MOBILE VIEW  | 

PLANTS-SOLANINE

Classification   |    Detailed evidence-based information

Therapeutic Toxic Class

    A) Solanine is a glycoalkaloid combination of an alkamine aglycone (solanidine) and a glycoside linkage to the sugars galactose, glucose, and rhamnose (Dalvi & Bowie, 1983).

Specific Substances

    1) SOLANUM TUBEROSUM/POTATO
    2) SOLANUM DULCAMARA/BITTERSWEET
    3) SOLANUM NIGRUM/BLACK NIGHTSHADE
    4) SOLANUM PSEUDOCAPSICUM/JERUSALEM CHERRY
    5) SOLANINE - PLANTS

Available Forms Sources

    A) SOURCES
    1) Found mainly in the Solanaceae plant family. Contained in such plants as potato, tomato, and eggplant. Related alkaloids such as solanocapsine (found in Jerusalem cherry) and chaconine (in green potatoes) (Eisen, 1988).
    2) CHACONINE (alpha): Differs from solanine because it has one glucose and two rhamnose sugars (Dalvi & Bowie, 1983).
    3) SOLANINE containing plants are found throughout the world. Solanine and related compounds are found in both food and non-food plants.

Life Support

    A) This overview assumes that basic life support measures have been instituted.

Clinical Effects

    0.2.1) SUMMARY OF EXPOSURE
    A) GENUS: Solanum. It is a very large genus with over 1700 species. Found mainly in the Solanaceae plant family; common species include Solanum americanum, S nigrum and the S nigrum complex (black nightshade, nightshade, poisonberry), S lycopersicum (tomato), S melongena (eggplant), S pseudocapiscum (Jerusalem cherry), S sodomeum (apple of sodom), Solanum tuberosum (the white potato; commonly cultivated vegetable). SPECIES: Solanine is contained in such common plants as potato, tomato, and eggplant. Related alkaloids include solanocapsine (found in Jerusalem cherry) and chaconine (in green potatoes).
    B) BACKGROUND: Solanine is a glycoalkaloid combination that contains an alkamine aglycone (solanidine) a glycoside (solanidine) and a glycoside linkage to the sugars galactose, glucose and rhamnose. Most plants coded to this management contain primarily solanine, but some may contain an anticholinergic. This has been reported historically, but there is very limited information describing human toxicity secondary to anticholinergic events. Solanine usually, but not always, dominates. If the patient develops evidence of anticholinergic toxicity see the PLANTS-ANTICHOLINERGIC management.
    C) PHARMACOLOGY: In animal studies, solanine is poorly absorbed from the gastrointestinal tract and is rapidly eliminated in the urine and feces.
    D) TOXICOLOGY: Solanine has weak cardiac activity, possibly due to its similar structure to other cardiac glycosides such as K-strophanthoside. It has been reported that solanine can inhibit cholinesterase activity in in vivo and in vitro studies but cholinergic effects (ie, bradycardia, sialorrhea ) were not observed in animal studies. The relationship to human toxicity is unknown. There have been rare reports of bradycardia following solanine poisoning. Solanine may inhibit hepatic microsomal enzymes. Similar to saponins, solanine can cause hemolytic and hemorrhagic damage to the gastrointestinal tract but these events have been reported infrequently in humans. Hemolysis has been noted in human, rat, and hamster cells after potato glycoalkaloids, there was no significant difference between species.
    E) EPIDEMIOLOGY: Exposure may occur but there are minimal reports of human cases in the medical literature with most cases reporting mild toxicity following ingestion of solanine. Parenteral exposure of solanine is considered very toxic.
    F) WITH POISONING/EXPOSURE
    1) MILD TO MODERATE TOXICITY: Solanine has a bitter taste and is irritating to the throat. The most common effects are nausea, vomiting, abdominal pain, diarrhea, and headache. Fever may be an early sign of poisoning. Drowsiness and fatigue may develop. Blurred vision can be present due to mydriasis from anticholinergic effects. INFREQUENT: Other neurological disturbances that have been reported infrequently include: confusion, weakness, hallucinations, apathy, agoraphobia, restlessness, and visual disturbances. Mild hypotension, muscular cramping, increased salivation and paresthesias are not common. ONSET: Most clinical effects are seen within 2 to 24 hours. In a small case series, the onset of GI symptoms occurred within 7 to 19 hours following the ingestion of a meal containing contaminated potatoes. In some cases, pain preceded other symptoms by 2 to 6 hours. DURATION: Gastrointestinal (ie, vomiting, diarrhea) symptoms may last 1 to 6 days.
    2) SEVERE TOXICITY: There are rare reports of severe toxicity following solanine exposure in humans. In severe cases, neurologic events may include: drowsiness, apathy, confusion, weakness, and hallucinations that may be followed by unconsciousness. CNS depression and coma are possible but not likely to occur. Bradycardia happens rarely and is primarily seen with solanocapsine. Tachycardia and other anticholinergic effects have been seen with nightshade berry poisoning. Both tachypnea and respiratory failure may occur; dyspnea leading to respiratory failure is possible but uncommon.
    0.2.3) VITAL SIGNS
    A) Fever may develop.
    0.2.5) CARDIOVASCULAR
    A) Solanocapsine has been shown to cause bradycardia. Mild hypotension may occur. Solanine may produce a positive inotropic effect. It has also caused significant tachycardia.
    0.2.20) REPRODUCTIVE
    A) Results of tests have been contradictory and may be due to variable absorption.
    B) HUMANS - Blighted potatoes were once implicated as a teratogenic agent causing neural tube defects. More recent experiments seem to have refuted these data, but considerable controversy still exists.
    0.2.21) CARCINOGENICITY
    A) At the time of this review, no data were available to assess the carcinogenic potential of this agent.

Laboratory Monitoring

    A) Few laboratories are able to identify solanine and related compounds; levels have no clinical significance.
    B) Electrolytes and renal function should be monitored in the setting of gastrointestinal symptoms.

Treatment Overview

    0.4.2) ORAL/PARENTERAL EXPOSURE
    A) MANAGEMENT OF MILD TO MODERATE TOXICITY
    1) Treatment is symptomatic and supportive. There is no specific antidote for solanine. Monitor fluids and electrolytes, if vomiting and diarrhea are extensive. Replace electrolytes as needed. Atropine is occasionally used to treat significant bradycardia.
    B) MANAGEMENT OF SEVERE TOXICITY
    1) Symptomatic and supportive treatment is the mainstay of solanine toxicity. Monitor vital signs and neurologic function. Severe gastrointestinal symptoms may produce fluid and electrolyte imbalances which should be monitored. Treat with IV fluids and electrolyte replacement as needed. Historically, it has been suggested that these plants may contain anticholinergics as well and patients should be monitored for these effects (eg, bradycardia, sialorrhea). However, this has been rarely reported in the literature. Physostigmine, if needed, should be reserved for life-threatening effects. Respiratory failure has rarely occurred late in the illness and should be managed supportively with intubation and ventilation as needed.
    C) DECONTAMINATION
    1) PREHOSPITAL: Consider prehospital administration of activated charcoal as an aqueous slurry in patients with a potentially toxic ingestion who are awake and able to protect their airway. However, activated charcoal is contraindicated, if the patient is already vomiting and/or the risk of aspiration may be present.
    2) HOSPITAL: Consider administration of activated charcoal in patients with a potentially toxic ingestion who are awake and able to protect their airway. Consider treating patients with solanine-like symptoms with activated charcoal even if they present 8 to 12 hours after exposure. Solanine is poorly absorbed; however, coingestion of atropine compounds may slow GI tract.
    D) AIRWAY MANAGEMENT
    1) Airway management is unlikely to be necessary following a mild to moderate exposure. Airway support including intubation and ventilation may be necessary following severe intoxication if the patient develops significant CNS effects or respiratory insufficiency. Respiratory failure has rarely occurred late in the course of illness.
    E) ANTIDOTE
    1) None.
    F) ENHANCED ELIMINATION
    1) Enhanced elimination is not anticipated to be necessary following exposure.
    G) PATIENT DISPOSITION
    1) HOME CRITERIA: Asymptomatic children (other than mild gastrointestinal symptoms) with an acute inadvertent ingestion may be monitored at home.
    2) OBSERVATION CRITERIA: Patients with deliberate ingestions and symptomatic patients should be sent to a health care facility for observation until symptoms are clearly improving.
    3) ADMISSION CRITERIA: Patients with significant persistent central nervous system toxicity (i.e., hallucinations, somnolence, coma) should be admitted. Patients with coma, seizures or delirium should be admitted to an intensive care setting.
    4) CONSULT CRITERIA: Consult a poison center or medical toxicologist for assistance in managing patients with severe toxicity (i.e, coma), or in whom the diagnosis is not clear.
    H) PHARMACOKINETICS
    1) The route of administration of solanine can influence potential toxicity (ie, parenteral administration more toxic compared to the oral route). Following oral exposure, solanine is poorly absorbed from the gastrointestinal tract. However, data indicates that uptake and alpha solanine absorption increases as the dose increases. Excretion is rapid from the fecal and urinary route as well as hydrolysis to the less toxic and poorly absorbed solanidine. There is significant variability among species in the development of toxicity. It appears that humans are more sensitive to the effects of solanine compared to animals. In a small case series, the onset of gastrointestinal symptoms occurred within 7 to 19 hours following ingestion of a meal containing contaminated potatoes. The duration of gastrointestinal (ie, vomiting, diarrhea) symptoms lasted 1 to 6 days. HUMANS: When 1 mg/kg was given via mashed potatoes, peak glycoalkaloid concentration of 6 to 21 nanograms/mL for chaconine and 3 to 11 nanograms/mL of solanine was seen at 4 to 8 hours postingestion.

Range Of Toxicity

    A) TOXIC DOSE: Minimum lethal human exposure is unknown. There is considerable species variation in toxicity. ESTIMATED TOXIC DOSE: 20 to 30 mg of solanine. ESTIMATED FATAL DOSE: 400 to 500 mg. Solanine is much more toxic via the parenteral route compared to an oral exposure.

Summary Of Exposure

    A) GENUS: Solanum. It is a very large genus with over 1700 species. Found mainly in the Solanaceae plant family; common species include Solanum americanum, S nigrum and the S nigrum complex (black nightshade, nightshade, poisonberry), S lycopersicum (tomato), S melongena (eggplant), S pseudocapiscum (Jerusalem cherry), S sodomeum (apple of sodom), Solanum tuberosum (the white potato; commonly cultivated vegetable). SPECIES: Solanine is contained in such common plants as potato, tomato, and eggplant. Related alkaloids include solanocapsine (found in Jerusalem cherry) and chaconine (in green potatoes).
    B) BACKGROUND: Solanine is a glycoalkaloid combination that contains an alkamine aglycone (solanidine) a glycoside (solanidine) and a glycoside linkage to the sugars galactose, glucose and rhamnose. Most plants coded to this management contain primarily solanine, but some may contain an anticholinergic. This has been reported historically, but there is very limited information describing human toxicity secondary to anticholinergic events. Solanine usually, but not always, dominates. If the patient develops evidence of anticholinergic toxicity see the PLANTS-ANTICHOLINERGIC management.
    C) PHARMACOLOGY: In animal studies, solanine is poorly absorbed from the gastrointestinal tract and is rapidly eliminated in the urine and feces.
    D) TOXICOLOGY: Solanine has weak cardiac activity, possibly due to its similar structure to other cardiac glycosides such as K-strophanthoside. It has been reported that solanine can inhibit cholinesterase activity in in vivo and in vitro studies but cholinergic effects (ie, bradycardia, sialorrhea ) were not observed in animal studies. The relationship to human toxicity is unknown. There have been rare reports of bradycardia following solanine poisoning. Solanine may inhibit hepatic microsomal enzymes. Similar to saponins, solanine can cause hemolytic and hemorrhagic damage to the gastrointestinal tract but these events have been reported infrequently in humans. Hemolysis has been noted in human, rat, and hamster cells after potato glycoalkaloids, there was no significant difference between species.
    E) EPIDEMIOLOGY: Exposure may occur but there are minimal reports of human cases in the medical literature with most cases reporting mild toxicity following ingestion of solanine. Parenteral exposure of solanine is considered very toxic.
    F) WITH POISONING/EXPOSURE
    1) MILD TO MODERATE TOXICITY: Solanine has a bitter taste and is irritating to the throat. The most common effects are nausea, vomiting, abdominal pain, diarrhea, and headache. Fever may be an early sign of poisoning. Drowsiness and fatigue may develop. Blurred vision can be present due to mydriasis from anticholinergic effects. INFREQUENT: Other neurological disturbances that have been reported infrequently include: confusion, weakness, hallucinations, apathy, agoraphobia, restlessness, and visual disturbances. Mild hypotension, muscular cramping, increased salivation and paresthesias are not common. ONSET: Most clinical effects are seen within 2 to 24 hours. In a small case series, the onset of GI symptoms occurred within 7 to 19 hours following the ingestion of a meal containing contaminated potatoes. In some cases, pain preceded other symptoms by 2 to 6 hours. DURATION: Gastrointestinal (ie, vomiting, diarrhea) symptoms may last 1 to 6 days.
    2) SEVERE TOXICITY: There are rare reports of severe toxicity following solanine exposure in humans. In severe cases, neurologic events may include: drowsiness, apathy, confusion, weakness, and hallucinations that may be followed by unconsciousness. CNS depression and coma are possible but not likely to occur. Bradycardia happens rarely and is primarily seen with solanocapsine. Tachycardia and other anticholinergic effects have been seen with nightshade berry poisoning. Both tachypnea and respiratory failure may occur; dyspnea leading to respiratory failure is possible but uncommon.

Vital Signs

    3.3.1) SUMMARY
    A) Fever may develop.
    3.3.3) TEMPERATURE
    A) FEVER: An elevated body temperature may be an early sign of poisoning with solanine (McMillan & Thompson, 1979) (Willimott, 1933).
    1) CASE REPORT: A 4-year-old who ingested an estimated 50 Solanum dulcamara berries had a temperature of 103 degrees F upon arrival to the emergency department. Anticholinergic signs predominated in this exposure (Ceha et al, 1997).

Heent

    3.4.3) EYES
    A) Visual disturbances, such as blurred vision, were reported after poisonings by these plants (Slanina, 1990).
    B) Ingestion of approximately 50 Solanum dulcamara berries produced dilated pupils in a 4-year-old. Anticholinergic signs predominated in this exposure (Ceha et al, 1997).

Cardiovascular

    3.5.1) SUMMARY
    A) Solanocapsine has been shown to cause bradycardia. Mild hypotension may occur. Solanine may produce a positive inotropic effect. It has also caused significant tachycardia.
    3.5.2) CLINICAL EFFECTS
    A) BRADYCARDIA
    1) WITH POISONING/EXPOSURE
    a) Bradycardia is rarely seen, primarily with solanocapsine.
    b) Volunteers given 60 to 84 mg of solanocapsine IV developed bradycardia for 30 minutes (Watt, 1932).
    B) TACHYCARDIA
    1) WITH POISONING/EXPOSURE
    a) In one study, rapid, weak pulse was reported following severe cases of solanine poisoning (McMillan & Thompson, 1979).
    C) TACHYARRHYTHMIA
    1) WITH POISONING/EXPOSURE
    a) Significant tachycardia along with other anticholinergic effects were reported in one case of nightshade berry poisoning (Ceha et al, 1997).
    b) CASE REPORT: Ingestion of Solanum dulcamara berries (estimated 50 berries) produced anticholinergic symptoms and tachycardia in a 4-year-old child. Heart rate ranged between 160 and 190 beats/min (Ceha et al, 1997).
    D) ELECTROCARDIOGRAM ABNORMAL
    1) WITH POISONING/EXPOSURE
    a) POSITIVE INOTROPIC ACTIONS: May occur due to solanine's similarity to cardiac glycosides.
    E) HYPOTENSIVE EPISODE
    1) WITH POISONING/EXPOSURE
    a) Mild hypotension has been reported in both animal and human poisonings (McMillan & Thompson, 1979; Slanina, 1990a).
    b) HUMAN EXPERIMENTS: Doses of 60 to 84 mg of solanocapsine IV produced a drop in systolic blood pressure for 30 minutes (Watt, 1932).
    3.5.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) BRADYCARDIA
    a) Solanocapsine has shown a marked slowing of pacemaker impulse formation in animals given intravenous, oral, or subcutaneous doses. Cardiac impulse propagation slowing was also seen (Watt, 1930; Watt, 1932).
    2) ECG ABNORMAL
    a) Positive inotropic action was reported on the isolated frog ventricle (Nishie et al, 1971).

Respiratory

    3.6.2) CLINICAL EFFECTS
    A) TACHYPNEA
    1) WITH POISONING/EXPOSURE
    a) Tachypnea has been reported. Dyspnea leading to respiratory failure is possible but uncommon (McMillan & Thompson, 1979).

Neurologic

    3.7.2) CLINICAL EFFECTS
    A) CENTRAL NERVOUS SYSTEM DEFICIT
    1) WITH POISONING/EXPOSURE
    a) In severe cases, neurologic events may include apathy, confusion, weakness, and hallucinations that may be followed by unconsciousness following solanine poisoning (Slanina, 1990a).
    B) DROWSY
    1) WITH POISONING/EXPOSURE
    a) Drowsiness may progress to significant CNS depression (Willimott, 1933).
    b) CASE REPORT: In one ingestion of approximately 50 Solanum dulcamara berries in a 4-year-old, lethargy was noted. Anticholinergic effects predominated (Ceha et al, 1997).
    C) HEADACHE
    1) Headache has been reported (Willimott, 1933) (Geehr, 1984). Headache has frequently accompanied the onset of gastrointestinal symptoms following solanine poisoning (McMillan & Thompson, 1979).
    D) PARESTHESIA
    1) WITH POISONING/EXPOSURE
    a) Solanocapsine poisoning may cause paresthesias (Geehr, 1984).
    E) FATIGUE
    1) WITH POISONING/EXPOSURE
    a) Weakness has been reported following solanine poisoning (Glover & Harmer, 2014; Slanina, 1990).
    F) NEUROPATHY
    1) WITH POISONING/EXPOSURE
    a) Other neurological disturbances sometimes reported include confusion, weakness, hallucinations, apathy, agoraphobia, restlessness, and visual disturbances (Frohne & Pfander, 1984).
    3.7.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) CNS DEPRESSION
    a) ANIMAL EXPERIMENTS: Death due to CNS depression was reported in rabbits (Nishie et al, 1971).
    b) Although reported infrequently, there have been reports of a nervous system type of toxicity that included stupor, depression, dullness, prostration and total indifference to the environment observed in animals (eg, horses, cattle, pigs and poultry) (Dalvi & Bowie, 1983a).

Gastrointestinal

    3.8.2) CLINICAL EFFECTS
    A) VOMITING
    1) WITH POISONING/EXPOSURE
    a) Nausea, vomiting, and abdominal pain are likely the most common findings after solanine ingestion (McMillan & Thompson, 1979; Eisen, 1988; Glover & Harmer, 2014) (Willimott, 1933) .
    b) Of 17 boys requiring hospitalization for solanine toxicity, vomiting and diarrhea developed 7 to 19 hours following the ingestion of a meal containing contaminated potatoes. In some cases, pain preceded other symptoms by 2 to 6 hours (McMillan & Thompson, 1979)
    B) DIARRHEA
    1) WITH POISONING/EXPOSURE
    a) Diarrhea is a common finding after solanine ingestion; blood and mucus may be present (McMillan & Thompson, 1979; Eisen, 1988). Of 17 boys requiring hospitalization for solanine toxicity, vomiting and diarrhea developed 7 to 19 hours following the ingestion of a meal containing contaminated potatoes. In some cases, pain preceded other symptoms by 2 to 6 hours (McMillan & Thompson, 1979).
    b) DURATION: Gastrointestinal (ie, vomiting, diarrhea) symptoms may last 1 to 6 days (McMillan & Thompson, 1979).
    C) EXCESSIVE SALIVATION
    1) WITH POISONING/EXPOSURE
    a) Excessive salivation may occur with solanocapsine poisoning (Geehr, 1984).

Hematologic

    3.13.2) CLINICAL EFFECTS
    A) HEMOLYSIS
    1) WITH POISONING/EXPOSURE
    a) Twenty micromoles of chaconine causes lysis of human erythrocytes in vitro (Roddick & Leonard, 1999). Addition of 0.5 millimoles of glucose-6-phosphate decreased the inhibition, and NADP reduced lysis. One millimole of either caused about a 50% inhibition of this effect.
    b) ANIMAL STUDIES: An oral mixture of alpha-solanine and alpha chaconine (1:1), was given to hamsters at doses of up to 50 mg/kg with no effect, but an intraperitoneal injection of 25 mg/kgor greater produced lethal bleeding in the gut of hamsters (Phillips et al, 1996).

Dermatologic

    3.14.2) CLINICAL EFFECTS
    A) EXCESSIVE SWEATING
    1) WITH POISONING/EXPOSURE
    a) Diaphoresis may occur in conjunction with elevated body temperature (Willimott, 1933).

Musculoskeletal

    3.15.2) CLINICAL EFFECTS
    A) INCREASED MUSCLE TONE
    1) WITH POISONING/EXPOSURE
    a) Muscle cramps may occur after solanocapsine ingestion.
    B) MUSCLE PAIN
    1) WITH THERAPEUTIC USE
    a) CASE REPORT: A 54-year-old woman prepared a meal containing a large number of susumber (Solanum torvum) berries (boiled prior to eating) and the next morning she developed nausea and vomiting, changes in her vision, speech, gait and diffuse myalgias along with difficulty ambulating and slurring of her speech. She was transported to the ED and found to have normal mentation but had developed miosis, opsoclonus, severe dysarthria, dysmetria, mild upper and lower extremity tenderness, weakness, and an inability to walk. Laboratory and diagnostic (ie, MRI and cerebrospinal fluid) studies were within normal limits. An electromyogram and nerve conduction studies were performed and indicated spontaneous activity, an early full recruitment pattern, and myotonia consistent with features of toxic myopathy. Following symptomatic care, the patient was discharged to home on day 3 with no further symptoms. Upon follow-up one month later, she had no recurrent symptoms. Serum analysis was positive for the toxic alkaloids solasodine and solanidine which decreased rapidly and followed her clinical improvement (Glover & Harmer, 2014).

Reproductive

    3.20.1) SUMMARY
    A) Results of tests have been contradictory and may be due to variable absorption.
    B) HUMANS - Blighted potatoes were once implicated as a teratogenic agent causing neural tube defects. More recent experiments seem to have refuted these data, but considerable controversy still exists.
    3.20.2) TERATOGENICITY
    A) CONGENITAL ANOMALY
    1) SUMMARY - Results of tests have been contradictory and may be due to variable absorption.
    2) HUMANS - Blighted potatoes were once implicated as a teratogenic agent causing neural tube defects. Some recent experiments seem to have refuted this, but considerable controversy still exists (Anon, 1975; Hopkins, 1995).
    a) The steroidal glycosides found in potatoes are inhibitors of acetylcholinesterase (AchE) and butyrylcholinesterase (BuChE), both of which are produced by human embryos during the early states of embriogenesis to attenuate the effects of xenobiotics via hydrolysis or sequesteration. BuChE is found primarily in the first trimester, AchE in the last trimester. The effect of the inhibition of these enzymes is unknown in humans (Morris & Lee, 1984; Massoulie et al, 1993; Nigg et al, 1996; Sternfeld et al, 1997; Brimijoin & Koenigsberger, 1999) Lauder & Schamber, 1999).
    b) It is possible that anencephaly and spina bifida are due to a yet unidentified substance in certain potato tubers (Renwick, 1972).
    3) ANIMALS - Solanidine-type alkaloids are known to induce malformations in hamsters (Keeler et al, 1976) 1978).
    a) HAMSTERS/POTATOES - Potato sprouts induced a 24% deformed litter incidence rate in hamsters (Keeler et al, 1990).

Carcinogenicity

    3.21.2) SUMMARY/HUMAN
    A) At the time of this review, no data were available to assess the carcinogenic potential of this agent.
    3.21.3) HUMAN STUDIES
    A) LACK OF INFORMATION
    1) At the time of this review, no data were available to assess the carcinogenic potential of this agent.

Monitoring Parameters Levels

    4.1.1) SUMMARY
    A) Few laboratories are able to identify solanine and related compounds; levels have no clinical significance.
    B) Electrolytes and renal function should be monitored in the setting of gastrointestinal symptoms.
    4.1.2) SERUM/BLOOD
    A) BLOOD/SERUM CHEMISTRY
    1) No specific tests are indicated. Levels are not useful. Clinical evaluation plus history is most important.
    2) Severe gastrointestinal symptoms may produce fluid and electrolyte imbalances which should be monitored and treated with appropriate intravenous fluids (Eisen, 1988).

Methods

    A) OTHER
    1) Few laboratories are capable of identifying solanine or solanocapsine.
    B) HIGH PERFORMANCE LIQUID-CHROMATOGRAPHY
    1) Identification of solanine and chaconine in blood serum samples has been performed by high-performance liquid chromatography (HPLC) (Hellanas, 1992).
    C) LIQUID CHROMATOGRAPHY/MASS SPECTROMETRY
    1) CASE REPORT: A 54-year-old woman prepared a meal containing a large number of susumber (Solanum torvum) berries that were boiled prior to consumption. The next morning she developed nausea and vomiting, changes in her vision, speech, gait and diffuse myalgias along with difficulty ambulating and slurring of her speech. An electromyogram and nerve conduction studies were performed and indicated spontaneous activity, an early full recruitment pattern, and myotonia consistent with features of toxic myopathy. Serum analysis was positive for the toxic alkaloids solasodine and solanidine, which decreased rapidly and followed her clinical improvement with supportive care. Leftover berries were analyzed using liquid chromatography-mass spectometry and various solanaceous glycoalkaloids (ie, solasonine, solamargine, solanine, and chaconine and associated free alkaloids, solasodine and/or solanidine) were detected (Glover & Harmer, 2014).

Life Support

    A) Support respiratory and cardiovascular function.

Patient Disposition

    6.3.1) DISPOSITION/ORAL EXPOSURE
    6.3.1.1) ADMISSION CRITERIA/ORAL
    A) Patients with significant persistent central nervous system toxicity (i.e., hallucinations, somnolence, coma) should be admitted. Patients with coma, seizures or delirium should be admitted to an intensive care setting.
    6.3.1.2) HOME CRITERIA/ORAL
    A) Asymptomatic children (other than mild gastrointestinal symptoms) with an acute inadvertent ingestion may be monitored at home.
    6.3.1.3) CONSULT CRITERIA/ORAL
    A) Consult a poison center or medical toxicologist for assistance in managing patients with severe toxicity (i.e, coma), or in whom the diagnosis is not clear.
    6.3.1.5) OBSERVATION CRITERIA/ORAL
    A) Patients with deliberate ingestions and symptomatic patients should be sent to a health care facility for observation until symptoms are clearly improving.

Monitoring

    A) Few laboratories are able to identify solanine and related compounds; levels have no clinical significance.
    B) Electrolytes and renal function should be monitored in the setting of gastrointestinal symptoms.

Oral Exposure

    6.5.1) PREVENTION OF ABSORPTION/PREHOSPITAL
    A) ACTIVATED CHARCOAL
    1) PREHOSPITAL ACTIVATED CHARCOAL ADMINISTRATION
    a) Consider prehospital administration of activated charcoal as an aqueous slurry in patients with a potentially toxic ingestion who are awake and able to protect their airway. Activated charcoal is most effective when administered within one hour of ingestion. Administration in the prehospital setting has the potential to significantly decrease the time from toxin ingestion to activated charcoal administration, although it has not been shown to affect outcome (Alaspaa et al, 2005; Thakore & Murphy, 2002; Spiller & Rogers, 2002).
    1) In patients who are at risk for the abrupt onset of seizures or mental status depression, activated charcoal should not be administered in the prehospital setting, due to the risk of aspiration in the event of spontaneous emesis.
    2) The addition of flavoring agents (cola drinks, chocolate milk, cherry syrup) to activated charcoal improves the palatability for children and may facilitate successful administration (Guenther Skokan et al, 2001; Dagnone et al, 2002).
    2) CHARCOAL DOSE
    a) Use a minimum of 240 milliliters of water per 30 grams charcoal (FDA, 1985). Optimum dose not established; usual dose is 25 to 100 grams in adults and adolescents; 25 to 50 grams in children aged 1 to 12 years (or 0.5 to 1 gram/kilogram body weight) ; and 0.5 to 1 gram/kilogram in infants up to 1 year old (Chyka et al, 2005).
    1) Routine use of a cathartic with activated charcoal is NOT recommended as there is no evidence that cathartics reduce drug absorption and cathartics are known to cause adverse effects such as nausea, vomiting, abdominal cramps, electrolyte imbalances and occasionally hypotension (None Listed, 2004).
    b) ADVERSE EFFECTS/CONTRAINDICATIONS
    1) Complications: emesis, aspiration (Chyka et al, 2005). Aspiration may be complicated by acute respiratory failure, ARDS, bronchiolitis obliterans or chronic lung disease (Golej et al, 2001; Graff et al, 2002; Pollack et al, 1981; Harris & Filandrinos, 1993; Elliot et al, 1989; Rau et al, 1988; Golej et al, 2001; Graff et al, 2002). Refer to the ACTIVATED CHARCOAL/TREATMENT management for further information.
    2) Contraindications: unprotected airway (increases risk/severity of aspiration) , nonfunctioning gastrointestinal tract, uncontrolled vomiting, and ingestion of most hydrocarbons (Chyka et al, 2005).
    6.5.2) PREVENTION OF ABSORPTION
    A) SUMMARY
    1) Consider administration of activated charcoal in patients with a potentially toxic ingestion who are awake and able to protect their airway. Consider treating patients with solanine-like symptoms with activated charcoal even if they present 8 to 12 hours after exposure. Solanine is poorly absorbed; however, coingestion of atropine compounds may slow GI tract.
    B) ACTIVATED CHARCOAL
    1) CHARCOAL ADMINISTRATION
    a) Consider administration of activated charcoal after a potentially toxic ingestion (Chyka et al, 2005). Administer charcoal as an aqueous slurry; most effective when administered within one hour of ingestion.
    2) CHARCOAL DOSE
    a) Use a minimum of 240 milliliters of water per 30 grams charcoal (FDA, 1985). Optimum dose not established; usual dose is 25 to 100 grams in adults and adolescents; 25 to 50 grams in children aged 1 to 12 years (or 0.5 to 1 gram/kilogram body weight) ; and 0.5 to 1 gram/kilogram in infants up to 1 year old (Chyka et al, 2005).
    1) Routine use of a cathartic with activated charcoal is NOT recommended as there is no evidence that cathartics reduce drug absorption and cathartics are known to cause adverse effects such as nausea, vomiting, abdominal cramps, electrolyte imbalances and occasionally hypotension (None Listed, 2004).
    b) ADVERSE EFFECTS/CONTRAINDICATIONS
    1) Complications: emesis, aspiration (Chyka et al, 2005). Aspiration may be complicated by acute respiratory failure, ARDS, bronchiolitis obliterans or chronic lung disease (Golej et al, 2001; Graff et al, 2002; Pollack et al, 1981; Harris & Filandrinos, 1993; Elliot et al, 1989; Rau et al, 1988; Golej et al, 2001; Graff et al, 2002). Refer to the ACTIVATED CHARCOAL/TREATMENT management for further information.
    2) Contraindications: unprotected airway (increases risk/severity of aspiration) , nonfunctioning gastrointestinal tract, uncontrolled vomiting, and ingestion of most hydrocarbons (Chyka et al, 2005).
    6.5.3) TREATMENT
    A) SUPPORT
    1) MANAGEMENT OF MILD TO MODERATE TOXICITY
    a) Treatment is symptomatic and supportive. There is no specific antidote for solanine. Monitor fluids and electrolytes, if vomiting and diarrhea are extensive. Replace electrolytes as needed. Atropine is occasionally used to treat significant bradycardia.
    2) MANAGEMENT OF SEVERE TOXICITY
    a) Symptomatic and supportive treatment is the mainstay of solanine toxicity. Monitor vital signs and neurologic function. Severe gastrointestinal symptoms may produce fluid and electrolyte imbalances which should be monitored. Treat with IV fluids and electrolyte replacement as needed. Historically, it has been suggested that these plants may contain anticholinergics as well and patients should be monitored for these effects (eg, bradycardia, sialorrhea). However, this has been rarely reported in the literature. Physostigmine, if needed, should be reserved for life-threatening effects. Respiratory failure has rarely occurred late in the illness and should be managed supportively with intubation and ventilation as needed
    B) MONITORING OF PATIENT
    1) Few laboratories are able to identify solanine and related compounds; levels have no clinical significance. Routine laboratory studies are not indicated following a mild exposure. Electrolytes and renal function should be monitored in the setting of moderate to severe gastrointestinal symptoms (ie, vomiting, diarrhea).
    C) FLUID/ELECTROLYTE BALANCE REGULATION
    1) SUMMARY: Severe gastrointestinal symptoms may produce fluid and electrolyte imbalances which should be monitored and treated with appropriate intravenous fluids. Replace electrolytes as needed. (Eisen, 1988).
    D) AIRWAY MANAGEMENT
    1) Respiratory failure has rarely occurred late in the course of an illness. Provide respiratory support when necessary.
    E) PHYSOSTIGMINE
    1) Based on limited human cases of solanine exposure, physostigmine is unlikely to be necessary. Most clinical events are self-limited and are more likely to produce gastrointestinal events (Slanina, 1990; Dalvi & Bowie, 1983a; McMillan & Thompson, 1979).
    2) PRECAUTIONS: Some ingestions may have mixed solanine and anticholinergic effects (Ceha et al, 1997). Administration of physostigmine may increase masked solanine symptoms. Physostigmine is not indicated unless there are life-threatening anticholinergic effects.
    3) CASE REPORT: Following a large nightshade ingestion a 4-year-old girl presented to an ED in acute anticholinergic crisis. The child received an initial dose of 0.2 mg of intravenous physostigmine (0.02 mg/kg) along with two additional equivalent doses with complete resolution of symptoms (Ceha et al, 1997).
    4) PHYSOSTIGMINE/INDICATIONS
    a) Physostigmine is indicated to reverse the CNS effects caused by clinical or toxic dosages of agents capable of producing anticholinergic syndrome; however, long lasting reversal of anticholinergic signs and symptoms is generally not achieved because of the relatively short duration of action of physostigmine (45 to 60 minutes) (Prod Info physostigmine salicylate intravenous injection, intramuscular injection, 2008). It is most often used diagnostically to distinguish anticholinergic delirium from other causes of altered mental status (Frascogna, 2007; Shannon, 1998).
    b) Physostigmine should not be used in patients with suspected tricyclic antidepressant overdose, or an ECG suggestive of tricyclic antidepressant overdose (eg, QRS widening). In the setting of tricyclic antidepressant overdose, use of physostigmine has precipitated seizures and intractable cardiac arrest (Stewart, 1979; Newton, 1975; Pentel & Peterson, 1980; Frascogna, 2007).
    5) DOSE
    a) ADULT: BOLUS: 2 mg IV at slow controlled rate, no more than 1 mg/min. May repeat doses at intervals of 10 to 30 min, if severe symptoms recur (Prod Info physostigmine salicylate intravenous injection, intramuscular injection, 2008). INFUSION: For patients with prolonged anticholinergic delirium, a continuous infusion of physostigmine may be considered. Starting dose is 2 mg/hr, titrate to effect (Eyer et al, 2008)
    b) CHILD: 0.02 mg/kg by slow IV injection, at a rate no more than 0.5 mg/minute. Repeat dosage at 5 to 10 minute intervals as long as the toxic effect persists and there is no sign of cholinergic effects. MAXIMUM DOSAGE: 2 mg total (Prod Info physostigmine salicylate intravenous injection, intramuscular injection, 2008).
    c) AVAILABILITY: Physostigmine salicylate is available in 2 mL ampules, each mL containing 1 mg of physostigmine salicylate in a vehicle containing sodium metabisulfite 0.1%, benzyl alcohol 2%, and water (Prod Info physostigmine salicylate intravenous injection, intramuscular injection, 2008).
    6) CAUTIONS
    a) Relative contraindications to the use of physostigmine are asthma, gangrene, diabetes, cardiovascular disease, intestinal or urogenital tract mechanical obstruction, peripheral vascular disease, cardiac conduction defects, atrioventricular block, and in patients receiving choline esters and depolarizing neuromuscular blocking agents (decamethonium, succinylcholine). It may cause anaphylactic symptoms and life-threatening or less severe asthmatic episodes in patients with sulfite sensitivity (Prod Info physostigmine salicylate intravenous injection, intramuscular injection, 2008).
    b) Too rapid IV administration of physostigmine has resulted in bradycardia, hypersalivation leading to respiratory difficulties, and possible seizures (Prod Info physostigmine salicylate intravenous injection, intramuscular injection, 2008).
    7) ATROPINE FOR PHYSOSTIGMINE TOXICITY
    a) Atropine should be available to reverse life-threatening physostigmine-induced, toxic cholinergic effects (Prod Info physostigmine salicylate intravenous injection, intramuscular injection, 2008; Frascogna, 2007). Atropine may be given at half the dose of previously given physostigmine dose (Daunderer, 1980).
    F) BRADYCARDIA
    1) Bradycardia has been infrequently reported following solanine exposure. Monitor vital signs. Atropine may be indicated to treat significant solanocapsine induced bradycardia.
    a) ATROPINE/DOSE
    1) ADULT BRADYCARDIA: BOLUS: Give 0.5 milligram IV, repeat every 3 to 5 minutes, if bradycardia persists. Maximum: 3 milligrams (0.04 milligram/kilogram) intravenously is a fully vagolytic dose in most adults. Doses less than 0.5 milligram may cause paradoxical bradycardia in adults (Neumar et al, 2010).
    2) PEDIATRIC DOSE: As premedication for emergency intubation in specific situations (eg, giving succinylchoine to facilitate intubation), give 0.02 milligram/kilogram intravenously or intraosseously (0.04 to 0.06 mg/kg via endotracheal tube followed by several positive pressure breaths) repeat once, if needed (de Caen et al, 2015; Kleinman et al, 2010). MAXIMUM SINGLE DOSE: Children: 0.5 milligram; adolescent: 1 mg.
    a) There is no minimum dose (de Caen et al, 2015).
    b) MAXIMUM TOTAL DOSE: Children: 1 milligram; adolescents: 2 milligrams (Kleinman et al, 2010).

Enhanced Elimination

    A) SUMMARY
    1) Enhanced elimination is unlikely to be necessary following exposure.

Summary

    A) TOXIC DOSE: Minimum lethal human exposure is unknown. There is considerable species variation in toxicity. ESTIMATED TOXIC DOSE: 20 to 30 mg of solanine. ESTIMATED FATAL DOSE: 400 to 500 mg. Solanine is much more toxic via the parenteral route compared to an oral exposure.

Minimum Lethal Exposure

    A) SUMMARY
    1) The oral toxic dose of solanidine alkaloids for humans is unknown (McMillan & Thompson, 1979).
    2) Based on older data, a suggested lethal dose range is 3 to 6 mg total glycoalkaloids/kilogram body weight. However, the results of older epidemiologic studies are difficult to evaluate (Slanina, 1990).
    3) Estimated fatal dose is less than 400 to 500 mg (Moeschlin, 1980).

Maximum Tolerated Exposure

    A) SUMMARY
    1) There is considerable species variation in toxicity. Solanine is much more toxic via the parenteral route compared to an oral exposure (Dalvi & Bowie, 1983a).
    2) In humans, oral doses of 2.8 mg/kg caused hyperesthesia, drowsiness, itching, and dyspnea while higher doses caused nausea and vomiting in humans (Dalvi & Bowie, 1983a)
    3) SOLANINE ESTIMATED TOXIC DOSE: 20 to 30 mg of solanine (Moeschlin, 1980). An estimated 2 to 5 milligrams glycol alkaloids per kilogram body weight has also been suggested (Slanina, 1990).
    B) SPECIFIC SUBSTANCE
    1) SOLANUM TUBEROSUM/POTATOES
    a) Solanine content greater than 0.02 percent is considered toxic for man (Sapeika, 1969).
    b) Most commercially grown potatoes from the US and Europe have total alkaloid levels of 20 to 150 mg/kg (0.002 to 0.015%) of unpeeled tuber. There is considerable variation (Slanina, 1990).
    2) SOLANUM DULCAMARA/BITTERSWEET
    a) SUMMARY: Up to 10 berries may be taken without significant effects. Toxicity is highly dependent on erratic absorption. The intraperitoneal LD50 in mice may be 42 mg/kg, but doses of up to 1000 mg/kg have been tolerated.
    b) HUMAN TOXIC DOSE: If the maximum fresh weight of a berry is 0.4 g and maximum alkaloid content is assumed, approximately 10 berries could be ingested without symptoms. A fatal dose would be nearly 200 berries (Frohne & Pfander, 1984).
    3) SOLANUM NIGRUM/BLACK NIGHTSHADE
    a) SUMMARY: Up to 2 or 3 green berries may be taken without significant symptoms.
    b) HUMAN TOXIC DOSE: If the maximum fresh weight of a berry is 0.4 g, and maximum alkaloid content from a green berry of a solanine-producing hybrid is used, 2 to 3 berries may be taken without serious symptoms (Frohne & Pfander, 1984).
    4) SOLANUM PSEUDOCAPSICUM/JERUSALEM CHERRY
    a) SUMMARY: There are few case reports, so a specific toxic dose is not available. There is little difference in toxicity due to ripeness of the fruit (der Marderosian et al, 1976).
    b) HUMAN TOXIC DOSE: A "few" berries produced mydriasis, drowsiness, and gastroenteritis (Frohne & Pfander, 1984; Brugsch & Klimmer, 1966).
    5) CESTRUM SPECIES/JESSAMINE
    a) Produces solanine poisoning when the berries are unripe, and anticholinergic poisoning when ripe.

Toxicity Information

    7.7.1) TOXICITY VALUES
    A) LD50- (INTRAPERITONEAL)MOUSE:
    1) 32 to 42 mg/kg (Dalvi & Bowie, 1983)
    B) LD50- (INTRAPERITONEAL)RAT:
    1) 75 mg/kg (Dalvi & Bowie, 1983)
    C) LD50- (ORAL)RAT:
    1) 590 mg/kg (Dalvi & Bowie, 1983)

Toxicologic Mechanism

    A) CARDIAC ACTIVITY: Solanine has weak cardiac activity, possibly due to its similarity in structure to cardiac glycosides such as K-strophanthoside (Nishie et al, 1971).
    B) HEPATIC ACTIVITY: Solanine may inhibit hepatic microsomal enzymes (Dalvi & Peeples, 1981; Lahiri et al, 1966).
    C) CHOLINESTERASE ACTIVITY: Both alpha chaconine and alpha solanine inhibits blood and brain cholinesterases in test animals. The relationship to toxicity is unknown (Alozie et al, 1978).
    D) HEMOLYSIS: Similar to saponins, solanine causes hemolytic and hemorrhagic damage to the gastrointestinal tract (Dalvi & Bowie, 1983). Lethal doses of these alkaloids have a disruptive effect on gastrointestinal tract membranes (Morris & Lee, 1984). Hemolysis has been noted in human, rat, and hamster cells after potato glycoalkaloids, there was no significant difference between species (Phillips et al, 1996).
    E) CYTOTOXICITY: Glycoalkaloids from the potato were found to be cytotoxic to Chinese hamster ovary cells (Phillips et al, 1996).

Physical Characteristics

    A) Solanine has a bitter taste and is irritating to the throat (Dalvi & Bowie, 1983).

Molecular Weight

    A) Solanine: 868

Clinical Effects

    11.1.1) AVIAN/BIRD
    A) POULTRY -
    1) Solanine poisoning may be characterized by CNS depression, dullness, indifference to the environment, prostration, and stupor (Clarke & Clarke, 1975).
    11.1.2) BOVINE/CATTLE
    A) Solanine poisoning may be characterized by CNS depression, dullness, indifference to the environment, prostration, and stupor (Clarke & Clarke, 1975).
    B) Ulcerative stomatitis, conjunctivitis, vesticular and scurfy eczema of the legs, and diarrhea have also been seen (Clarke & Clarke, 1975).
    C) Postmortem examination shows gastroenteritis and congestion of the cerebral membranes and kidneys (Dalvi & Bowie, 1983).
    11.1.5) EQUINE/HORSE
    A) Solanine poisoning may be characterized by CNS depression, dullness, indifference to the environment, prostration, and stupor (Clarke & Clarke, 1975).
    11.1.10) PORCINE/SWINE
    A) Solanine poisoning may be characterized by CNS depression, dullness, indifference to the environment, prostration, and stupor (Clarke & Clarke, 1975).
    B) Ulcerative stomatitis, conjunctivitis, vesticular and scurfy eczema of the legs, and diarrhea have also been seen (Clarke & Clarke, 1975).
    C) Postmortem examination shows gastroenteritis and congestion of the cerebral membranes and kidneys (Dalvi & Bowie, 1983).

General Bibliography

    1) Alaspaa AO, Kuisma MJ, Hoppu K, et al: Out-of-hospital administration of activated charcoal by emergency medical services. Ann Emerg Med 2005; 45:207-12.
    2) Alozie SO, Sharma RP, & Salunkhe DK: Inhibition of rat cholinesterase isoenzymes in vitro and in vivo by the potato alkaloid, a-chaconine. J Fd Biochem 1978; 2:259-276.
    3) Anon: End of the potato avoidance hypothesis. Br Med J 1975; 4:308-309.
    4) Brimijoin S & Koenigsberger C: Cholinesterase in neural development: new findings and toxicologic implication. Environ Health Perspect 1999; 107(suppl 1):59-64.
    5) Brugsch H & Klimmer OR: Vergiftungen im Kindsalter, 2nd ed, F Enke, Stuttgart, Germany, 1966, pp 438.
    6) Ceha LJ, Presperin C, & Young E: Anticholinergic toxicity from nightshade berry poisoning responsive to physostigmine. J Emerg Med 1997; 15:65-69.
    7) Chyka PA, Seger D, Krenzelok EP, et al: Position paper: Single-dose activated charcoal. Clin Toxicol (Phila) 2005; 43(2):61-87.
    8) Clarke EGG & Clarke ML: Veterinary Toxicology, 1st ed, Williams & Williams Co, Baltimore, MD, 1975, pp 359-360.
    9) Coxon DT: The glycoalkaloid content of potato berries. J Sci food Agric 1981; 32:412-414.
    10) Dagnone D, Matsui D, & Rieder MJ: Assessment of the palatability of vehicles for activated charcoal in pediatric volunteers. Pediatr Emerg Care 2002; 18:19-21.
    11) Dalvi RR & Bowie WC: Toxicology of solanine: an overview. Vet Hum Toxicol 1983; 25:13-15.
    12) Dalvi RR & Bowie WC: Toxicology of solanine: an overview. Vet Hum Toxicol 1983a; 25(1):13-15.
    13) Dalvi RR & Peeples A: In vitro effect of toxic alkaloids on drug metabolism. J Pharm Pharmacol 1981; 33:51-53.
    14) Daunderer M: Physostigmine salicylate as an antidote. Int J Clin Pharmacol Ther Toxicol 1980; 18(12):523-535.
    15) Eisen T: Plant alkaloid. Clin Toxicol Rev 1988; 11:1-2.
    16) Elliot CG, Colby TV, & Kelly TM: Charcoal lung. Bronchiolitis obliterans after aspiration of activated charcoal. Chest 1989; 96:672-674.
    17) Eyer F, Jetzinger E, Pfab R, et al: Withdrawal from high-dose tranylcypromine. Clin Toxicol (Phila) 2008; 46(3):261-263.
    18) FDA: Poison treatment drug product for over-the-counter human use; tentative final monograph. FDA: Fed Register 1985; 50:2244-2262.
    19) Frascogna N: Physostigmine: is there a role for this antidote in pediatric poisonings?. Curr Opin Pediatr 2007; 19(2):201-205.
    20) Frohne D & Pfander HJ: A Colour Atlas of Poisonous Plants, Wolfe Publishing Ltd, London, England, 1984.
    21) Geehr E: Common toxic plant ingestions. Emerg Med Clin N Amer 1984; 2:553-562.
    22) Glover D & Harmer V: Radiotherapy-induced skin reactions: assessment and management. Br J Nurs 2014; 23(4):S28, S30- S35.
    23) Golej J, Boigner H, Burda G, et al: Severe respiratory failure following charcoal application in a toddler. Resuscitation 2001; 49:315-318.
    24) Graff GR, Stark J, & Berkenbosch JW: Chronic lung disease after activated charcoal aspiration. Pediatrics 2002; 109:959-961.
    25) Guenther Skokan E, Junkins EP, & Corneli HM: Taste test: children rate flavoring agents used with activated charcoal. Arch Pediatr Adolesc Med 2001; 155:683-686.
    26) Harris CR & Filandrinos D: Accidental administration of activated charcoal into the lung: aspiration by proxy. Ann Emerg Med 1993; 22:1470-1473.
    27) Hellenas KE, Nyman A, & Slanina P: Determination of potato glycoalkaloids and their aglycone in blood serum by high-performance liquid chromatography. Application to pharmacokinetic studies in humans. J Chromatog 1992; 573:69-78.
    28) Hopkins J: The glycoalkaloids: naturally of interest (but a hot potato?). Food Chem Toxicol 1995; 33:323-328.
    29) Jadhav SJ, Sharma RB, & Salunkhe DK: Naturally occurring toxic alkaloids in foods. CRC Crit Rev Tox 1981; 9:21-104.
    30) Jayhay SJ: Formation and control of chlorophyll and glycoalkaloids in tubers of Solanum tuberosum L. and evaluation of glycoalkaloid toxicity. Adv Food Res 1975; 21:307-354.
    31) Jones PG & Fenwick GR: The glycoalkaloid content of some edible Solanaceous fruits and potato products. J Sci Food Agric 1981; 32:419-421.
    32) Keeler RF, Baker DC, & Gaffield W: Spirosolane - containing Solanum species and induction of congenital craniofacial malformations. Toxicon 1990; 28:873-884.
    33) Keeler RF, Young S, & Brown D: Spina bifida, exencephaly and cranial bleb produced in hamsters by the Solanum alkaloid solasodine. Res Commun Chem Pathol Pharmacol 1976; 13:723-730.
    34) Kleinman ME, Chameides L, Schexnayder SM, et al: 2010 American Heart Association guidelines for cardiopulmonary resuscitation and emergency cardiovascular care. Part 14: pediatric advanced life support. Circulation 2010; 122(18 Suppl.3):S876-S908.
    35) Lahiri SC, Maiti PC, & Chatterjee I: Pharmacological properties of a glycoalkaloidal fraction obtained from Solanum auricuatum Ait. Experientia 1966; 22:464.
    36) Massoulie J, Pezzementi L, & Bon S: Molecular and cellular biology of cholinesterases. Prog in Neurobiol 1993; 14:31-91.
    37) Mathe I Jr & Mathe I Sr: Variation in alkaloids in Solanum dulcamara L., in Hawkes et al (eds): The biology and taxonomy of the Solanaceae, Academic Press, Burlington, MA, 1979, pp 221-222.
    38) McMillan M & Thompson JC: An outbreak of suspected solanine poisoning in schoolboys: Examinations of criteria of solanine poisoning. Q J Med 1979; 48(190):227-243.
    39) Moeschlin S: Klinik und therapie der Vergiftungen, 6th ed, G Thieme, Stuttgart, Germany, 1980, pp 640.
    40) Morris SC & Lee TH: The toxicity and teratogenicity of Solanaceae glycoalkaloids, particularly those of the potato (Solanum tuberosum): a review. Fd Technol Aust 1984; 36:118-124.
    41) Neumar RW , Otto CW , Link MS , et al: Part 8: adult advanced cardiovascular life support: 2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Circulation 2010; 122(18 Suppl 3):S729-S767.
    42) Newton RW: Physostigmine salicylate in the treatment of tricyclic antidepressant overdosage. JAMA 1975; 231:941-943.
    43) Nigg H, Ramos L, & Graham E: Inhibition of human plasma and serum butyrlycholinesterase by alpha-chaconine and alpha-solanine. Fundam Appl Toxicol 1996; 33:272-281.
    44) Nishie K, Gumbmann MR, & Keyl A: Pharmacology of solanine. Toxicol Appl Pharmacol 1971; 19:81-92.
    45) None Listed: Position paper: cathartics. J Toxicol Clin Toxicol 2004; 42(3):243-253.
    46) Pentel P & Peterson CD: Asystole complicating physostigmine treatment of tricyclic antidepressant overdose. Ann Emerg Med 1980; 9:588-590.
    47) Phillips BJ, Hughes JA, & Phillips JC: A study of the toxic hazard that might be associated with the consumption of green potato tops. Food Chem Toxicol 1996; 34(5):439-448.
    48) Pollack MM, Dunbar BS, & Holbrook PR: Aspiration of activated charcoal and gastric contents. Ann Emerg Med 1981; 10:528-529.
    49) Porter WL: A note on the melting point of alpha solanine. Am Pot J 1972; 49:4303-4306.
    50) Product Information: physostigmine salicylate intravenous injection, intramuscular injection, physostigmine salicylate intravenous injection, intramuscular injection. Akorn, Inc. (per Manufacturer), Lake Forest, IL, 2008.
    51) Rau NR, Nagaraj MV, Prakash PS, et al: Fatal pulmonary aspiration of oral activated charcoal. Br Med J 1988; 297:918-919.
    52) Roddick JG & Leonard AL: Amelioration by glucose-6-phosphate and NADP of potato glycoalkaloid inhibition in cell, enzyme and liposome assays. Phytochemistry 1999; 51(1):23-27.
    53) Sapeika N: Food Pharmacology, CC Thomas, Springfield, IL, 1969, pp 67.
    54) Schreiber K: Uber das Vorkommen von Solasodingly Kosiden in Solanum nigrum L. und ihre industrielle Verwertung. Planta Med 1958; 6:435-439.
    55) Shannon M: Toxicology reviews: physostigmine. Pediatr Emerg Care 1998; 14(3):224-226.
    56) Slanina P: Solanine (glycoalkaloids) in potatoes: toxicological evaluation. Fd Chem Toxicol 1990; 28:759-761.
    57) Slanina P: Solanine (glycoalkaloids) in potatoes: toxicological evaluation. Food ChemToxicol 1990a; 28(11):759-761.
    58) Spiller HA & Rogers GC: Evaluation of administration of activated charcoal in the home. Pediatrics 2002; 108:E100.
    59) Sternfeld M, Rachmilewitz J, & Lowenstein-Lichtenstein Y: Normal and atypical butyrylcholinesterases in placental development, function, and malformation. Cell Mol Neurobiol 1997; 17(3):315-332.
    60) Stewart GO: Convulsions after physostigmine (letter). Anaesth Intens Care 1979; 7:283.
    61) Thakore S & Murphy N: The potential role of prehospital administration of activated charcoal. Emerg Med J 2002; 19:63-65.
    62) Watt JM: J Pharm Exp Ther 1930; 39:387-395.
    63) Watt JM: S Afr Med J 1932; 6:562-563.
    64) de Caen AR, Berg MD, Chameides L, et al: Part 12: Pediatric Advanced Life Support: 2015 American Heart Association Guidelines Update for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Circulation 2015; 132(18 Suppl 2):S526-S542.
    65) der Marderosian A, Giller FB, & Roja FC Jr: Phytochemical and toxicological screening of household ornamental plants potentially toxic to humans. J Toxicol Environ Health 1976; 1:939-953.