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VALINOMYCIN

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Classification   |    Detailed evidence-based information

Substances Included Synonyms

Therapeutic Toxic Class

    A) Valinomycin is a cyclododecadepsipeptide ionophore antibiotic produced by Streptomycetes fulvissimus and is related to enniatin compounds. It is composed of three moles each of L-lactic acid, D-valine, D-alpha-hydroxyisovaleric acid, and L-valine alternately linked and forming a 36-membered ring compound (Budavari, 1996).

Specific Substances

    A) No Synonyms were found in group or single elements
    1.2.1) MOLECULAR FORMULA
    1) C54-H90-N6-O18

Available Forms Sources

    A) SOURCES
    1) SOURCES
    a) Valinomycin is produced by Streptomycetes fulvissimus (Budavari, 1996).
    B) USES
    1) Valinomycin is used as an insecticide and nematocide, although it is not currently registered as a pesticide in the United States or in the European Union (EPA, 1985; Budavari, 1996).
    2) Valinomycin has been used as an experimental antineoplastic drug (Daoud & Juliano, 1986).
    3) It is also used as a research tool in the study of biological membranes and ion transport processes (Gad et al, 1985).

Overview

Life Support

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

Clinical Effects

    0.2.1) SUMMARY OF EXPOSURE
    A) There are no reported cases of human toxicity due to valinomycin exposure. In isolated mouse and rabbit eye lenses, a 4-hour incubation in a valinomycin solution caused imbalances of the sodium-potassium gradient and cataract formation. Direct eye instillation or subconjunctival injection caused decreased intraocular pressure in rabbits and monkeys. Topical conjunctival application also caused corneal edema. Dermal absorption occurs.
    B) It has been speculated that valinomycin might cause toxicity to the central and peripheral nervous systems, heart, and kidneys as is seen with other ionophore antibiotics such as amphotericin B. However, no such effects were seen in some animal experiments.
    C) In other animal experiments, valinomycin has produced aggressive behavior, tremors, seizures, and peripheral nervous system effects. Tolerance develops to some of the behavioral effects. It has caused cardiotoxicity at high doses in experimental animals.
    0.2.4) HEENT
    A) Intraocular pressure, ion imbalance, cataract formation, and corneal edema have been observed.
    0.2.5) CARDIOVASCULAR
    A) Cardiotoxicity is possible.
    0.2.7) NEUROLOGIC
    A) Neurotoxicity and seizures are possible effects.
    0.2.10) GENITOURINARY
    A) Nephrotoxicity is possible.
    0.2.14) DERMATOLOGIC
    A) Percutaneous absorption can result in systemic toxicity.
    0.2.20) REPRODUCTIVE
    A) At the time of this review, no data were available to assess the possible reproductive hazards of valinomycin.
    0.2.21) CARCINOGENICITY
    A) Antineoplastic activity may be observed.
    0.2.22) OTHER
    A) Valinomycin may enhance or prevent uptake or toxicity of other substances.

Laboratory Monitoring

    A) A number of chemicals produce abnormalities of the hematopoietic system, liver, and kidneys. Monitoring complete blood count, urinalysis, and liver and kidney function tests is suggested for patients with significant exposure.

Treatment Overview

    0.4.2) ORAL/PARENTERAL EXPOSURE
    A) ACTIVATED CHARCOAL: Administer charcoal as a slurry (240 mL water/30 g charcoal). Usual dose: 25 to 100 g in adults/adolescents, 25 to 50 g in children (1 to 12 years), and 1 g/kg in infants less than 1 year old.
    B) GASTRIC LAVAGE: Consider after ingestion of a potentially life-threatening amount of poison if it can be performed soon after ingestion (generally within 1 hour). Protect airway by placement in the head down left lateral decubitus position or by endotracheal intubation. Control any seizures first.
    1) CONTRAINDICATIONS: Loss of airway protective reflexes or decreased level of consciousness in unintubated patients; following ingestion of corrosives; hydrocarbons (high aspiration potential); patients at risk of hemorrhage or gastrointestinal perforation; and trivial or non-toxic ingestion.
    C) Carefully observe patients with ingestion exposure for the development of any systemic signs or symptoms and administer symptomatic treatment as necessary.
    D) If cardiotoxicity is suspected, obtain and monitor cardiac enzymes and electrocardiogram. Appropriate neurophysiologic tests and scans should be obtained, based on neurological signs and symptoms if present.
    E) SEIZURES: Administer a benzodiazepine; DIAZEPAM (ADULT: 5 to 10 mg IV initially; repeat every 5 to 20 minutes as needed. CHILD: 0.1 to 0.5 mg/kg IV over 2 to 5 minutes; up to a maximum of 10 mg/dose. May repeat dose every 5 to 10 minutes as needed) or LORAZEPAM (ADULT: 2 to 4 mg IV initially; repeat every 5 to 10 minutes as needed, if seizures persist. CHILD: 0.05 to 0.1 mg/kg IV over 2 to 5 minutes, up to a maximum of 4 mg/dose; may repeat in 5 to 15 minutes as needed, if seizures continue).
    1) Consider phenobarbital or propofol if seizures recur after diazepam 30 mg (adults) or 10 mg (children greater than 5 years).
    2) Monitor for hypotension, dysrhythmias, respiratory depression, and need for endotracheal intubation. Evaluate for hypoglycemia, electrolyte disturbances, and hypoxia.
    0.4.3) INHALATION EXPOSURE
    A) INHALATION: Move patient to fresh air. Monitor for respiratory distress. If cough or difficulty breathing develops, evaluate for respiratory tract irritation, bronchitis, or pneumonitis. Administer oxygen and assist ventilation as required. Treat bronchospasm with an inhaled beta2-adrenergic agonist. Consider systemic corticosteroids in patients with significant bronchospasm.
    B) Carefully observe patients with inhalation exposure for the development of any systemic signs or symptoms and administer symptomatic treatment as necessary.
    0.4.4) EYE EXPOSURE
    A) DECONTAMINATION: Remove contact lenses and irrigate exposed eyes with copious amounts of room temperature 0.9% saline or water for at least 15 minutes. If irritation, pain, swelling, lacrimation, or photophobia persist after 15 minutes of irrigation, the patient should be seen in a healthcare facility.
    B) Prolonged initial flushing and early ophthalmologic consultation are advisable.
    0.4.5) DERMAL EXPOSURE
    A) OVERVIEW
    1) DECONTAMINATION: Remove contaminated clothing and jewelry and place them in plastic bags. Wash exposed areas with soap and water for 10 to 15 minutes with gentle sponging to avoid skin breakdown. A physician may need to examine the area if irritation or pain persists (Burgess et al, 1999).
    2) Some chemicals can produce systemic poisoning by absorption through intact skin. Carefully observe patients with dermal exposure for the development of any systemic signs or symptoms and administer symptomatic treatment as necessary.

Range Of Toxicity

    A) Minimum lethal human exposure is unknown.

Clinical Effects

Summary Of Exposure

    A) There are no reported cases of human toxicity due to valinomycin exposure. In isolated mouse and rabbit eye lenses, a 4-hour incubation in a valinomycin solution caused imbalances of the sodium-potassium gradient and cataract formation. Direct eye instillation or subconjunctival injection caused decreased intraocular pressure in rabbits and monkeys. Topical conjunctival application also caused corneal edema. Dermal absorption occurs.
    B) It has been speculated that valinomycin might cause toxicity to the central and peripheral nervous systems, heart, and kidneys as is seen with other ionophore antibiotics such as amphotericin B. However, no such effects were seen in some animal experiments.
    C) In other animal experiments, valinomycin has produced aggressive behavior, tremors, seizures, and peripheral nervous system effects. Tolerance develops to some of the behavioral effects. It has caused cardiotoxicity at high doses in experimental animals.

Heent

    3.4.1) SUMMARY
    A) Intraocular pressure, ion imbalance, cataract formation, and corneal edema have been observed.
    3.4.3) EYES
    A) INTRAOCULAR PRESSURE - Topical application or subconjunctival injection of valinomycin has caused decreased intraocular pressure in experimental animals (Lee & Lam, 1973). This effect has not been reported in exposed humans.
    B) ION IMBALANCE - Sodium-potassium gradient imbalances were noted in mouse and rabbit isolated eye lenses incubated in valinomycin (Iwata & Horiuchi, 1980).
    C) CATARACT FORMATION - Cataract formation was noted in mouse and rabbit isolated eye lenses incubated in valinomycin (Iwata & Horiuchi, 1980).
    D) CORNEAL EDEMA and eye irritation were noted in monkeys and rabbits following direct topical conjunctival valinomycin application (Lee & Lam, 1973).

Cardiovascular

    3.5.1) SUMMARY
    A) Cardiotoxicity is possible.
    3.5.2) CLINICAL EFFECTS
    A) CARDIOVASCULAR FINDING
    1) CARDIOTOXICITY
    a) It has been speculated that valinomycin might cause toxicity to the heart as is seen with other ionophore antibiotics such as amphotericin B (Daoud & Juliano, 1986). No such effects were seen in some animal experiments (Daoud & Juliano, 1986), but were noted in other experimental animal studies (Gad et al, 1985).

Neurologic

    3.7.1) SUMMARY
    A) Neurotoxicity and seizures are possible effects.
    3.7.2) CLINICAL EFFECTS
    A) NEUROPATHY
    1) SEIZURES
    a) It has been speculated that valinomycin might cause toxicity to the central and peripheral nervous systems as is seen with other ionophore antibiotics such as amphotericin B (Daoud & Juliano, 1986). However, no such effects were seen in some animal experiments (Daoud & Juliano, 1986) while in others, seizures, tremors, and agressive behavior were noted (Gad et al, 1985).
    B) SECONDARY PERIPHERAL NEUROPATHY
    1) Peripheral nervous system effects have been observed in animal experiments (Gad et al, 1985).

Genitourinary

    3.10.1) SUMMARY
    A) Nephrotoxicity is possible.
    3.10.2) CLINICAL EFFECTS
    A) ABNORMAL RENAL FUNCTION
    1) LACK OF EFFECT
    a) It has been speculated that valinomycin might cause toxicity to the kidneys as is seen with other ionophore antibiotics such as amphotericin B (Daoud & Juliano, 1986). However, no such effects were seen in animal experiments (Daoud & Juliano, 1986).

Dermatologic

    3.14.1) SUMMARY
    A) Percutaneous absorption can result in systemic toxicity.
    3.14.2) CLINICAL EFFECTS
    A) POISONING
    1) Dermal absorption can result in systemic toxicity (RTECS, 1996; (Gad et al, 1985).

Reproductive

    3.20.1) SUMMARY
    A) At the time of this review, no data were available to assess the possible reproductive hazards of valinomycin.
    3.20.2) TERATOGENICITY
    A) LACK OF INFORMATION
    1) At the time of this review, no data were available to assess the teratogenic potential of this agent.
    3.20.3) EFFECTS IN PREGNANCY
    A) LACK OF INFORMATION
    1) At the time of this review, no data were available to assess the potential effects of exposure to this agent during pregnancy or lactation.

Carcinogenicity

    3.21.1) IARC CATEGORY
    A) IARC Carcinogenicity Ratings for CAS2001-95-8 (International Agency for Research on Cancer (IARC), 2016; International Agency for Research on Cancer, 2015; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010a; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2008; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2007; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2006; IARC, 2004):
    1) Not Listed
    3.21.2) SUMMARY/HUMAN
    A) Antineoplastic activity may be observed.
    3.21.3) HUMAN STUDIES
    A) CARCINOMA
    1) ANTINEOPLASTIC ACTIVITY -
    a) Valinomycin has been shown to have antineoplastic activity in experimental animals (Daoud & Juliano, 1986).

Genotoxicity

    A) Valinomycin can induce DNA damage in human cells.

Laboratory Monitoring

Monitoring Parameters Levels

    4.1.1) SUMMARY
    A) A number of chemicals produce abnormalities of the hematopoietic system, liver, and kidneys. Monitoring complete blood count, urinalysis, and liver and kidney function tests is suggested for patients with significant exposure.
    4.1.2) SERUM/BLOOD
    A) BLOOD/SERUM CHEMISTRY
    1) A number of chemicals produce abnormalities of the hematopoietic system, liver, and kidneys. Monitoring complete blood count and liver and kidney function tests is suggested for patients with significant exposure.
    4.1.3) URINE
    A) URINALYSIS
    1) A number of chemicals produce abnormalities of the hematopoietic system, liver, and kidneys. Monitoring urinalysis is suggested for patients with significant exposure.
    4.1.4) OTHER
    A) OTHER
    1) MONITORING
    a) If cardiotoxicity is suspected, obtain and monitor cardiac enzymes and electrocardiogram.
    2) ELECTROPHYSIOLOGICAL TESTING
    a) If neurotoxicity is suspected, appropriate neurophysiologic tests and scans should be obtained, based on the patient's complaints and physical findings.

Treatment

Life Support

    A) Support respiratory and cardiovascular function.

Patient Disposition

    6.3.1) DISPOSITION/ORAL EXPOSURE
    6.3.1.5) OBSERVATION CRITERIA/ORAL
    A) Patients symptomatic following exposure should be observed in a controlled setting until all signs and symptoms have fully resolved.

Monitoring

    A) A number of chemicals produce abnormalities of the hematopoietic system, liver, and kidneys. Monitoring complete blood count, urinalysis, and liver and kidney function tests is suggested for patients with significant exposure.

Oral Exposure

    6.5.1) PREVENTION OF ABSORPTION/PREHOSPITAL
    A) SUMMARY
    1) Move victims of inhalation exposure from the toxic environment and administer 100 percent humidified supplemental oxygen with assisted ventilation as required. Exposed eyes and skin should be copiously flushed with water. Ingestions have not been reported, but measures to decrease absorption might be beneficial.
    6.5.2) PREVENTION OF ABSORPTION
    A) 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).
    B) GASTRIC LAVAGE
    1) INDICATIONS: Consider gastric lavage with a large-bore orogastric tube (ADULT: 36 to 40 French or 30 English gauge tube {external diameter 12 to 13.3 mm}; CHILD: 24 to 28 French {diameter 7.8 to 9.3 mm}) after a potentially life threatening ingestion if it can be performed soon after ingestion (generally within 60 minutes).
    a) Consider lavage more than 60 minutes after ingestion of sustained-release formulations and substances known to form bezoars or concretions.
    2) PRECAUTIONS:
    a) SEIZURE CONTROL: Is mandatory prior to gastric lavage.
    b) AIRWAY PROTECTION: Place patients in the head down left lateral decubitus position, with suction available. Patients with depressed mental status should be intubated with a cuffed endotracheal tube prior to lavage.
    3) LAVAGE FLUID:
    a) Use small aliquots of liquid. Lavage with 200 to 300 milliliters warm tap water (preferably 38 degrees Celsius) or saline per wash (in older children or adults) and 10 milliliters/kilogram body weight of normal saline in young children(Vale et al, 2004) and repeat until lavage return is clear.
    b) The volume of lavage return should approximate amount of fluid given to avoid fluid-electrolyte imbalance.
    c) CAUTION: Water should be avoided in young children because of the risk of electrolyte imbalance and water intoxication. Warm fluids avoid the risk of hypothermia in very young children and the elderly.
    4) COMPLICATIONS:
    a) Complications of gastric lavage have included: aspiration pneumonia, hypoxia, hypercapnia, mechanical injury to the throat, esophagus, or stomach, fluid and electrolyte imbalance (Vale, 1997). Combative patients may be at greater risk for complications (Caravati et al, 2001).
    b) Gastric lavage can cause significant morbidity; it should NOT be performed routinely in all poisoned patients (Vale, 1997).
    5) CONTRAINDICATIONS:
    a) Loss of airway protective reflexes or decreased level of consciousness if patient is not intubated, following ingestion of corrosive substances, hydrocarbons (high aspiration potential), patients at risk of hemorrhage or gastrointestinal perforation, or trivial or non-toxic ingestion.
    6.5.3) TREATMENT
    A) OBSERVATION REGIMES
    1) Carefully observe patients with ingestion exposure for the development of any systemic signs or symptoms and administer symptomatic treatment as necessary.
    2) Patients symptomatic following exposure should be observed in a controlled setting until all signs and symptoms have fully resolved.
    B) MONITORING OF PATIENT
    1) A number of chemicals produce abnormalities of the hematopoietic system, liver, and kidneys. Monitoring complete blood count, urinalysis, and liver and kidney function tests is suggested for patients with significant exposure.
    2) If cardiotoxicity is suspected, obtain and monitor cardiac enzymes and electrocardiogram.
    3) If neurotoxicity is suspected, appropriate neurophysiologic tests and scans should be obtained, based on the patient's complaints and physical findings.
    C) SEIZURE
    1) SUMMARY
    a) Attempt initial control with a benzodiazepine (eg, diazepam, lorazepam). If seizures persist or recur, administer phenobarbital or propofol.
    b) Monitor for respiratory depression, hypotension, and dysrhythmias. Endotracheal intubation should be performed in patients with persistent seizures.
    c) Evaluate for hypoxia, electrolyte disturbances, and hypoglycemia (or, if immediate bedside glucose testing is not available, treat with intravenous dextrose).
    2) DIAZEPAM
    a) ADULT DOSE: Initially 5 to 10 mg IV, OR 0.15 mg/kg IV up to 10 mg per dose up to a rate of 5 mg/minute; may be repeated every 5 to 20 minutes as needed (Brophy et al, 2012; Prod Info diazepam IM, IV injection, 2008; Manno, 2003).
    b) PEDIATRIC DOSE: 0.1 to 0.5 mg/kg IV over 2 to 5 minutes; up to a maximum of 10 mg/dose. May repeat dose every 5 to 10 minutes as needed (Loddenkemper & Goodkin, 2011; Hegenbarth & American Academy of Pediatrics Committee on Drugs, 2008).
    c) Monitor for hypotension, respiratory depression, and the need for endotracheal intubation. Consider a second agent if seizures persist or recur after repeated doses of diazepam .
    3) NO INTRAVENOUS ACCESS
    a) DIAZEPAM may be given rectally or intramuscularly (Manno, 2003). RECTAL DOSE: CHILD: Greater than 12 years: 0.2 mg/kg; 6 to 11 years: 0.3 mg/kg; 2 to 5 years: 0.5 mg/kg (Brophy et al, 2012).
    b) MIDAZOLAM has been used intramuscularly and intranasally, particularly in children when intravenous access has not been established. ADULT DOSE: 0.2 mg/kg IM, up to a maximum dose of 10 mg (Brophy et al, 2012). PEDIATRIC DOSE: INTRAMUSCULAR: 0.2 mg/kg IM, up to a maximum dose of 7 mg (Chamberlain et al, 1997) OR 10 mg IM (weight greater than 40 kg); 5 mg IM (weight 13 to 40 kg); INTRANASAL: 0.2 to 0.5 mg/kg up to a maximum of 10 mg/dose (Loddenkemper & Goodkin, 2011; Brophy et al, 2012). BUCCAL midazolam, 10 mg, has been used in adolescents and older children (5-years-old or more) to control seizures when intravenous access was not established (Scott et al, 1999).
    4) LORAZEPAM
    a) MAXIMUM RATE: The rate of intravenous administration of lorazepam should not exceed 2 mg/min (Brophy et al, 2012; Prod Info lorazepam IM, IV injection, 2008).
    b) ADULT DOSE: 2 to 4 mg IV initially; repeat every 5 to 10 minutes as needed, if seizures persist (Manno, 2003; Brophy et al, 2012).
    c) PEDIATRIC DOSE: 0.05 to 0.1 mg/kg IV over 2 to 5 minutes, up to a maximum of 4 mg/dose; may repeat in 5 to 15 minutes as needed, if seizures continue (Brophy et al, 2012; Loddenkemper & Goodkin, 2011; Hegenbarth & American Academy of Pediatrics Committee on Drugs, 2008; Sreenath et al, 2009; Chin et al, 2008).
    5) PHENOBARBITAL
    a) ADULT LOADING DOSE: 20 mg/kg IV at an infusion rate of 50 to 100 mg/minute IV. An additional 5 to 10 mg/kg dose may be given 10 minutes after loading infusion if seizures persist or recur (Brophy et al, 2012).
    b) Patients receiving high doses will require endotracheal intubation and may require vasopressor support (Brophy et al, 2012).
    c) PEDIATRIC LOADING DOSE: 20 mg/kg may be given as single or divided application (2 mg/kg/minute in children weighing less than 40 kg up to 100 mg/min in children weighing greater than 40 kg). A plasma concentration of about 20 mg/L will be achieved by this dose (Loddenkemper & Goodkin, 2011).
    d) REPEAT PEDIATRIC DOSE: Repeat doses of 5 to 20 mg/kg may be given every 15 to 20 minutes if seizures persist, with cardiorespiratory monitoring (Loddenkemper & Goodkin, 2011).
    e) MONITOR: For hypotension, respiratory depression, and the need for endotracheal intubation (Loddenkemper & Goodkin, 2011; Manno, 2003).
    f) SERUM CONCENTRATION MONITORING: Monitor serum concentrations over the next 12 to 24 hours. Therapeutic serum concentrations of phenobarbital range from 10 to 40 mcg/mL, although the optimal plasma concentration for some individuals may vary outside this range (Hvidberg & Dam, 1976; Choonara & Rane, 1990; AMA Department of Drugs, 1992).
    6) OTHER AGENTS
    a) If seizures persist after phenobarbital, propofol or pentobarbital infusion, or neuromuscular paralysis with general anesthesia (isoflurane) and continuous EEG monitoring should be considered (Manno, 2003). Other anticonvulsants can be considered (eg, valproate sodium, levetiracetam, lacosamide, topiramate) if seizures persist or recur; however, there is very little data regarding their use in toxin induced seizures, controlled trials are not available to define the optimal dosage ranges for these agents in status epilepticus (Brophy et al, 2012):
    1) VALPROATE SODIUM: ADULT DOSE: An initial dose of 20 to 40 mg/kg IV, at a rate of 3 to 6 mg/kg/minute; may give an additional dose of 20 mg/kg 10 minutes after loading infusion. PEDIATRIC DOSE: 1.5 to 3 mg/kg/minute (Brophy et al, 2012).
    2) LEVETIRACETAM: ADULT DOSE: 1000 to 3000 mg IV, at a rate of 2 to 5 mg/kg/min IV. PEDIATRIC DOSE: 20 to 60 mg/kg IV (Brophy et al, 2012; Loddenkemper & Goodkin, 2011).
    3) LACOSAMIDE: ADULT DOSE: 200 to 400 mg IV; 200 mg IV over 15 minutes (Brophy et al, 2012). PEDIATRIC DOSE: In one study, median starting doses of 1.3 mg/kg/day and maintenance doses of 4.7 mg/kg/day were used in children 8 years and older (Loddenkemper & Goodkin, 2011).
    4) TOPIRAMATE: ADULT DOSE: 200 to 400 mg nasogastric/orally OR 300 to 1600 mg/day orally divided in 2 to 4 times daily (Brophy et al, 2012).

Inhalation Exposure

    6.7.1) DECONTAMINATION
    A) Move patient from the toxic environment to fresh air. Monitor for respiratory distress. If cough or difficulty in breathing develops, evaluate for hypoxia, respiratory tract irritation, bronchitis, or pneumonitis.
    B) OBSERVATION: Carefully observe patients with inhalation exposure for the development of any systemic signs or symptoms and administer symptomatic treatment as necessary.
    C) INITIAL TREATMENT: Administer 100% humidified supplemental oxygen, perform endotracheal intubation and provide assisted ventilation as required. Administer inhaled beta-2 adrenergic agonists, if bronchospasm develops. Consider systemic corticosteroids in patients with significant bronchospasm (National Heart,Lung,and Blood Institute, 2007). Exposed skin and eyes should be flushed with copious amounts of water.
    6.7.2) TREATMENT
    A) OBSERVATION REGIMES
    1) Carefully observe patients with inhalation exposure for the development of any systemic signs or symptoms and administer symptomatic treatment as necessary.
    B) MONITORING OF PATIENT
    1) A number of chemicals produce abnormalities of the hematopoietic system, liver, and kidneys. Monitoring complete blood count, urinalysis, and liver and kidney function tests is suggested for patients with significant exposure.
    2) If cardiotoxicity is suspected, obtain and monitor cardiac enzymes and electrocardiogram.
    3) If neurotoxicity is suspected, appropriate neurophysiologic tests and scans should be obtained, based on the patient's complaints and physical findings.
    C) Treatment should include recommendations listed in the ORAL EXPOSURE section when appropriate.

Eye Exposure

    6.8.1) DECONTAMINATION
    A) EYE IRRIGATION, ROUTINE: Remove contact lenses and irrigate exposed eyes with copious amounts of room temperature 0.9% saline or water for at least 15 minutes. If irritation, pain, swelling, lacrimation, or photophobia persist after 15 minutes of irrigation, an ophthalmologic examination should be performed (Peate, 2007; Naradzay & Barish, 2006).
    6.8.2) TREATMENT
    A) OPHTHALMIC EXAMINATION AND EVALUATION
    1) CONSULTATION - Because of the potential for eye irritation, corneal edema, intraocular pressure changes, and possible cataract formation, prolonged initial flushing and early ophthalmologic consultation are advisable.
    B) Treatment should include recommendations listed in the ORAL EXPOSURE section when appropriate.

Dermal Exposure

    6.9.1) DECONTAMINATION
    A) DERMAL DECONTAMINATION
    1) DECONTAMINATION: Remove contaminated clothing and wash exposed area thoroughly with soap and water for 10 to 15 minutes. A physician may need to examine the area if irritation or pain persists (Burgess et al, 1999).
    6.9.2) TREATMENT
    A) SKIN ABSORPTION
    1) Percutaneous valinomycin absorption can result in systemic toxicity (RTECS, 1996; (Gad et al, 1985).
    2) Some chemicals can produce systemic poisoning by absorption through intact skin. Carefully observe patients with dermal exposure for the development of any systemic signs or symptoms and administer symptomatic treatment as necessary.
    B) MONITORING OF PATIENT
    1) A number of chemicals produce abnormalities of the hematopoietic system, liver, and kidneys. Monitoring complete blood count, urinalysis, and liver and kidney function tests is suggested for patients with significant exposure.
    2) If cardiotoxicity is suspected, obtain and monitor cardiac enzymes and electrocardiogram.
    3) If neurotoxicity is suspected, appropriate neurophysiologic tests and scans should be obtained, based on the patient's complaints and physical findings.
    C) Treatment should include recommendations listed in the ORAL EXPOSURE section when appropriate.

Enhanced Elimination

    A) EFFICACY
    1) No studies have addressed the utilization of extracorporeal elimination techniques in poisoning with this agent.

Range Of Toxicity

Summary

    A) Minimum lethal human exposure is unknown.

Minimum Lethal Exposure

    A) GENERAL/SUMMARY
    1) The minimum lethal human dose to this agent has not been delineated.

Maximum Tolerated Exposure

    A) GENERAL/SUMMARY
    1) The maximum tolerated human exposure to this agent has not been delineated.
    B) ANIMAL DATA
    1) Incubation in a 10(-6) molar valinomycin solution caused an imbalance of the sodium-potassium gradient and cataract formation in isolated rabbit and mouse eye lenses (Grant, 1986; Iwata & Horiuchi, 1980).

Workplace Standards

    A) ACGIH TLV Values for CAS2001-95-8 (American Conference of Governmental Industrial Hygienists, 2010):
    1) Not Listed

    B) NIOSH REL and IDLH Values for CAS2001-95-8 (National Institute for Occupational Safety and Health, 2007):
    1) Not Listed

    C) Carcinogenicity Ratings for CAS2001-95-8 :
    1) ACGIH (American Conference of Governmental Industrial Hygienists, 2010): Not Listed
    2) EPA (U.S. Environmental Protection Agency, 2011): Not Listed
    3) IARC (International Agency for Research on Cancer (IARC), 2016; International Agency for Research on Cancer, 2015; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010a; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2008; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2007; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2006; IARC, 2004): Not Listed
    4) NIOSH (National Institute for Occupational Safety and Health, 2007): Not Listed
    5) MAK (DFG, 2002): Not Listed
    6) NTP (U.S. Department of Health and Human Services, Public Health Service, National Toxicology Project ): Not Listed

    D) OSHA PEL Values for CAS2001-95-8 (U.S. Occupational Safety, and Health Administration (OSHA), 2010):
    1) Not Listed

Toxicity Information

    7.7.1) TOXICITY VALUES
    A) References: (RTECS, 1996; Gad et al, 1985
    1) LD50- (INTRAPERITONEAL)MOUSE:
    a) 390 mcg/kg
    b) 1 mg/kg
    2) LD50- (ORAL)MOUSE:
    a) 2500 mcg/kg
    3) LD50- (SUBCUTANEOUS)MOUSE:
    a) 4140 mcg/kg
    4) LD50- (INTRAPERITONEAL)RAT:
    a) 800 mcg/kg
    5) LD50- (ORAL)RAT:
    a) 4 mg/kg

Pharmacology Toxicology

Pharmacologic Mechanism

    A) Valinomycin is a potassium ionophore (McNulty et al, 1995). It makes biological membranes selectively permeable to potassium ions, thereby creating hyperpolarization (McNulty et al, 1995).
    1) Valinomycin effects the sodium-potassium gradient across cellular and mitochondrial membranes (Grant, 1986; Iwata & Horiuchi, 1980; Daoud & Juliano, 1986; Gad et al, 1985).
    2) It also presumably uncouples mitochondrial oxidative phosphorylation, as evidenced by decreased ATP production (Daoud & Juliano, 1986).

Toxicologic Mechanism

    A) Valinomycin is a potassium ionophore (McNulty et al, 1995). It makes biological membranes selectively permeable to potassium ions, thereby creating hyperpolarization (McNulty et al, 1995).
    1) Valinomycin effects the sodium-potassium gradient across cellular and mitochondrial membranes (Grant, 1986; Iwata & Horiuchi, 1980; Daoud & Juliano, 1986; Gad et al, 1985).
    2) It also presumably uncouples mitochondrial oxidative phosphorylation, as evidenced by decreased ATP production (Daoud & Juliano, 1986).
    B) The exact mechanism of cataract formation caused by valinomycin is not currently known (Iwata & Horiuchi, 1980).

Physicochemical

Physical Characteristics

    A) Valinomycin is a shiny rectangular crystalline solid; it has also been described as shiny rectangular platelets from dibutyl ether (Budavari, 1996) Lewis, 1982; (EPA, 1985).

Ph

    A) Neutral reaction (Budavari, 1996)

Molecular Weight

    A) 1111.36 (Budavari, 1996)

References

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