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CYCLOHEXIMIDE

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Classification   |    Detailed evidence-based information

Substances Included Synonyms

Therapeutic Toxic Class

    A) Cycloheximide is an antibiotic fungicide that was isolated from beers of streptomycin-producing strains of Streptomyces griseus (Budavari, 1989; Gosselin et al, 1984).

Specific Substances

    1) 4-(2-(3,5-Dimethyl-2-oxocyclohexyl)-2-hydroxyethyl)-2,6-piperidinedione
    2) 3-(2-(3,5-dimethyl-2-oxocyclohexyl)-2-hydroxyethyl-)glutarimide
    3) Naramycin A
    4) Actidione(R)
    5) Hizarocin
    6) Kaken
    7) Neocycloheximide
    8) U-4527
    9) CAS 66-81-9
    1.2.1) MOLECULAR FORMULA
    1) C15-H23-N-O4

Available Forms Sources

    A) FORMS
    1) RELATED MIXTURES (Thomson, 1984)
    1) Acti-dione Thiram (0.75% Acti-dione and 75% Thiram)
    2) Acti-dione R2 (1.3% Acti-dione and 75% pentachloronitrobenzene)
    3) Acti-dione TGF (2.1% Acti-dione)
    4) Acti-dione PM (0.27% Acti-dione)
    2) OTHER NAMES (Sax, 1984)
    1) Acti-Aid
    2) Actidione
    3) Actidone
    4) Neocycloheximide
    5) Actispray (FMC Corp)
    6) Hizarocin
    7) Kaken (Japan)
    B) SOURCES
    1) Cycloheximide is marketed under the trade name of Actidione by the Upjohn Company. It is available in two of their agricultural products, Acti-Dione RZ and Acti-Dione Thiram.
    2) Cycloheximide is an antibiotic substance obtained from the beers of streptomycin-producing strains of Streptomyces griseus (Budavari, 1989).
    C) USES
    1) Cycloheximide is a foliar fungicide used to control powdery mildew on ornamentals, rusts and leaf spot diseases on lawns, and as a growth regulator on citrus fruit and olives (Hartley & Kidd, 1987).
    2) Cycloheximide is used in agriculture and has no antibacterial activity. It acts by inhibiting protein synthesis. It is used as a fungicide and plant growth regulator (Budavari, 1989; Gosselin et al, 1984).
    3) Cycloheximide is used as a fungicide, pesticide, antibiotic, medication in cancer therapy, plant growth regulator and protein synthesis inhibitor. It is also used for the abscission of citrus fruit in harvesting, and for turf disease control (Budavari, 1989; Sax & Lewis, 1987; Sax & Lewis, 1989; EPA, 1985).
    4) Cycloheximide is extremely repellent to rats (Budavari, 1989) and has been investigated as a rodent repellent (HSDB , 1991).
    5) Cycloheximide is used in laboratory media as a selective agent to permit isolation of pathogenic and non-pathogenic fungi from sputa and feces which may contain other fungi (HSDB , 1991).

Overview

Life Support

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

Clinical Effects

    0.2.1) SUMMARY OF EXPOSURE
    A) Cycloheximide is a potent irritant. When ingested gastrointestinal symptoms of nausea, vomiting, diarrhea, melena, and excessive salivation have been reported. Other signs of poisoning are transient CNS excitement and tremors. Cycloheximide is irritating to the skin.
    0.2.5) CARDIOVASCULAR
    A) Deaths in animals has been due to cardiovascular collapse.
    0.2.7) NEUROLOGIC
    A) Transient CNS excitement and tremors may occur.
    0.2.8) GASTROINTESTINAL
    A) Nausea and vomiting may be noted
    B) Excessive salivation may occur.
    C) Diarrhea and melena have been reported.
    0.2.9) HEPATIC
    A) Liver congestion has been found in animal studies.
    0.2.10) GENITOURINARY
    A) Elevated BUN may be noted.
    B) Renal damage has been found in animal studies.
    0.2.14) DERMATOLOGIC
    A) Dermal application may result in skin irritation ranging from erythema to sloughing and may not appear for 6 to 24 hours after application.
    0.2.16) ENDOCRINE
    A) Enlarged adrenal glands were found in animal studies.
    0.2.20) REPRODUCTIVE
    A) Cycloheximide has been reported to be teratogenic in rats.

Laboratory Monitoring

    A) Obtain baseline BUN. No other specific lab work (CBC, electrolyte, urinalysis) is needed unless otherwise indicated.

Treatment Overview

    0.4.2) ORAL/PARENTERAL EXPOSURE
    A) 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.
    B) 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.
    C) Hydrocortisone (1 mg/kg) should be considered in symptomatic patients.
    D) Atropine may be useful for cholinergic effects.
    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.
    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.
    0.4.5) DERMAL EXPOSURE
    A) OVERVIEW
    1) Cycloheximide is a potent skin irritant.
    2) 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).

Range Of Toxicity

    A) This material is extremely toxic. There is insufficient information in the literature to accurately assess the range of toxicity of cycloheximide in humans. Humans with fungal disease have tolerated up to 180 mg/day IV. Orally, a 10 mg single dose regularly causes intense nausea in adults.

Clinical Effects

Summary Of Exposure

    A) Cycloheximide is a potent irritant. When ingested gastrointestinal symptoms of nausea, vomiting, diarrhea, melena, and excessive salivation have been reported. Other signs of poisoning are transient CNS excitement and tremors. Cycloheximide is irritating to the skin.

Cardiovascular

    3.5.1) SUMMARY
    A) Deaths in animals has been due to cardiovascular collapse.
    3.5.2) CLINICAL EFFECTS
    A) HYPOTENSIVE EPISODE
    1) ANIMALS - Deaths in animals has been due to cardiovascular collapse and is usually preceded by coma (Gosselin et al, 1984).

Neurologic

    3.7.1) SUMMARY
    A) Transient CNS excitement and tremors may occur.
    3.7.2) CLINICAL EFFECTS
    A) CENTRAL STIMULANT ADVERSE REACTION
    1) Transient central nervous system excitment and tremors may occur (Gosselin et al, 1984; Morgan, 1989).
    B) DROWSY
    1) Cancer patients receiving cycloheximide investigationally by intravenous infusion (0.2 mg/kg/hr) reported the onset of drowsiness to be delayed by 90 to 180 minutes after the IV infusion was started (Young & Dowling, 1975).
    3.7.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) MENINGISM
    a) DOGS - Irritation of the meninges was reported in dogs (Gosselin et al, 1984).

Gastrointestinal

    3.8.1) SUMMARY
    A) Nausea and vomiting may be noted
    B) Excessive salivation may occur.
    C) Diarrhea and melena have been reported.
    3.8.2) CLINICAL EFFECTS
    A) NAUSEA AND VOMITING
    1) Nausea and vomiting have been reported following ingestion of cycloheximide (Gosselin et al, 1984; Morgan, 1989). Nausea has also been reported following administratoin of cycloheximide by intravenous infusion (0.2 mg/kg/hr) in cancer patients (Young & Dowling, 1975).
    B) EXCESSIVE SALIVATION
    1) Excessive salivation may occur in a cycloheximide poisoning (Gosselin et al, 1984; Morgan, 1989).
    C) DIARRHEA
    1) Diarrhea and bloody diarrhea has been reported following cycloheximide ingestion (Gosselin et al, 1984; Morgan, 1989).

Hepatic

    3.9.1) SUMMARY
    A) Liver congestion has been found in animal studies.
    3.9.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) HEPATOCELLULAR DAMAGE
    a) RATS - Liver congestion has been found on autopsy in rats (Gosselin et al, 1984; Greig & Gibbons, 1959).

Genitourinary

    3.10.1) SUMMARY
    A) Elevated BUN may be noted.
    B) Renal damage has been found in animal studies.
    3.10.2) CLINICAL EFFECTS
    A) BLOOD UREA ABNORMAL
    1) Overdosage presents with an elevated blood urea nitrogen (BUN).
    3.10.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) RENAL FUNCTION ABNORMAL
    a) RATS - Renal damage has been found on autopsy in rats (Gosselin et al, 1984; Greig & Gibbons, 1959).

Dermatologic

    3.14.1) SUMMARY
    A) Dermal application may result in skin irritation ranging from erythema to sloughing and may not appear for 6 to 24 hours after application.

Endocrine

    3.16.1) SUMMARY
    A) Enlarged adrenal glands were found in animal studies.
    3.16.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) ENDOCRINE DISORDER
    a) RATS - Enlarged adrenal glands were found on autopsy in rats (Gosselin et al, 1984).

Reproductive

    3.20.1) SUMMARY
    A) Cycloheximide has been reported to be teratogenic in rats.
    3.20.2) TERATOGENICITY
    A) SKELETAL MALFORMATION
    1) MICE - Cycloheximide produced skeletal defects and dactyly in mice (Schardein, 1985).
    2) RATS - Teratogenic effects in rats have included cardiovascular defects, hepatobiliary defects, CNS defects, and craniofacial defects (RTECS , 1990).
    3.20.3) EFFECTS IN PREGNANCY
    A) CERVIX LESION
    1) RATS/MICE - Observed maternal toxic effects in rats include changes in the uterus, cervix and vagina. Post-implantation mortality was also observed in rats and mice. In both the rabbit and hamster, toxic effects on fertility were observed (RTECS , 1991).

Carcinogenicity

    3.21.1) IARC CATEGORY
    A) IARC Carcinogenicity Ratings for CAS66-81-9 (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

Laboratory Monitoring

Monitoring Parameters Levels

    4.1.1) SUMMARY
    A) Obtain baseline BUN. No other specific lab work (CBC, electrolyte, urinalysis) is needed unless otherwise indicated.
    4.1.2) SERUM/BLOOD
    A) BLOOD/SERUM CHEMISTRY
    1) BUN determination.

Treatment

Life Support

    A) Support respiratory and cardiovascular function.

Monitoring

    A) Obtain baseline BUN. No other specific lab work (CBC, electrolyte, urinalysis) is needed unless otherwise indicated.

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) 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.
    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) FLUID/ELECTROLYTE BALANCE REGULATION
    1) IV FLUIDS: Intravenous fluids may be of benefit by accelerating cycloheximide excretion (Morgan, 1989).
    B) ATROPINE
    1) Atropine may be of value to alleviate the cholinergic symptoms. (Adult: 0.4 to 0.6 milligram subcutaneously, intravenously, or intramuscularly; Child: 0.1 (infants) to 0.6 (older children) milligram subcutaneously) (Morgan, 1989).
    C) EXPERIMENTAL THERAPY
    1) Hydrocortisone increased survival in poisoned rats, and may be administered intravenously in doses of approximately 1 milligram/kilogram. Additional protection was achieved in animals by using therapeutic doses of epinephrine, methoxyphenamine, or hexamethonium (Morgan, 1989).

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.

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).

Dermal Exposure

    6.9.1) DECONTAMINATION
    A) DERMAL DECONTAMINATION
    1) Cycloheximide is a potent skin irritant.
    2) 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).

Range Of Toxicity

Summary

    A) This material is extremely toxic. There is insufficient information in the literature to accurately assess the range of toxicity of cycloheximide in humans. Humans with fungal disease have tolerated up to 180 mg/day IV. Orally, a 10 mg single dose regularly causes intense nausea in adults.

Therapeutic Dose

    7.2.1) ADULT
    A) GENERAL
    1) Cycloheximide (infusion rate of 0.2 milligram/kilogram/hour) was administered to 15 patients with Hodgkin's disease or other malignant neoplasms to study the antipyretic effect of cycloheximide (Young & Dowling, 1975).

Minimum Lethal Exposure

    A) ACUTE
    1) The probable oral lethal dose in humans is 5 to 50 mg/kg, or 7 drops to 1 teaspoonful for a 150 pound person (EPA, 1985).

Maximum Tolerated Exposure

    A) GENERAL/SUMMARY
    1) Humans with fungal disease have tolerated 30 milligrams 4 times a day intramuscularly and 180 milligrams/day intravenously.
    2) Orally, 10 milligram single doses regularly cause intense nausea in adults.
    B) ANIMAL DATA
    1) A dose of 1 pph/24h (Standard Draize Test, skin route) caused moderate skin irritation in test rabbits (RTECS , 1990).

Workplace Standards

    A) ACGIH TLV Values for CAS66-81-9 (American Conference of Governmental Industrial Hygienists, 2010):
    1) Not Listed

    B) NIOSH REL and IDLH Values for CAS66-81-9 (National Institute for Occupational Safety and Health, 2007):
    1) Not Listed

    C) Carcinogenicity Ratings for CAS66-81-9 :
    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 CAS66-81-9 (U.S. Occupational Safety, and Health Administration (OSHA), 2010):
    1) Not Listed

Toxicity Information

    7.7.1) TOXICITY VALUES
    A) References: RTECS, 1990 Sax & Lewis, 1989 ITI, 1988
    1) LD50- (INTRAPERITONEAL)MOUSE:
    a) 100 mg/kg
    b) 150 mg/kg
    2) LD50- (ORAL)MOUSE:
    a) 133 mg/kg
    3) LD50- (SUBCUTANEOUS)MOUSE:
    a) 160 mg/kg
    4) LD50- (INTRAPERITONEAL)RAT:
    a) 3700 mcg/kg
    5) LD50- (ORAL)RAT:
    a) 2 mg/kg
    6) LD50- (SUBCUTANEOUS)RAT:
    a) 2500 mcg/kg
    b) 3 mg/kg

Pharmacology Toxicology

Pharmacologic Mechanism

    A) Cycloheximide, an antibiotic isolated from Streptomyces griseus, is highly active against a large number of yeasts, but has no marked antibacterial activity. It has been used commercially in the treatment of various fungal infections of plants and clinically in the treatment of disseminated candidiasis and in cryptococcus meningitis in man.
    B) It is a potent inhibitor of protein synthesis in mammals and can be used to inhibit the induction of hepatic microsomal drug-metabolizing enzymes. It has also been used clinically in combination with other agents for treatment of various types of cancer.

Toxicologic Mechanism

    A) Cycloheximide is a potent irritant of the gut and skin (Morgan, 1982; Reynolds, 1982). Exact mechanism of toxicity is not well defined. Renal injury, damage to the adrenal cortex, and stimulation of sympathetic and parasympathetic nervous systems have been proposed as mechanisms of toxicity (Morgan, 1982).
    B) Cycloheximide has been reported to alter protein metabolism in man and may inhibit the induction of hepatic microsomal drug-metabolizing enzymes (Young & Dowling, 1975; Selye, 1970).

Physicochemical

Physical Characteristics

    A) Cycloheximide is a colorless crystal (Sax & Lewis, 1989; EPA, 1985; Meister et al, 1985). Plates are formed from amyl acetate, water, or 30% methanol (Budavari, 1989).

Molecular Weight

    A) 281.34
    B) 281.39

Animal Toxicology

Clinical Effects

    11.1.1) AVIAN/BIRD
    A) Acute oral administration resulted in ataxia, polydipsia, regurgitation, inbalance, wing-drop, wing shivers, tremors, hypoactivity, and prostration, beginning 10 minutes postingestion, in mallard ducks and pheasants (HSDB , 1990).
    11.1.3) CANINE/DOG
    A) Acute oral administration of lethal doses to dogs resulted in salivation, diarrhea, bloody feces, transient CNS excitement, tremors, meningeal irritation, coma, and cardiovascular collapse (Gosselin et al, 1984).

References

General Bibliography

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    2) 40 CFR 372.65: Environmental Protection Agency - Toxic Chemical Release Reporting, Community Right-To-Know, Chemicals and Chemical Categories to which this part applies. National Archives and Records Association (NARA) and the Government Printing Office (GPO), Washington, DC. Final rules current as of Apr 3, 2006.
    3) 49 CFR 172.101 - App. B: Department of Transportation - Table of Hazardous Materials, Appendix B: List of Marine Pollutants. National Archives and Records Administration (NARA) and the Government Printing Office (GPO), Washington, DC. Final rules current as of Aug 29, 2005.
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    10) 67 FR 7164: Notice of the National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances - Proposed AEGL Values, Environmental Protection Agency, NAC/AEGL Committee. National Archives and Records Administration (NARA) and the Government Publishing Office (GPO), Washington, DC, 2002.
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    12) 69 FR 54144: Notice of the National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances - Proposed AEGL Values, Environmental Protection Agency, NAC/AEGL Committee. National Archives and Records Administration (NARA) and the Government Publishing Office (GPO), Washington, DC, 2004.
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