National Toxicology Program

Selected toxicity information from HSDB, one of the National Library of Medicine's databases. ¹

Names (NTP)

• Isoniazid
• INH
• 4-PYRIDINECARBOXYLIC ACID, HYDRAZIDE (9CI)
• ISONIAZID (AIDS)
• ISONICOTINIC ACID HYDRAZIDE

Human Toxicity Excerpts

• SIGNS AND SYMPTOMS: Patients may be asymptomatic for 30 minutes to 2 hours after an acute overdose. Early symptoms include nausea and vomiting, dizziness, slurred speech, lethargy, disorientation, and hyperreflexia. Seizures usually occur within 1 to 3 hours after ingestion, and are often repetitive and refractory to usual anticonvulsants. Lactic acid accumulation produces an anion gap metabolic acidosis within a few hours, which is often severe and refractory to sodium bicarbonate. Hyperglycemia, glycosuria, and ketonuria have also been reported. [Thomson.Micromedex. Drug Information for the Health Care Professional. 24th ed. Volume 1. Plus Updates. Content Reviewed by the United States Pharmacopeial Convention, Inc. Greenwood Village, CO. 2004., p. 1692]**PEER REVIEWED**
  
• SIGNS AND SYMPTOMS: Overdosage of isoniazid has produced nausea, vomiting, dizziness. slurred speech, blurred vision, and visual hallucinations (including bright colors and strange designs). Symptoms of overdosage usually occur within 30 minutes to 3 hours following ingestion of the drug. After marked overdosage, respiratory distress and CNS depression, progressing rapidly from stupor to coma, severe intractable seizures, metabolic acidosis, acetonuria, and hyperglycemia have occurred. If untreated or treated inadequately, isoniazid overdosage may be fatal. Isoniazid-induced seizures are thought to be associated with decreased gamma-aminobutyric acid (GABA) concentrations in the CNS, possibly resulting from inhibition by isoniazid of brain pyridoxal-5-phosphate activity. [McEvoy, G.K. (ed.). American Hospital Formulary Service- Drug Information 2004. Bethesda, MD: American Society of Health-System Pharmacists, Inc. 2004 (Plus Supplements)., p. 559]**PEER REVIEWED**
  
• CASE REPORTS: Accidental or intentional isoniazid overdose is not uncommon. Two patients suffering from pulmonary tuberculosis ingested isoniazid (9 g and 12 g respectively) intentionally following acute personal stress. One patient presented with oliguria and coma whereas seizures were the dominant feature in the second case. Serum levels of isoniazid were high in both cases. Satisfactory clinical recovery followed after the administration of iv pyridoxine. [Gilhotra R et al; Int J Clin Pharmacol Ther Toxicol 25 (5): 259-61 (1987) ]**PEER REVIEWED**
  
• CASE REPORTS: Two cases of acute isoniazid poisoning in patients who ingested 7.5 g and 5.0 g of isoniazid respectively, with the intention of committing suicide are presented. Both were admitted unconscious, with ventilatory insufficiency and convulsions. Hepatic dysfunction and peripheral neuropathy were notable complications. [Gurnani A et al; Anaesthesia 47 (9): 781-3 (1992) ]**PEER REVIEWED**
  

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Non-Human Toxicity Excerpts

• LABORATORY ANIMALS: Acute Exposure: In rabbits isoniazid penetrates readily into the eye either following topical orsystemic administration but without notable toxic effect. Massive doses injected SC in rabbits have been shown to cause hemorrhage in the meninges at the base of the brain and in the region of the optic nerves, but no inflammatory or degenerative changes in the nerves themselves. Intrathecal injection of isoniazid in rabbits was more seriously damaging, and it is felt that the route of administration was a critical factor in causing optic neuritis in a series of patients who were treated by intrathecal administration of isoniazid for tuberculous meningitis. [Grant, W.M. Toxicology of the Eye. 3rd ed. Springfield, IL: Charles C. Thomas Publisher, 1986., p. 537]**PEER REVIEWED**
  
• LABORATORY ANIMALS: Subchronic or Prechronic Exposure: The subacute effect of a low dose of isoniazid (10 mg/kg/day for 11 days) in phenobarbitone sodium pretreated rabbits (60 mg/kg/day for 4 days) on various lipid parameters in plasma, liver and adipose tissue was investigated. While treatment with phenobarbitone sodium or isoniazid alone did not alter the lipid levels in plasma and tissues, isoniazid treatment in phenobarbitone sodium pretreated rabbits elevated the levels of plasma total lipid and cholesterol. In adipose tissue there was a decrease in total lipid, triglyceride and cholesterol and an elevation in free fatty acid. In contrast, all these parameters were found to be elevated in the liver. It is proposed that the enhanced release of primary amine functional groups from isoniazid during microsomal induction by phenobarbitone sodium treatment caused increased deposition of lipids in the liver, which is presumably an outcome of enhanced breakdown and mobilization of lipids from the adipose tissue. [Krishnamoorthy MS, Karthikeyan S; Pharmacol Res 24 (3): 219-25 (1991) ]**PEER REVIEWED**
  
• LABORATORY ANIMALS: Chronic Exposure or Carcinogenicity: ... CB/SE RATS /WERE GIVEN/ DAILY DOSES OF ABOUT 35 MG INH IN DRINKING WATER FOR 48 WEEKS. OF MALES, 1/49 DEVELOPED LIVER TUMOR AND 2/49 ... LUNG TUMORS. OF FEMALES, 11/40 HAD FIBROADENOMAS OF MAMMARY GLAND. NO ... TUMORS WERE FOUND IN ... CONTROLS ... KILLED AT 104 WEEKS. [IARC. Monographs on the Evaluation of the Carcinogenic Risk of Chemicals to Man. Geneva: World Health Organization, International Agency for Research on Cancer, 1972-PRESENT. (Multivolume work)., p. V4 164 (1974)]**PEER REVIEWED**
  
• LABORATORY ANIMALS: Chronic Exposure or Carcinogenicity: ... DD MICE /WERE INJECTED/ SC WITH 2 MG INH EVERY 2 DAYS FOR 18 WEEKS. INCIDENCE OF PULMONARY TUMORS (ADENOMAS) IN 15 ANIMALS SURVIVING 7 MON WAS 53% IN EXPTL GROUP AND 11% IN 9 CONTROL ANIMALS. [IARC. Monographs on the Evaluation of the Carcinogenic Risk of Chemicals to Man. Geneva: World Health Organization, International Agency for Research on Cancer, 1972-PRESENT. (Multivolume work)., p. V4 164 (1974)]**PEER REVIEWED**
  
• LABORATORY ANIMALS: Chronic Exposure or Carcinogenicity: WITH TOTAL /IP/ DOSES OF 40-55 MG/MOUSE, TUMORS (MAINLY MEDIASTINAL LYMPHOSARCOMAS AND MYELOID LEUKEMIAS) DEVELOPED IN 15/50 MICE WITHIN 13 MONTHS. ONLY 1/50 CONTROL MICE DEVELOPED A MYELOID LEUKEMIA ... . [IARC. Monographs on the Evaluation of the Carcinogenic Risk of Chemicals to Man. Geneva: World Health Organization, International Agency for Research on Cancer, 1972-PRESENT. (Multivolume work)., p. V4 165 (1974)]**PEER REVIEWED**
  
• LABORATORY ANIMALS: Chronic Exposure or Carcinogenicity: ... LUNG TUMORS /WERE NOTED/ IN 17/45 R3 STRAIN MICE AFTER DAILY /IP/ DOSES OF 1.25 MG INH/MOUSE ADMIN FOR 87 DAYS, STARTING WHEN MICE WERE 6 MONTHS OF AGE. NO LUNG TUMORS WERE SEEN IN ... 45 CONTROL MICE, NOR IN 380 CONTROLS KILLED AT VARIOUS AGES. [IARC. Monographs on the Evaluation of the Carcinogenic Risk of Chemicals to Man. Geneva: World Health Organization, International Agency for Research on Cancer, 1972-PRESENT. (Multivolume work)., p. V4 165]**PEER REVIEWED**
  
• LABORATORY ANIMALS: Chronic Exposure or Carcinogenicity: Isoniazid has been shown to cause pulmonary tumors in a number of strains of mice. [Thomson.Micromedex. Drug Information for the Health Care Professional. 24th ed. Volume 1. Plus Updates. Content Reviewed by the United States Pharmacopeial Convention, Inc. Greenwood Village, CO. 2004., p. 1690]**PEER REVIEWED**
  
• LABORATORY ANIMALS: Chronic Exposure or Carcinogenicity: In dogs chronic feeding of isoniazid has been reported to have caused no histologic abnormalities of the retina, but to have produced mild pathologic changes in the optic nerves and tracts. No ophthalmoscopic examinations were reported. Histologic damage was found in the brains, and in both motor and sensory nerves in these animals. [Haddad, L.M. and Winchester, J.F. Clinical Management of Poisoning and Drug Overdosage. Philadelphia, PA: W.B. Saunders Co., 1983., p. 538]**PEER REVIEWED**
  
• LABORATORY ANIMALS: Chronic Exposure or Carcinogenicity: In order to evaluate possible carcinogenesis, young adult male Sprague Dawley rats were fed diets of hydralazine, phenelzine, and isoniazid at levels of 0.020-0.035% for 87 wk. Hydralazine and isoniazid were also tested by the sc route at weekly dosages of 17 and 83 mg/kg, respectively, in both intact and partially hepatectomized rats, but many succumbed after 7 to 49 wk of treatment. Gastrointestinal lesions were absent and, of the miscellaneous changes, sc lesions occurred sporadically among the control and drug treated groups. As a further criterion, male weanlings were placed on the diets and, starting on day 15, 1,2-dimethylhydrazine was injected sc at 9.0 mg/kg once weekly for the first 7 wk and twice per wk for a total of 23 treatments. The rats were killed 22 wk after the last injection, at which time colon adenocarcinomas were observed in over 80% per group, the total number being significantly greater for the isoniazid group due to heightened tumor occurrence at the distal colon. The tumor number in the descending colon for phenelzine was also increased but the overall score, as with the hydralazine group, was in the range of the 1,2-dimethylhydrazine injected controls. Small intestinal adenocarcinomas were lower in number and involved fewer rats on the hydralazine and phenelzine diets as compared to the isoniazid and control groups. Based on the current data, it is concluded that on long term exposure of 1,2-dimethylhydrazine treated rats to the monoamine oxidase inhibitors, hydralazine and phenelzine are not colon carcinogenic, whereas isoniazid enhances colon carcinogenicity. [Gershbein LL, Rao KC; Oncol Res 4 (3): 121-7 (1992) ]**PEER REVIEWED**
  
• LABORATORY ANIMALS: Developmental or Reproductive Toxicity: Studies in rats and rabbits have shown that isoniazid may be embryocidal. However, isoniazid has not been shown to be teratogenic in mice, rats, or rabbits. [Thomson.Micromedex. Drug Information for the Health Care Professional. 24th ed. Volume 1. Plus Updates. Content Reviewed by the United States Pharmacopeial Convention, Inc. Greenwood Village, CO. 2004., p. 1690]**PEER REVIEWED**
  
• LABORATORY ANIMALS: Developmental or Reproductive Toxicity: The developmental toxicity of isoniazid and the metabolites acetylhydrazide and isonicotinic acid were examined with the frog embryo teratogenesis assay-Xenopus. Late Xenopus laevis blastulae were exposed to isoniazid, acetylhydrazide, and isonicotinic acid for 96 hr in two separate static renewal tests with and without the presence of three differently induced metabolic activation systems. The metabolic activation system consisted of uninduced, Aroclor 1254 induced, and isoniazid induced rat liver microsomes. Addition of the isoniazid induced metabolic activation system decreased the 96 hr LC50 of isoniazid and acetylhydrazide approximately 1.6 fold and 7.9 fold, respectively. The 96 hr EC50 (malformation) of isoniazid was virtuall unaffected; however, the isoniazid metabolic activation system decreased the teratogenic index (96 hr LC50/96 hr EC50 (malformation)) nearly 1.8 fold. The 96 hr EC50 (malformation) of acetylhydrazide increased approximately 2.0 fold, decreasing the teratogenic index value 15.8 fold. Isonicotinic acid yielded a teratogenic index value of 2.5. Neither the uninduced metabolic activation system nor the Aroclor 1254 induced metabolic activation system had an effect on any of the cmpd tested and none of the metabolic activation systems affected the developmental toxicity of isonicotinic acid. Results from this study suggest that mixed functional oxidase metabolism may alter the developmental toxicity of isoniazid in vitro by producing a more embryolethal, but less teratogenic metabolite(s) than isoniazid or acetylhydrazide themselves. Results are indicative of the utility and versatility of frog embryo teratogenesis assay-Xenopus in evaluating toxicological mechanisms of teratogenesis in vitro. [Fort DJ, Bantle JA; Teratog Carcinog Mutagen 10 (6): 463-76 (1990) ]**PEER REVIEWED**
  
• LABORATORY ANIMALS: Developmental or Reproductive Toxicity: In chick embryos treated with a 4 hr pulse of 7.2X10-5 M isonicotinic acid hydrazide the cell population growth is inhibited with an increased population doubling time. Teratogenised blastoderm cells complete their ongoing cell cycle and arrest in G1 phase. A chase with an equimolar concentration of pyridoxal-5-phosphate restores the growth rate after a lag of 4 hr equivalent to the duration of treatment with isonicotinic acid hydrazide. Presumptive mesoblast cells invaginated through the primitive streak and neuroectoblast cells induced prior to the application of isonicotinic acid hydrazide differentiate, while the teratogen inhibits morphogenesis and organization of organ primordia. [Joshi MV et al; Indian J Exp Biol 29 (1): 12-5 (1991) ]**PEER REVIEWED**
  
• GENOTOXICITY: Isoniazid (98% pure) caused DNA damage (as judged by a positive effect in an alkaline elution test) in lung DNA (but not liver DNA) of mice treated in vivo. [IARC. Monographs on the Evaluation of the Carcinogenic Risk of Chemicals to Man. Geneva: World Health Organization, International Agency for Research on Cancer, 1972-PRESENT. (Multivolume work)., p. S4 147 (1982)]**PEER REVIEWED**
  

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Human Toxicity Values

• None found

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Non-Human Toxicity Values

• LD50 Mouse ip 100 mg/kg [Sax, N.I. Dangerous Properties of Industrial Materials. 6th ed. New York, NY: Van Nostrand Reinhold, 1984., p. 1644]**PEER REVIEWED**
  
• LD50 Rat oral 650 mg/kg [Sax, N.I. Dangerous Properties of Industrial Materials. 6th ed. New York, NY: Van Nostrand Reinhold, 1984., p. 1644]**PEER REVIEWED**
  

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Absorption, Distribution and Excretion

• ISONIAZID DIFFUSES READILY INTO ALL BODY FLUIDS AND CELLS. THE DRUG IS DETECTABLE IN SIGNIFICANT QUANTITIES IN PLEURAL AND ASCITIC FLUIDS; CONCENTRATIONS IN CEREBROSPINAL FLUID ARE SIMILAR TO THOSE IN THE PLASMA. ISONIAZID PENETRATES WELL INTO CASEOUS MATERIAL. THE CONCENTRATION OF THE AGENT IS INITIALLY HIGHER IN THE PLASMA AND MUSCLE THAN IN THE INFECTED TISSUE, BUT THE LATTER RETAINS THE DRUG FOR A LONG TIME IN QUANTITIES WELL ABOVE THOSE REQUIRED FOR BACTERIOSTASIS. [Hardman, J.G., L.E. Limbird, P.B. Molinoff, R.W. Ruddon, A.G. Goodman (eds.). Goodman and Gilman's The Pharmacological Basis of Therapeutics. 9th ed. New York, NY: McGraw-Hill, 1996., p. 1157]**PEER REVIEWED**
  
• FROM 75 TO 95% OF A DOSE OF ISONIAZID IS EXCRETED IN THE URINE WITHIN 24 HR, MOSTLY AS METABOLITES. [Hardman, J.G., L.E. Limbird, P.B. Molinoff, R.W. Ruddon, A.G. Goodman (eds.). Goodman and Gilman's The Pharmacological Basis of Therapeutics. 9th ed. New York, NY: McGraw-Hill, 1996., p. 1157]**PEER REVIEWED**
  
• Readily absorbed following oral administration; however, may undergo significant first pass metabolism. Absorption and bioavailability were reduced when isoniazid was administered with food. [Thomson.Micromedex. Drug Information for the Health Care Professional. 24th ed. Volume 1. Plus Updates. Content Reviewed by the United States Pharmacopeial Convention, Inc. Greenwood Village, CO. 2004., p. 1689]**PEER REVIEWED**
  
• Widely distributed to all fluids and tissues, including cerebrospinal fluid, pleural and ascitic fluids, skin, sputum, saliva, lungs, muscle, and caseous tissue. Crosses the placenta and is excreted in breast milk. [Thomson.Micromedex. Drug Information for the Health Care Professional. 24th ed. Volume 1. Plus Updates. Content Reviewed by the United States Pharmacopeial Convention, Inc. Greenwood Village, CO. 2004., p. 1689]**PEER REVIEWED**
  
• Volume of distribution = 0.57 to 0.76 L/kg. [Thomson.Micromedex. Drug Information for the Health Care Professional. 24th ed. Volume 1. Plus Updates. Content Reviewed by the United States Pharmacopeial Convention, Inc. Greenwood Village, CO. 2004., p. 1689]**PEER REVIEWED**
  
• Protein binding; very low (0-10%). [Thomson.Micromedex. Drug Information for the Health Care Professional. 24th ed. Volume 1. Plus Updates. Content Reviewed by the United States Pharmacopeial Convention, Inc. Greenwood Village, CO. 2004., p. 1689]**PEER REVIEWED**
  
• Peak serum concentration: 3 to 7 ug/ml after a single 300 mg oral dose; Time to peak serum concentration: 1 to 2 hr. [Thomson.Micromedex. Drug Information for the Health Care Professional. 24th ed. Volume 1. Plus Updates. Content Reviewed by the United States Pharmacopeial Convention, Inc. Greenwood Village, CO. 2004., p. 1689]**PEER REVIEWED**
  
• Approximately 75-95% /is/ excreted by the kidneys within 24 hours, primarily as the inactive metabolites, N-acetylisoniazid and isonicotinic acid; of this amount, 93% of the isoniazid excreted in the urine may occur as the acetylated form in fast acetylators and 63% in slow acetylators, with the remainder, in both cases, occurring as the free or conjugated form. Small amounts are excreted in feces. [Thomson.Micromedex. Drug Information for the Health Care Professional. 24th ed. Volume 1. Plus Updates. Content Reviewed by the United States Pharmacopeial Convention, Inc. Greenwood Village, CO. 2004., p. 1690]**PEER REVIEWED**
  
• The clearance of isoniazid is dependent to only a small degree on the status of renal function, but patients who are slow inactivators of the drug may accumulate toxic concentrations if their renal function is impaired. [Hardman, J.G., L.E. Limbird, P.B. Molinoff, R.W. Ruddon, A.G. Goodman (eds.). Goodman and Gilman's The Pharmacological Basis of Therapeutics. 9th ed. New York, NY: McGraw-Hill, 1996., p. 1158]**PEER REVIEWED**
  
• In a single-dose study in healthy fasting males, the extent of absorption (as measured by area under the plasma concentration-time curve) of isoniazid, rifampin, or pyrazinamide in dosages of 250, 6O0, or 1500 mg, respectively, was similar whether the drugs were administered individually as capsules (rifampin) and tablets (isoniazid and pyrazinamide) or as a fixed combination containing isoniazid 50 mg, rifampin 120 mg, and pyrazinamide 300 mg per tablet. [Thomson.Micromedex. Drug Information for the Health Care Professional. 24th ed. Volume 1. Plus Updates. Content Reviewed by the United States Pharmacopeial Convention, Inc. Greenwood Village, CO. 2004., p. 559]**PEER REVIEWED**
  

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Metabolism/Metabolites

• Isoniazid is inactivated in the liver, mainly by acetylation and dehydrazination. Metabolites of the drug include acetylisoniazid, isonicotinic acid, monoacetylhydrazine, diacetylhydrazine, and isonicotinyl glycine. [McEvoy, G.K. (ed.). American Hospital Formulary Service- Drug Information 2004. Bethesda, MD: American Society of Health-System Pharmacists, Inc. 2004 (Plus Supplements)., p. 560]**PEER REVIEWED**
  
• IN MAN: ... MOST IMPORTANT METABOLITES OF INH IN URINE /WERE FOUND/ TO BE 1-ACETYL-2-ISONICOTINOYLHYDRAZINE (ACETYL INH), N-ACETYL-N'-ISONICOTINIC ACID, ISONICOTINYLGLYCINE, PYRUVIC ACID ISONICOTINYLHYDRAZONE AND ALPHA-OXOGLUTARIC ACID ISONICOTINYLHYDRAZONE ... . [IARC. Monographs on the Evaluation of the Carcinogenic Risk of Chemicals to Man. Geneva: World Health Organization, International Agency for Research on Cancer, 1972-PRESENT. (Multivolume work)., p. V4 166 (1974)]**PEER REVIEWED**
  
• IN VIVO METABOLISM OF INH IN RABBIT ... YIELDS ISONICOTINIC ACID AND AMMONIA, LATTER BEING DERIVED FROM RAPID BREAKDOWN OF HYDRAZINE GROUP ... . [IARC. Monographs on the Evaluation of the Carcinogenic Risk of Chemicals to Man. Geneva: World Health Organization, International Agency for Research on Cancer, 1972-PRESENT. (Multivolume work)., p. V4 165 (1974)]**PEER REVIEWED**
  
• Acetylation of acetylisoniazid results in the formation of monoacetylhydrazine which has been shown to be a potent hepatotoxin in animals. Microsomal metabolism of monoacetylhydrazine in animals results in production of a reactive acylating species capable of covalently binding with tissue macromolecules (i.e., liver protein) and subsequently causing hepatic necrosis. [McEvoy, G.K. (ed.). American Hospital Formulary Service- Drug Information 2004. Bethesda, MD: American Society of Health-System Pharmacists, Inc. 2004 (Plus Supplements)., p. 560]**PEER REVIEWED**
  
• Hepatic; isoniazid is acetylated by N-acetyl transferase to N-acetylisoniazid; it is then biotransformed to isonicotinic acid and monoacetylhydrazine. Monoacetylhydrazine is associated with hepatotoxicity via formation of a reactive intermediate metabolite when N-hydroxylated by the cytochrome p450 mixed oxidase system. The rate of acetylation is genetically determined; slow acetylators are characterized by a relative lack of hepatic N-acetyl transferase. [Thomson.Micromedex. Drug Information for the Health Care Professional. 24th ed. Volume 1. Plus Updates. Content Reviewed by the United States Pharmacopeial Convention, Inc. Greenwood Village, CO. 2004., p. 1689]**PEER REVIEWED**
  
• Most cases with antituberculosis drug-induced hepatitis have been attributed to isoniazid. Isoniazid is metabolized by hepatic N-acetyltransferase (NAT) and cytochrome P450 2E1 (CYP2E1) to form hepatotoxins. However, the role of CYP2E1 in this hepatotoxicity has not yet been reported. The aim of this study was to evaluate whether the polymorphism of the CYP2E1 gene is associated with antituberculosis drug-induced hepatitis. A total of 318 tuberculosis patients who received antituberculosis treatment were followed prospectively. Their CYP2E1 and NAT2 genotypes were determined using a polymerase chain reaction with restriction fragment length polymorphism method. Twenty-one healthy volunteers were recruited for CYP2E1 phenotype study using a chlorzoxazone test. Forty-nine (15.4%) patients were diagnosed to have drug-induced hepatotoxicity. Patients with homozygous wild genotype CYP2E1 c1/c1 had a higher risk of hepatotoxicity (20.0%; odds ratio [OR], 2.52) than those with mutant allele c2 (CYP2E1 c1/c2 or c2/c2, 9.0%, P =.009). If CYP2E1 c1/c2 or c2/c2 genotype combined with rapid acetylator status was regarded as the reference group, the risk of hepatotoxicity increased from 3.94 for CYP2E1 c1/c1 with rapid acetylator status to 7.43 for CYP2E1 c1/c1 with slow acetylator status. After adjustment for acetylator status and age, the CYP2E1 c1/c1 genotype remained an independent risk factor for hepatotoxicity (OR, 2.38; P =.017). Furthermore, under the administration of isoniazid, the volunteers with CYP2E1 c1/c1 genotype had higher CYP2E1 activity than those with other genotypes had and, hence, might produce more hepatotoxins. In conclusion, CYP 2E1 genetic polymorphism may be associated with susceptibility to antituberculosis drug-induced hepatitis. [Huang YS et al; Hepatology 37 (4): 924-30 (2003) ]**PEER REVIEWED**
  

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TSCA Test Submissions

• None found

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Footnotes

¹ Source: the National Library of Medicine's Hazardous Substance Database, 10/28/2007.