| Name | cytochrome P450 (protein family or complex) |
|---|---|
| Synonyms | cytochrome P450; cytochrome P 450; CYP450; CYP 450 |
| Name | carbon disulfide |
|---|---|
| CAS | carbon disulfide |
| PubMed | Abstract | RScore(About this table) | |
|---|---|---|---|
| 3127944 | Snyderwine EG, Kroll R, Rubin RJ: The possible role of the -inducible isozyme of cytochrome P450 in the metabolism and distribution of carbon disulfide. Toxicol Appl Pharmacol. 1988 Mar 30;93(1):11-21. |
83(1,1,1,3) | Details |
| 3439888 | Dalvi RR: Cytochrome P-450-dependent covalent binding of carbon disulfide to rat liver microsomal protein in vitro and its prevention by Arch Toxicol. 1987 Dec;61(2):155-7. |
82(1,1,1,2) | Details |
| 755667 | Dalvi RR, Howell CD: Interaction of parathion and malathion with hepatic cytochrome P-450 from rats treated with phenobarbital and carbon disulfide. Drug Chem Toxicol. 1978;1(2):191-202. |
63(0,2,2,3) | Details |
| 237636 | Dalvi RR, HUNTER AL, Neal RA: Toxicological implications of the mixed-function oxidase catalyzed metabolism of carbon disulfide. Chem Biol Interact. 1975 May;10(5):347-61. The results of these studies have indicated that the decrease in the activity of the hepatic mixed-function oxidase enzyme system and the concentration of cytochrome P-450 seen on incubation of carbon disulfide (CS2) with rat liver microsomes in the presence of is the result of the binding of the released in the mixed-function oxidase catalyzed metabolism of CS2 to carbonyl sulfide (COS). |
33(0,1,1,3) | Details |
| 7801330 | Mizutani T, Nakahori Y, Yamamoto K: p-Dichlorobenzene-induced hepatotoxicity in mice depleted of by treatment with buthionine sulfoximine. Toxicology. 1994 Nov-Dec;94(1-3):57-67. Treatment with inhibitors of hepatic cytochrome P-450-dependent monooxygenases, carbon disulfide, and piperonyl butoxide also prevented the hepatotoxicity. |
32(0,1,1,2) | Details |
| 3432735 | Mizutani T, Nomura H, Nakanishi K, Fujita S: Effects of drug metabolism modifiers on pulegone-induced hepatotoxicity in mice. Res Commun Chem Pathol Pharmacol. 1987 Oct;58(1):75-83. Treatments of mice with the cytochrome P-450 enzyme inhibitors, SKF-525A, piperonyl butoxide, and carbon disulfide (CS2), prevented or markedly alleviated the hepatotoxicity of pulegone. |
31(0,1,1,1) | Details |
| 7712112 | Mizutani T, Irie Y, Nakanishi K: Styrene-induced hepatotoxicity in mice depleted of . Res Commun Mol Pathol Pharmacol. 1994 Dec;86(3):361-74. Treatment with inhibitors of hepatic cytochrome P-450-dependent monooxygenases such as carbon disulfide, methoxsalen, piperonyl butoxide, and SKF-525A prevented or tended to reduce the hepatotoxic effect of styrene given in combination with BSO. |
31(0,1,1,1) | Details |
| 3778518 | Masuda Y, Yasoshima M, Nakayama N: Early, selective and reversible suppression of cytochrome P-450-dependent monooxygenase of liver microsomes following the administration of low doses of carbon disulfide in mice. Biochem Pharmacol. 1986 Nov 15;35(22):3941-7. |
31(0,1,1,1) | Details |
| 3390203 | Masuda Y, Yasoshima M: Loss of 3-methylcholanthrene-inducible form of cytochrome P-450 in liver microsomes following administration of carbon disulfide in C57BL/6 Cr mice. Biochem Pharmacol. 1988 Jun 15;37(12):2363-71. |
7(0,0,1,2) | Details |
| 7406873 | Obrebska MJ, Kentish P, Parke DV: The effects of carbon disulphide on rat liver microsomal mixed-function oxidases, in vivo and in vitro. Biochem J. 1980 Apr 15;188(1):107-12. An intraperitoneal dose of CS (2) (500mg/kg) to male rats resulted in loss of liver microsomal mixed-function-oxidase activity (85% loss of biphenyl 4-hydroxylase), followed by denaturation of liver cytochrome P-450 to cytochrome P-420, and degradative loss of both cytochromes (50% loss). |
5(0,0,0,5) | Details |
| 3760457 | Wronska-Nofer T, Klimczak J, Wisniewska-Knypl JM, Jajte J, Opalska B: Combined effect of and carbon disulphide on cytochrome P-450 mono-oxygenase, lipid peroxidation and ultrastructure of the liver in chronically exposed rats. J Appl Toxicol. 1986 Aug;6(4):297-302. |
5(0,0,0,5) | Details |
| 7044288 | Neal RA, Halpert J: Toxicology of thiono- compounds. Annu Rev Pharmacol Toxicol. 1982;22:321-39. These toxic effects of thiono--containing compounds appear to be at least partially the result of their metabolism to reactive intermediates by the cytochrome P-450-containing monooxygenase enzyme systems. |
4(0,0,0,4) | Details |
| 4082194 | Borin C, Periquet A, Mitjavila S: Studies on the mechanism of nabam- and zineb-induced inhibition of the hepatic microsomal monooxygenases of the male rat. Toxicol Appl Pharmacol. 1985 Dec;81(3 Pt 1):460-8. Incubation of nabam and zineb with hepatic microsomes, without leads to an inhibition of the metabolism of aminopyrine and and to a denaturation of cytochrome P-450 into cytochrome P-420; in addition nabam causes the destruction of cytochrome P-450. We studied the in vitro effects of three of the chief breakdown products of these fungicides: ethylene bis-isothiocyanate sulfide (EBIS), ethylene thiourea (ETU), and carbon disulfide (CS2). |
3(0,0,0,3) | Details |
| 3175344 | Chengelis CP: Paradoxical effect of cobaltous on carbon disulfide induced hepatotoxicity in rats. Res Commun Chem Pathol Pharmacol. 1988 Jul;61(1):83-96. CS2 caused an approximate 50% decrease in hepatic cytochrome P-450 when given alone, but an approximate 85% decrease when given with CoCl2. |
2(0,0,0,2) | Details |
| 3109439 | Furukawa N, Nakamura H, Sato M, Suzuki Y: Induction of the hepatic microsomal cytochrome P-450 system by trialkyl phosphorothioates in rats. Biochem Pharmacol. 1987 Apr 15;36(8):1291-6. Triethyl the analog of OOO-Et (S), also caused an increase of the reductase activity, but carbon disulfide had no influence on this activity. |
2(0,0,0,2) | Details |
| 7717875 | Kivisto H, Elovaara E, Riihimaki V, Aitio A: Effect of cytochrome P450 isozyme induction and depletion on the metabolism of CS2 to TTCA in rats. Arch Toxicol. 1995;69(3):185-90. Analysis of 2-thiothiazolidine-4-carboxylic acid (TTCA), a metabolite of carbon disulfide (CS2), is used in the biological monitoring exposure to CS2 at work. |
2(0,0,0,2) | Details |
| 3841135 | Wilkie IW, Seawright AA, Hrdlicka J: The hepatotoxicity of carbon disulphide in sheep. J Appl Toxicol. 1985 Dec;5(6):360-7. At 24 h after dosing with CS2 there was an increase in total liver water, and ions but without an increase in the concentration of these cations in total liver water, and a 50% reduction in microsomal cytochrome P450 levels. |
2(0,0,0,2) | Details |
| 1489528 | Yang M, Luo Y, Liu Y: Potential use of luminol-dependent chemiluminescence for estimation of free radicals produced in hepatic microsomes and reconstituted cytochrome P-450 systems. Biomed Environ Sci. 1992 Dec;5(4):336-48. The study of CL in detecting free radicals formed by biotransformation of 44 xenobiotics suggested that some of the compounds known as free radicals producing agents by bioactivation increased the light emission in cytochrome P-450 enzyme system, such as carbon tetrachloride, chloroform, tetrachloroethylene etc., the others forming toxic metabolites by biotransformation induced the CL in some cases, such as carbon disulfide, methyldursban, methylparathion etc. or decreased the light emission, such as parathion, and polychlorinated byphenyls etc., and still others whose toxic effects have no relationship with their biotransformation had no influence or an inhibitory effect on the CL, such as aminopyrine, TOCP, and acrylamide. |
2(0,0,0,2) | Details |
| 5084788 | Atkin SD, Palmer ED, English PD, Morgan B, Cawthorne MA, Green J: The role of cytochrome P-450 in biogenesis and catabolism. . Biochem J. 1972 Jun;128(2):237-42. |
2(0,0,0,2) | Details |
| 4035665 | Green EC, Hunter A: Toxicity of carbon disulfide in developing rats: LD50 values and effects on the hepatic mixed-function oxidase enzyme system. Toxicol Appl Pharmacol. 1985 Mar 30;78(1):130-8. Twenty-four hours after administration of CS2 (375 mg/kg, ip) to 1-, 5-, 10-, 20-, 30-, and 40-day-old rats, significant inhibition of cytochrome P-450 and hydroxylation was observed in rats of all ages studied except the 1-day-old rats. |
2(0,0,0,2) | Details |
| 3005542 | Nakayama N, Masuda Y: Suppression of phenacetin-induced methemoglobinemia by diethyldithiocarbamate and carbon disulfide and its relation to phenacetin metabolism in mice. J Pharmacobiodyn. 1985 Oct;8(10):868-76. The suppression of methemoglobinemia by DTC and CS2 may result from an inhibition of metabolic conversion of p-phenetidine to methemoglobin-forming substances such as N--p-phenetidine which is of most importance, and 2--p-phenetidine by the microsomal cytochrome P-450-containing monooxygenase system in the liver. |
1(0,0,0,1) | Details |
| 6315019 | Masuda Y, Nakayama N: Protective action of diethyldithiocarbamate and carbon disulfide against renal injury induced by chloroform in mice. Biochem Pharmacol. 1983 Nov 1;32(21):3127-35. DTC and CS2 per se markedly decreased kidney microsomal hydroxylase and p-nitroanisole demethylase activities at 1 hr after oral administration, accompanying a moderate loss of cytochrome P-450 content, in both normal and CCl4-treated mice. |
1(0,0,0,1) | Details |
| 4693833 | Magos L, Butler WH, White IN: Hepatotoxicity of CS 2 in rats: relation to postexposure liver weight and pre-exposure cytochrome P-450 level. Biochem Pharmacol. 1973 Apr 15;22(8):992-4. |
1(0,0,0,1) | Details |
| 6291543 | Masuda Y, Nakayama N: Protective effect of diethyldithiocarbamate and carbon disulfide against liver injury induced by various hepatotoxic agents. Biochem Pharmacol. 1982 Sep 1;31(17):2713-25. DTC and SC, alone, given orally, decreased microsomal metabolism of several substrates p-nitroanisole, hexobarbital, zoxazolamine, aminopyrine and 3,4-benzopyrene), CC14-induced lipid peroxidation, and cytochrome P-450 content. |
1(0,0,0,1) | Details |
| 7447701 | Tucker SP, Lovell DP, Seawright AA, Cunningham VJ: Variation in the hepatotoxic effects of carbon disulphide between different strains of rat. Arch Toxicol. 1980 Oct;45(4):287-96. Analysis of variance of the accompanying changes in liver weight and water content and in total liver cytochrome P450 content gave statistical confirmation of a strain effect in the response to carbon disulphide. |
1(0,0,0,1) | Details |
| 929623 | Vacha J, Seifert J: Biosynthesis of nucleotides and level of cytochrome P-450 in rat liver after administration of carbon tetrachloride. Toxicology. 1977 Oct;8(2):157-64. |
1(0,0,0,1) | Details |
| 3814176 | Chengelis CP, Neal RA: Oxidative metabolism of carbon disulfide by isolated rat hepatocytes and microsomes. Biochem Pharmacol. 1987 Feb 1;36(3):363-8. These data are consistent with the hypothesis that CS2 is oxidized predominantly by the cytochrome P-450 containing monooxygenase system, and the product of this reaction is an unstable intermediate which reacts with water to form monothiocarbonate and reactive species. |
1(0,0,0,1) | Details |
| 6087497 | Masuda Y, Nakayama N: Prevention of butylated hydroxytoluene-induced lung damage by diethyldithiocarbamate and carbon disulfide in mice. Toxicol Appl Pharmacol. 1984 Aug;75(1):81-90. CS2 also reduced various drug metabolizing enzyme activities and the cytochrome P-450 content of the lung microsomal fraction. |
1(0,0,0,1) | Details |
| 7184939 | Freundt KJ, Romer KG, Kamal AM: The inhibitory action of dithiocarbamates and carbon disulphide on malondialdehyde formation resulting from lipid peroxidation in rat liver microsomes. J Appl Toxicol. 1981 Aug;1(4):215-9. In parallel with the inhibition of MDA formation, oxidative destruction of microsomal cytochrome P-450 was delayed with increasing concentrations of the DTCs. |
1(0,0,0,1) | Details |
| 3798451 | Mizutani T, Nomura H, Nakanishi K, Fujita S: Hepatotoxicity of butylated hydroxytoluene and its analogs in mice depleted of hepatic Toxicol Appl Pharmacol. 1987 Jan;87(1):166-76. As judged by the observation of normal serum GPT, drug metabolism inhibitors such as SKF-525A, piperonyl butoxide, and carbon disulfide prevented the hepatotoxic effect of BHT given in combination with BSO. These results suggest that BHT is activated by a cytochrome-P-450-dependent metabolic reaction and that the hepatotoxic effect is caused by inadequate rates of detoxification of the reactive metabolite in mice depleted of hepatic GSH by BSO administration. |
1(0,0,0,1) | Details |
| 2047567 | Mizutani T, Satoh K, Nomura H, Nakanishi K: Hepatotoxicity of in mice depleted of by treatment with DL-buthionine sulfoximine. Res Commun Chem Pathol Pharmacol. 1991 Feb;71(2):219-30. Drug metabolism inhibitors such as carbon disulfide, methoxsalen, and piperonyl butoxide prevented or significantly reduced the hepatotoxic effect of given in combination with BSO. These results suggest that is activated by a cytochrome-P-450-dependent metabolic reaction and that the liver injury is caused by inadequate rates of detoxification of the resulting metabolite in mice depleted of hepatic GSH by BSO treatment. |
1(0,0,0,1) | Details |
| 3953292 | Dalvi RR, Deoras DP: Metabolism of a dithiocarbamate fungicide thiram to carbon disulfide in the rat and its hepatotoxic implications. Acta Pharmacol Toxicol. 1986 Jan;58(1):38-42. Furthermore, measurement of the activities of hepatic microsomal and serum enzymes at 5 hrs and 24 hrs following thiram treatment indicated that thiram caused significant loss of cytochrome P-450 and benzphetamine N-demethylase activity only at 24 hrs interval whereas there was significant elevation of sorbitol dehydrogenase (SDH) and serum glutamic oxalacetic transaminase (SGOT) activity at 5 and 24 hrs after treatment. |
1(0,0,0,1) | Details |
| 402793 | Jarvisalo J, Savolainen H, Elovaara E, Vainio H: The in vivo toxicity of CS2 to liver microsomes: binding of labelled CS2 and changes of the microsomal enzyme activities. Acta Pharmacol Toxicol. 1977 Feb;40(2):329-36. The level of hepatic cytochrome P-450, the activities of epoxide hydratase and UDP-glucuronosyltransferase were analyzed in the same animals. |
1(0,0,0,1) | Details |
| 3175345 | Chengelis CP: Changes in hepatic concentrations during carbon disulfide induced hepatotoxicity in the rat. Res Commun Chem Pathol Pharmacol. 1988 Jul;61(1):97-109. These results support the hypothesis that the hepatotoxicity of CS2 requires metabolism by the cytochrome P-450 containing monooxygenase system. |
1(0,0,0,1) | Details |