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Toxicity Effects

CAS Registry Number: 108-98-5

Selected toxicity information from HSDB, one of the National Library of Medicine's databases. 2.

Names 1

  • Benzenethiol
  • Phenyl Mercaptan
  • Thiophenol II

Human Toxicity Excerpts

  • ALTERNATIVE and IN VITRO TESTS: Thiophenol and aminothiophenol were used to study levels of toxicity in human red blood cells. Thiophenols caused conversion of oxyhemoglobin to methemoglobin. Reduction of corresponding disulfides by intracellular glutathione caused cyclic reduction/oxidation reactions, resulting in increased oxidative flux. Three levels of oxidative stress were observed in these experiments; the lowest level resulted from incubation with 0.25 mM thiophenol; the intermediate level with 0.50 mM thiophenol or 0.25 mM 4-aminothiophenol; the highest levels with 0.50 mM 4-aminothiophenol. Methemoglobin formation increased with increasing level of oxidative stress. Glycolysis and the hexose monophosphate shunt were inhibited at the intermediate and highest levels of stress, respectively. Above the highest level of stress non-intact hemoglobin was formed and cell lysis occurred. These metabolic responses were reflected in cellular levels of NADH, NADPH and reduced glutathione. At the lowest level of oxidative stress, both glycolysis and hexose monophosphate shunt were increased such that near-normal levels of NADH, NADPH and reduced glutathione were maintained and methemglobin formation was kept to a minimum. The response of red cells to 0.25 mM thiophenol appears to represent a level of oxidative stress to which the cell is capable of adaptive metabolic response. Glycolysis contributes approximately one quarter of the total reducing equivalents from glucose metabolism in response to the oxidative challenge by thiophenol.[Amrolia P et al; J Appl Toxicol 9 (2): 113-8 (1989)] **PEER REVIEWED** PubMed Abstract

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Non-Human Toxicity Excerpts

  • GENOTOXICITY: Heteroatomic analogs of 4,4'-methylenedianiline, including thiophenol, in Salmonella typhimurium tester strains TA100 & TA98 showed relative mutagenic response with & without metabolic activation.[LAVOIE ET AL; MUTAT RES 67 (2): 123 (1979)] **PEER REVIEWED** PubMed Abstract
  • LABORATORY ANIMALS: Acute Exposure: ... Application of a drop to rabbit eyes caused severe irritation, moderate redness, & chemosis of the conjunctiva with discharge for 3-4 days ... corneas developed opacities which gradually increased during 2-3 wk, becoming opalescent & obscuring details of pupil & iris. However, in ... 2 months the eyes recovered .[Grant, W.M. Toxicology of the Eye. 3rd ed. Springfield, IL: Charles C. Thomas Publisher, 1986., p. 141] **PEER REVIEWED**
  • LABORATORY ANIMALS: Developmental or Reproductive Toxicity: The potential reproductive toxicity of thiophenol in S-D rats was evaluated using the Reproductive Assessment by Continuous Breeding protocol. Thiophenol was nominated for testing due to the relative lack of reproductive toxicity information; it is used as a chemical intermediate and mosquito larvicide. Thiophenol in corn oil was administered by oral gavage at doses of 9, 18, and 35 mg/kg/day to 20 animals/sex/group. Rats were individually housed for one week and then cohabitated for 16 weeks. During cohabitation, litters were euthanized after evaluation on postnatal day (PND) 1. Litters born after Week 17 were reared until PND 21 and selected weanlings were administered the same dose levels as their respective parents. On PND 81 +/- 10, F1 animals were cohabitated within groups for one week and necropsied following delivery of the litters. During 16 weeks of cohabitation, adjusted live pup weight was decreased by 4 and 6% in the 9 and 35 mg/kg dose groups, respectively. At the crossover mating trial to determine the affected sex, the pups born to 35 mg/kg females weighed 8-9% less; no effects were observed in litters from thiophenol-treated males. In the F1 mating trial, live F2 pup weight was decreased by 9 and 12% in the 18 and 35 mg/kg dose groups, respectively. Throughout the study, the body weights of the F0 and F1 35 mg/kg males were consistently decreased. F0 and F1 liver and kidney weights increased with increasing dose and were associated with centrilobular hepatocellular hypertrophy and renal tubule degeneration. Decreased (5-6%) sperm motility was observed in the 18 and 35 mg/kg F0 group. Inhibited spermiation was observed in all treated F1 males but not the F0 males. In conclusion, thiophenol is not a selective reproductive toxicant, because the effects on male (decreased sperm motility and inhibited spermiation) and female (decreased live pup weight during the crossover mating) endpoints occurred concomitant with, or at doses greater than, those that produced hepatic or renal effects.[Wolfe GW et al; Toxicologist 1996 Mar;30(1 Pt 2):119] **PEER REVIEWED**

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Human Toxicity Values

  • None found

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Non-Human Toxicity Values

  • LC50 Mouse inhalation 28 ppm/4 hr[Lewis, R.J. Sr. (ed) Sax's Dangerous Properties of Industrial Materials. 11th Edition. Wiley-Interscience, Wiley & Sons, Inc. Hoboken, NJ. 2004., p. 2921] **PEER REVIEWED**
  • LC50 Rat inhalation 33 ppm/4 hr[Lewis, R.J. Sr. (ed) Sax's Dangerous Properties of Industrial Materials. 11th Edition. Wiley-Interscience, Wiley & Sons, Inc. Hoboken, NJ. 2004., p. 2921] **PEER REVIEWED**
  • LD50 Mouse ip 25 mg/kg[Lewis, R.J. Sr. (ed) Sax's Dangerous Properties of Industrial Materials. 11th Edition. Wiley-Interscience, Wiley & Sons, Inc. Hoboken, NJ. 2004., p. 2921] **PEER REVIEWED**
  • LD50 Rat dermal 300 mg/kg[Lewis, R.J. Sr. (ed) Sax's Dangerous Properties of Industrial Materials. 11th Edition. Wiley-Interscience, Wiley & Sons, Inc. Hoboken, NJ. 2004., p. 2921] **PEER REVIEWED**
  • LD50 Rat ip 10 mg/kg[Lewis, R.J. Sr. (ed) Sax's Dangerous Properties of Industrial Materials. 11th Edition. Wiley-Interscience, Wiley & Sons, Inc. Hoboken, NJ. 2004., p. 2921] **PEER REVIEWED**
  • LD50 Rat oral 46 mg/kg[Lewis, R.J. Sr. (ed) Sax's Dangerous Properties of Industrial Materials. 11th Edition. Wiley-Interscience, Wiley & Sons, Inc. Hoboken, NJ. 2004., p. 2921] **PEER REVIEWED**

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Absorption, Distribution And Excretion

  • None found

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Metabolism/Metabolites

  • N-Acetylcysteine was ... elevated in the urine of smokers compared to nonsmoking humans. ... Studies with ... /a human volunteer/ with (14)C-benzene revealed the thiophenol excreted to be derived from the benzene metabolite S-phenyl-N-acetylcysteine. Human smokers also exhibited elevated urinary thiophenol levels.[Dehnen W; Zentralbl Hyg Umweltmed 189 (5): 441-51 (1990)] **PEER REVIEWED** PubMed Abstract
  • Studies with rats receiving xenobiotics known to be metabolized via glutathione conjugation, revealed increases in urinary total thiols and thiophenol. ... Further studies with rats with (14)C benzene revealed the thiophenol excreted to be derived from the benzene metabolite S-phenyl-N-acetylcysteine. ...[Dehnen W; Zentralbl Hyg Umweltmed; 189 (5): 441-51 (1990)] **PEER REVIEWED** PubMed Abstract
  • Thiopurine methyltransferase (TPMT) catalyzes the S-methylation of thiopurine and thiopyrimidine drugs. Several nonheterocyclic aromatic thiol compounds, including thiophenol, were discovered to be substrates for thiopurine methyltransferase. Apparent Km constants for some of these aromatic thiol compounds were in the nanomolar range, several orders of magnitude lower than those of the thiopurines & thiopyrimidines previously thought to be the only substrates for thiopurine methyltransferase. These observations suggested that aryl thiol methyltransferase might be a better name than thiopurine methyltransferase for this enzyme. ...[Woodson LC et al; Mol Pharmacol 24 (3): 471-8 (1983)] **PEER REVIEWED** PubMed Abstract
  • Yields methyl phenyl thioether probably in rats; phenylthio-beta-d-glucoside in crickets & cockroaches; & phenylthio-beta-d-glucuronide in mice. /From table/[Goodwin, B.L. Handbook of Intermediary Metabolism of Aromatic Compounds. New York: Wiley, 1976., p. T-12] **PEER REVIEWED**

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Tsca Test Submissions

  • None found

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Footnotes

1 Source: the NTP's CEBS database.

2 Source: the National Library of Medicine's Hazardous Substance Database, 02/28/2017.

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