Role of glutathione conjugation in 1-bromobutane-induced hepatotoxicity in mice.

doi:10.1016/j.fct.2010.06.044

Paper

Role of glutathione conjugation in 1-bromobutane-induced hepatotoxicity in mice.

Published Oct 1, 2010 · Sang Kyu Lee, Dong Ju Lee, G. Ko

Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association

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Abstract

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Non-RCT

Animal Study

Study Snapshot

1-bromobutane can cause hepatotoxicity and depletion of glutathione content in mice due to the formation of GSH conjugates.

PopulationOlder adults (50-71 years)

Sample size24

MethodsObservational

OutcomesBody Mass Index projections

ResultsSocial networks mitigate obesity in older groups.

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Paper

Role of glutathione conjugation in 1-bromobutane-induced hepatotoxicity in mice.

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References

Role of Metabolism In 1-Bromopropane-Induced Hepatotoxicity in Mice

Formation of reactive metabolites by CYP and depletion of glutathione may play important roles in 1-bromopropane-induced hepatotoxicity in mice.

Glutathione depletion in isolated hepatocytes: its relation to lipid peroxidation and cell damage.

Glutathione depletion in hepatocytes can lead to lipid peroxidation and hepatocellular lysis, with certain compounds preventing these effects.

Hepatotoxic and Immunotoxic Effects produced by 1,3‐Dibromopropane and Its Conjugation with Glutathione in Female BALB/c Mice

1,3-dibromopropane-induced hepatotoxicity and immunotoxicity in female BALB/c mice may be mediated by the formation of GSH conjugate, which depletes cellular GSH and damages the cellular anti-oxidative system.

Role of glutathione conjugation in the hepatotoxicity and immunotoxicity induced by 1‐bromopropane in female BALB/c mice

1bromopropane can cause hepatotoxicity and immunotoxicity in female BALB/c mice, with the formation of GSH conjugates contributing to the depletion of GSH content.

Identification of glutathione conjugates and mercapturic acids of 1,2-dibromopropane in female BALB/c mice by liquid chromatography-electrospray ionization tandem mass spectrometry

Oral treatment with 1,2-dibromopropane reduces hepatic glutathione levels in female BALB/c mice, with dose-dependent production of glutathione conjugates and mercapturic acids in the liver.

Citations

Preliminary characterization of a murine model for 1-bromopropane neurotoxicity: Role of cytochrome P450.

Controlling hepatic P450 activity with 1-aminobenzotriazole (1-ABT) allows mice to experience higher concentrations of 1-bromopropane neurotoxicity, potentially providing better models for 1-bromopropane-induced neurotoxicity.

Report on carcinogens monograph on 1-bromopropane.

1-bromopropane is reasonably anticipated to be a human carcinogen based on sufficient evidence from studies in experimental animals, including skin tumors in male rats and large intestine tumors in female mice.