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p-Dichlorobenzene-induced hepatotoxicity in mice depleted of glutathione by treatment with buthionine sulfoximine.

Abstract：

:p-Dichlorobenzene (p-DCB) is widely used as a moth repellent and a space deodorant. In mice pretreated with DL-buthionine sulfoximine (BSO; 2 mmol/kg or higher doses, i.p.), an inhibitor of glutathione (GSH) synthesis, administration of p-DCB (100-400 mg/kg, p.o.) resulted in dose-dependent hepatotoxicity as judged by increased serum alanine aminotransferase (ALT) activities and liver calcium concentrations and by histological examination of the liver, p-DCB alone (up to 1200 mg/kg) resulted in no hepatotoxicity. Administration of GSH monoethyl ester, which is known as a useful means for increasing organ GSH levels, protected against the hepatotoxicity caused by p-DCB in combination with BSO. Treatment with inhibitors of hepatic cytochrome P-450-dependent monooxygenases, carbon disulfide, metyrapone and piperonyl butoxide also prevented the hepatotoxicity. These results suggest that p-DCB is activated by a cytochrome P-450-dependent metabolic reaction and that the hepatotoxicity is caused by inadequate rates of detoxification of the resulting metabolite in mice depleted of hepatic GSH by BSO treatment. The liver injury was preceded by an extensive depletion of hepatic GSH but not accompanied by significant changes in hepatic contents of lipid peroxides and protein thiols.

journal_name

Toxicology

journal_title

Toxicology

authors

Mizutani T,Nakahori Y,Yamamoto K

doi

10.1016/0300-483x(94)90028-0

subject

Has Abstract

pub_date

1994-11-01 00:00:00

pages

57-67

issue

1-3

eissn

0300-483X

issn

1879-3185

pii

0300-483X(94)90028-0

journal_volume

94

pub_type

杂志文章

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