BSO 유도 루타치온 저감 흰쥐에서 1, 2, 4-trichlorobenzene의 급성독성에 관한 연구

The Acute Toxicity of 1, 2, 4-Trichlorobenzene in Sprague-Dawley Rats Depleted of Glutathione by Treatment with Buthionine Sulfoximine

1, 2, 4-Trichlorobenzene (1, 2, 4-TCB) is used as a dye carrier, as an intermediate in the synthesis of herbicides, as a flame retardant, and for other purpose. After a single oral administration of 1, 2, 4-TCB (200 mg/kg, 400 mg/kg) in rats, toxic effects were studied by means of serum biochemical and heatological analysis, and liver calcium concentration. Administration of 1, 2, 4-TCB resulted in dose-dependent liver and kidney damage as estimated by increased serum alanine aminotransferase (ALT) activities, liver calcium concentration and blood urea nitrogen (BUN). Pretreatment with DL-buthionine sulfoximine (BSO, 2 mmol/kg, i.p. ) considerably decreased liver glutathione concentration, which was accompanied by markedly elevated serum ALT activites. It is well-known that toxicity of halogenated benzene such as bromobenzene, 1, 4-dichlorobenzene is increased by pretreatment of henobarbital (PB), and protected by pretreatment of cytochrome P450 inhibitor including metyrapone (MP). However, there was no obvious alterations in toxicity of 1, 2, 4-TCB by pretreatment of phenobarbital or metyrapone. In comparison with control group, treatment groups exhibited significant changes in some parameters of hematological analysis but all hematological values remined within normal ranges.