机构地区:[1]DepartmentofToxicology,SecondMilitaryMedicalUniversity,Shanghai,200433,China [2]InstituteofPharmacologya
出 处:《Biomedical and Environmental Sciences》1992年第4期303-313,共11页生物医学与环境科学(英文版)
摘 要:The hepatotoxicity and the relationship between the hepatotoxicity and free radical induced by 1,1,2-trichloroethane (1,1,2-TCE) and 1,1,1-trichloroethane (1,1,1-TCE) were studied by whole animals test and the isolated perfused rat liver test. Enzymatic parameters measured during the test included the assay of levels of glutamic pyruvic transaminase (GPT), sorbital dehydrogenase (SDH) and glutamate dehydrogenase (GDH). The observation of the pathologic changes of the liver by the light microscope and the measurement of the relative total free radical concentration in the liver were also made. The results showed that 1,1,2-TCE caused definite pathologic changes of rat liver. It led to much higher values for GPT, SDH and GDH both in serum and perfusate than 1,1,1-TCE did (P<0.01). The concentration of perfusate K+ caused by 1,1,2-TCE was higher than that by 1,1,1 -TCE (P < 0.01). The value of the relative total free radical concentration induced by 1,1,2-TCE was also greater than that by 1,1,1-TCE (P<0.05). The results suggested that the hepatotoxicity of 1,1,2-TCE was stronger than that of 1,1,1-TCE. The free radical concentration was increased proportionally to the increase of the hepatotoxicity of 1,1,2-TCE and 1,1,1 -TCE. It appeared that free radical may play an important role in the mechanism of the hepatic injury induced by 1,1,2-TCE.The hepatotoxicity and the relationship between the hepatotoxicity and free radical induced by 1,1,2-trichloroethane (1,1,2-TCE) and 1,1,1-trichloroethane (1,1,1-TCE) were studied by whole animals test and the isolated perfused rat liver test. Enzymatic parameters measured during the test included the assay of levels of glutamic pyruvic transaminase (GPT), sorbital dehydrogenase (SDH) and glutamate dehydrogenase (GDH). The observation of the pathologic changes of the liver by the light microscope and the measurement of the relative total free radical concentration in the liver were also made. The results showed that 1,1,2-TCE caused definite pathologic changes of rat liver. It led to much higher values for GPT, SDH and GDH both in serum and perfusate than 1,1,1-TCE did (P<0.01). The concentration of perfusate K+ caused by 1,1,2-TCE was higher than that by 1,1,1 -TCE (P < 0.01). The value of the relative total free radical concentration induced by 1,1,2-TCE was also greater than that by 1,1,1-TCE (P<0.05). The results suggested that the hepatotoxicity of 1,1,2-TCE was stronger than that of 1,1,1-TCE. The free radical concentration was increased proportionally to the increase of the hepatotoxicity of 1,1,2-TCE and 1,1,1 -TCE. It appeared that free radical may play an important role in the mechanism of the hepatic injury induced by 1,1,2-TCE.
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