Histological Evidence for Dissociation of Lipid Peroxidation and Cell Necrosis in Bromotrichloromethane Hepatotoxicity in the Perfused Rat liver.
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概要
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Bromotrichloromethane (CBrCl<SUB>3</SUB>)-induced hepatic lipid peroxidation and cell necrosis were studied histologically and biochemically, using isolated perfused livers from phenobarbital-pretreated rats. Lipid peroxidation was assessed by fuchsin staining of the liver slices and release of thiobarbituric acid reactive substances (TBARS) into the perfusate; necrosis was assessed by trypan blue uptake and lactate dehydrogenase (LDH) leakage. A good correlation was observed between the Schiffpositive reaction and TBARS release under various experimental conditions, supporting the validity of the fuchsin staining method for histological detection of lipid peroxidation. Lobular localization of lipid peroxidation and necrosis was as follows: Under high oxygen supply (95% O<SUB>2</SUB>-saturated buffer), infusion of CBrCl<SUB>3</SUB> caused the Schiffpositive reaction in the pericentral to midzonal hepatocytes, irrespective of the direction of perfusion, but did not produce necrosis. Under low oxygen supply (20% O<SUB>2</SUB>) with retrograde perfusion, dissociation of lipid peroxidation and necrosis was observed, i.e., trypan blue uptake in the periportal zones and Schiff-positive staining in the pericentral hepatocytes. Thus, lipid peroxidation by itself may have a relatively minor role in the development of CBrCl<SUB>3</SUB>-induced acute hepatic cell death.
- 公益社団法人 日本薬理学会の論文
著者
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Masuda Yasusuke
Division Of Toxicology Niigata College Of Pharmacy
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Yamamori Yasuko
Division of Toxicology, Niigata College of Pharmacy
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- Histological Evidence for Dissociation of Lipid Peroxidation and Cell Necrosis in Bromotrichloromethane Hepatotoxicity in the Perfused Rat liver.