1988XenobioticaRequires access

Effects of 1,2-dibromoethane on isolated hepatocytes: Functional alterations and induction of lipid peroxidation

Arthur A. J. Van Iersel, Ineke van Holsteijn, Bas J. Blaauboer

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Abstract

1. Isolated rat hepatocytes were exposed to the fumigant 1,2-dibromoethane (DBE) and cytotoxicity was evaluated by studying parameters of cellular function and lipid peroxidation. 2. DBE caused plasma membrane damage, as determined by leakage of lactate dehydrogenase, and was more severe in shaken suspensions than stationary suspensions, suggesting that cells were more fragile after DBE exposure. 3. DBE decreased hepatocyte glycogen content and stimulated albumin synthesis in hepatocyte suspensions. 4. Lipid peroxidation resulted from DBE exposure and was greater in cells isolated from phenobarbital-pretreated rats. Shaking the suspensions enhanced lipid peroxidation. Ethane production did not parallel formation of thiobarbituric acid reactants, suggesting that these parameters of lipid peroxidation reflect different mechanisms of molecular interaction of DBE.

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What this paper is about

1. Isolated rat hepatocytes were exposed to the fumigant 1,2-dibromoethane (DBE) and cytotoxicity was evaluated by studying parameters of cellular function and lipid peroxidation. 2. DBE caused plasma membrane damage, as determined by leakage of lactate dehydrogenase, and was more severe in shaken suspensions than stationary suspensions, suggesting that cells were more fragile after DBE exposure. 3. DBE decreased hepatocyte glycogen content and stimulated albumin synthesis in hepatocyte suspensions. 4. Lipid peroxidation resulted from DBE exposure and was greater in cells isolated from phenobarbital-pretreated rats. Shaking the suspensions enhanced lipid peroxidation. Ethane production did not parallel formation of thiobarbituric acid reactants, suggesting that these parameters of lipid peroxidation reflect different mechanisms of molecular interaction of DBE.

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Available abstract

1. Isolated rat hepatocytes were exposed to the fumigant 1,2-dibromoethane (DBE) and cytotoxicity was evaluated by studying parameters of cellular function and lipid peroxidation. 2. DBE caused plasma membrane damage, as determined by leakage of lactate dehydrogenase, and was more severe in shaken suspensions than stationary suspensions, suggesting that cells were more fragile after DBE exposure. 3. DBE decreased hepatocyte glycogen content and stimulated albumin synthesis in hepatocyte suspensions. 4. Lipid peroxidation resulted from DBE exposure and was greater in cells isolated from phenobarbital-pretreated rats. Shaking the suspensions enhanced lipid peroxidation. Ethane production did not parallel formation of thiobarbituric acid reactants, suggesting that these parameters of lipid peroxidation reflect different mechanisms of molecular interaction of DBE.

Key concepts: Lipid peroxidation, Hepatocyte, Chemistry, Lactate dehydrogenase, Biochemistry, Albumin, Glycogen, Phenobarbital

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Effects of 1,2-dibromoethane on isolated hepatocytes: Functional alterations and induction of lipid peroxidation — Research Paper | ScholarLens