Variations in peroxisomal catalase of neonatal rat hepatocyte subpopulations
Autor: | Renau-Piqueras J, C. Guerri, D Tolosa, María Sancho-Tello, Inmaculada Azorin |
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Rok vydání: | 1995 |
Předmět: |
medicine.medical_specialty
Time Factors Antioxidant medicine.medical_treatment Immunoblotting Microbodies Pathology and Forensic Medicine chemistry.chemical_compound Pregnancy Internal medicine medicine Animals Molecular Biology chemistry.chemical_classification Ethanol biology Acetaldehyde Cell Biology General Medicine Peroxisome Catalase Immunohistochemistry Rats Enzyme medicine.anatomical_structure Endocrinology Animals Newborn Liver chemistry Biochemistry Prenatal Exposure Delayed Effects Hepatocyte Toxicity biology.protein Female |
Zdroj: | Virchows Archiv. 427 |
ISSN: | 1432-2307 0945-6317 |
DOI: | 10.1007/bf00203400 |
Popis: | Alcohol consumption during pregnancy is teratogenic and induces severe alterations in hepatocytes. In the hepatocyte peroxisomal system, ethanol is converted in the presence of H2O2 to acetaldehyde and water. Therefore, peroxisomal catalase also acts as an antioxidant defence mechanism by removing H2O2 and preventing the formation of hydroxyl radicals in the cell. Alterations in peroxisomal catalase after pre- and pre+postnatal alcohol exposure were investigated in the rat. The effect of pre- and postnatal exposure to ethanol on hepatocyte subpopulations was analysed in isolated hepatocytes originating from periportal, intermediate and perivenous zones. Analysis of catalase revealed that the total activity and content of this enzyme were higher in 12-day-old cells than in cells from newborns and that this increment was more pronounced in treated cells. In controls, the amount of peroxisomal catalase increased mainly in periportal cells, whereas alcohol exposure induced a significant increase in the catalase of perivenous hepatocytes. We conclude that pre- and postnatal alcohol exposure mainly affects the perivenous hepatocyte peroxisomes and that the increase in peroxisomal catalase could constitute a defence mechanism against free radical generation induced by alcohol exposure during the perinatal period. |
Databáze: | OpenAIRE |
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