Cobalt chloride induces hepatotoxicity in adult rats and their suckling pups.
Identifieur interne : 000050 ( PubMed/Checkpoint ); précédent : 000049; suivant : 000051Cobalt chloride induces hepatotoxicity in adult rats and their suckling pups.
Auteurs : El Mouldi Garoui [Tunisie] ; Hamadi Fetoui ; Fatma Ayadi Makni ; Tahia Boudawara ; Najiba ZeghalSource :
- Experimental and toxicologic pathology : official journal of the Gesellschaft fur Toxikologische Pathologie [ 1618-1433 ] ; 2011.
Descripteurs français
- KwdFr :
- Administration par voie orale, Animaux, Animaux allaités, Antioxydants (métabolisme), Cobalt (pharmacocinétique), Cobalt (toxicité), Consommation de boisson, Effets différés de l'exposition prénatale aux facteurs de risque (), Effets différés de l'exposition prénatale aux facteurs de risque (anatomopathologie), Exposition maternelle (effets indésirables), Femelle, Grossesse, Polluants environnementaux (pharmacocinétique), Polluants environnementaux (toxicité), Rat Wistar, Rats, Tests de la fonction hépatique, Âge gestationnel.
- MESH :
- anatomopathologie : Effets différés de l'exposition prénatale aux facteurs de risque.
- effets indésirables : Exposition maternelle.
- métabolisme : Antioxydants.
- pharmacocinétique : Cobalt, Polluants environnementaux.
- toxicité : Cobalt, Polluants environnementaux.
- Administration par voie orale, Animaux, Animaux allaités, Consommation de boisson, Effets différés de l'exposition prénatale aux facteurs de risque, Femelle, Grossesse, Rat Wistar, Rats, Tests de la fonction hépatique, Âge gestationnel.
English descriptors
- KwdEn :
- Administration, Oral, Animals, Animals, Suckling, Antioxidants (metabolism), Cobalt (pharmacokinetics), Cobalt (toxicity), Drinking, Drug-Induced Liver Injury (enzymology), Drug-Induced Liver Injury (etiology), Environmental Pollutants (pharmacokinetics), Environmental Pollutants (toxicity), Female, Gestational Age, Liver Function Tests, Maternal Exposure (adverse effects), Pregnancy, Prenatal Exposure Delayed Effects (chemically induced), Prenatal Exposure Delayed Effects (pathology), Rats, Rats, Wistar.
- MESH :
- chemical , metabolism : Antioxidants.
- chemical , pharmacokinetics : Cobalt, Environmental Pollutants.
- chemical , toxicity : Cobalt, Environmental Pollutants.
- adverse effects : Maternal Exposure.
- chemically induced : Prenatal Exposure Delayed Effects.
- enzymology : Drug-Induced Liver Injury.
- etiology : Drug-Induced Liver Injury.
- pathology : Prenatal Exposure Delayed Effects.
- Administration, Oral, Animals, Animals, Suckling, Drinking, Female, Gestational Age, Liver Function Tests, Pregnancy, Rats, Rats, Wistar.
Abstract
To assess liver damages in pregnant and lactating rats and in their suckling pups, wistar female rats were given through drinking water 350 ppm of CoCl(2) (157 ppm Co(2+)) from the 14th day of pregnancy until day 14 after delivery. The effects of cobalt chloride on lipid peroxidation levels, antioxidant enzyme activities, lipid profile and histopathology aspects of liver were evaluated. Biochemical results showed that lipid peroxidation increased significantly in Co-treated rats, as evidenced by high liver thiobarbituric acid-reactive substance (TBARS) levels. Alteration of the antioxidant system in treated group was confirmed by the significant decline of superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx) activities and reduced glutathione (GSH) content in liver of suckling pups and their mothers. Moreover, CoCl(2) exposure induced an increase in the activities of the aspartate transaminase (AST), alanine transaminase (ALT), lactate deshydrogenase (LDH) and bilirubin levels in pups and their mothers while liver LDH activity and plasma albumin level were significantly decreased. On the other hand, cobalt chloride induced a marked hypoglycemia, a significant decline in triglycerides and total cholesterol levels. Histological studies showed an infiltration of mononuclear cells and vascular congestion in liver of pups and their mothers. Based on the present findings, exposure of rats to CoCl(2) during late pregnancy and early postnatal period affects antioxidant enzyme activities and lipid peroxidation indicating liver damage in mothers and their offspring.
DOI: 10.1016/j.etp.2009.09.003
PubMed: 19819122
Affiliations:
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pubmed:19819122Le document en format XML
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<front><div type="abstract" xml:lang="en">To assess liver damages in pregnant and lactating rats and in their suckling pups, wistar female rats were given through drinking water 350 ppm of CoCl(2) (157 ppm Co(2+)) from the 14th day of pregnancy until day 14 after delivery. The effects of cobalt chloride on lipid peroxidation levels, antioxidant enzyme activities, lipid profile and histopathology aspects of liver were evaluated. Biochemical results showed that lipid peroxidation increased significantly in Co-treated rats, as evidenced by high liver thiobarbituric acid-reactive substance (TBARS) levels. Alteration of the antioxidant system in treated group was confirmed by the significant decline of superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx) activities and reduced glutathione (GSH) content in liver of suckling pups and their mothers. Moreover, CoCl(2) exposure induced an increase in the activities of the aspartate transaminase (AST), alanine transaminase (ALT), lactate deshydrogenase (LDH) and bilirubin levels in pups and their mothers while liver LDH activity and plasma albumin level were significantly decreased. On the other hand, cobalt chloride induced a marked hypoglycemia, a significant decline in triglycerides and total cholesterol levels. Histological studies showed an infiltration of mononuclear cells and vascular congestion in liver of pups and their mothers. Based on the present findings, exposure of rats to CoCl(2) during late pregnancy and early postnatal period affects antioxidant enzyme activities and lipid peroxidation indicating liver damage in mothers and their offspring.</div>
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<Abstract><AbstractText>To assess liver damages in pregnant and lactating rats and in their suckling pups, wistar female rats were given through drinking water 350 ppm of CoCl(2) (157 ppm Co(2+)) from the 14th day of pregnancy until day 14 after delivery. The effects of cobalt chloride on lipid peroxidation levels, antioxidant enzyme activities, lipid profile and histopathology aspects of liver were evaluated. Biochemical results showed that lipid peroxidation increased significantly in Co-treated rats, as evidenced by high liver thiobarbituric acid-reactive substance (TBARS) levels. Alteration of the antioxidant system in treated group was confirmed by the significant decline of superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx) activities and reduced glutathione (GSH) content in liver of suckling pups and their mothers. Moreover, CoCl(2) exposure induced an increase in the activities of the aspartate transaminase (AST), alanine transaminase (ALT), lactate deshydrogenase (LDH) and bilirubin levels in pups and their mothers while liver LDH activity and plasma albumin level were significantly decreased. On the other hand, cobalt chloride induced a marked hypoglycemia, a significant decline in triglycerides and total cholesterol levels. Histological studies showed an infiltration of mononuclear cells and vascular congestion in liver of pups and their mothers. Based on the present findings, exposure of rats to CoCl(2) during late pregnancy and early postnatal period affects antioxidant enzyme activities and lipid peroxidation indicating liver damage in mothers and their offspring.</AbstractText>
<CopyrightInformation>Copyright © 2009 Elsevier GmbH. All rights reserved.</CopyrightInformation>
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