Cobalt chloride induces hepatotoxicity in adult rats and their suckling pups
Identifieur interne : 000555 ( Main/Exploration ); précédent : 000554; suivant : 000556Cobalt chloride induces hepatotoxicity in adult rats and their suckling pups
Auteurs : EL MOULDI GAROUI [Tunisie] ; Hamadi Fetoui [Tunisie] ; FATMA AYADI MAKNI [Tunisie] ; Tahia Boudawara [Tunisie] ; Najiba Zeghal [Tunisie]Source :
- Experimental and toxicologic pathology : (Print) [ 0940-2993 ] ; 2011.
Descripteurs français
- Pascal (Inist)
English descriptors
- KwdEn :
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 CoCl2 (157 ppm Co2+) 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, CoCl2 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 CoCl2 during late pregnancy and early postnatal period affects antioxidant enzyme activities and lipid peroxidation indicating liver damage in mothers and their offspring.
Affiliations:
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Sciences, Animal Physiology Laboratory, UR 08-73, Sciences Faculty of Sfax, BP 1171</s1><s2>3000 Sfax</s2><s3>TUN</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>5 aut.</sZ></inist:fA14><country>Tunisie</country><wicri:noRegion>3000 Sfax</wicri:noRegion></affiliation></author><author><name sortKey="Fatma Ayadi Makni" sort="Fatma Ayadi Makni" uniqKey="Fatma Ayadi Makni" last="Fatma Ayadi Makni">FATMA AYADI MAKNI</name><affiliation wicri:level="1"><inist:fA14 i1="02"><s1>Biochemistry Laboratory, CHU Habib Bouguiba</s1><s2>3029 Sfax</s2><s3>TUN</s3><sZ>3 aut.</sZ></inist:fA14><country>Tunisie</country><wicri:noRegion>3029 Sfax</wicri:noRegion></affiliation></author><author><name sortKey="Boudawara, Tahia" sort="Boudawara, Tahia" uniqKey="Boudawara T" first="Tahia" last="Boudawara">Tahia Boudawara</name><affiliation wicri:level="1"><inist:fA14 i1="03"><s1>Histopathology Laboratory, CHU Habib Bourguiba</s1><s2>3029 Sfax</s2><s3>TUN</s3><sZ>4 aut.</sZ></inist:fA14><country>Tunisie</country><wicri:noRegion>3029 Sfax</wicri:noRegion></affiliation></author><author><name sortKey="Zeghal, Najiba" sort="Zeghal, Najiba" uniqKey="Zeghal N" first="Najiba" last="Zeghal">Najiba Zeghal</name><affiliation wicri:level="1"><inist:fA14 i1="01"><s1>Department of Life Sciences, Animal Physiology Laboratory, UR 08-73, Sciences Faculty of Sfax, BP 1171</s1><s2>3000 Sfax</s2><s3>TUN</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>5 aut.</sZ></inist:fA14><country>Tunisie</country><wicri:noRegion>3000 Sfax</wicri:noRegion></affiliation></author></analytic><series><title level="j" type="main">Experimental and toxicologic pathology : (Print)</title><title level="j" type="abbreviated">Exp. toxicol. pathol. : (Print)</title><idno type="ISSN">0940-2993</idno><imprint><date when="2011">2011</date></imprint></series></biblStruct></sourceDesc><seriesStmt><title level="j" type="main">Experimental and toxicologic pathology : (Print)</title><title level="j" type="abbreviated">Exp. toxicol. pathol. : (Print)</title><idno type="ISSN">0940-2993</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Adult animal</term><term>Anatomic pathology</term><term>Breast feeding</term><term>Cobalt chloride</term><term>Hepatotoxicity</term><term>Liver</term><term>Oxidative stress</term><term>Pregnancy</term><term>Rat</term><term>Toxicity</term></keywords><keywords scheme="Pascal" xml:lang="fr"><term>Chlorure de cobalt</term><term>Toxicité</term><term>Hépatotoxicité</term><term>Animal adulte</term><term>Rat</term><term>Gestation</term><term>Allaitement</term><term>Foie</term><term>Stress oxydatif</term><term>Anatomopathologie</term></keywords></textClass></profileDesc></teiHeader><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<sub>2</sub> (157 ppm Co<sup>2+</sup>) 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<sub>2</sub> 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<sub>2</sub> during late pregnancy and early postnatal period affects antioxidant enzyme activities and lipid peroxidation indicating liver damage in mothers and their offspring.</div></front></TEI><affiliations><list><country><li>Tunisie</li></country></list><tree><country name="Tunisie"><noRegion><name sortKey="El Mouldi Garoui" sort="El Mouldi Garoui" uniqKey="El Mouldi Garoui" last="El Mouldi Garoui">EL MOULDI GAROUI</name></noRegion><name sortKey="Boudawara, Tahia" sort="Boudawara, Tahia" uniqKey="Boudawara T" first="Tahia" last="Boudawara">Tahia Boudawara</name><name sortKey="Fatma Ayadi Makni" sort="Fatma Ayadi Makni" uniqKey="Fatma Ayadi Makni" last="Fatma Ayadi Makni">FATMA AYADI MAKNI</name><name sortKey="Fetoui, Hamadi" sort="Fetoui, Hamadi" uniqKey="Fetoui H" first="Hamadi" last="Fetoui">Hamadi Fetoui</name><name sortKey="Zeghal, Najiba" sort="Zeghal, Najiba" uniqKey="Zeghal N" first="Najiba" last="Zeghal">Najiba Zeghal</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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