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Oxidative Stress, Biochemical and Histopathological Alterations in the Liver and Kidney of Female Rats Exposed to Low Doses of Deltamethrin (DM):A Molecular Assessment

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Biomedical and Environmental Sciences 2012年第6期25卷 672-683页

作者： CHARGUI Issam grissa intissar BENSASSI Fatma HRIRA Mohamed Yahia HAOUEM Samir HAOUAS Zohra BENCHEIKH Hassen Laboratory of Histology-Cytology and Genetics (02/UR/08-03) Faculty of Medicine 5019 Monastir Tunisia Laboratory of Research on Biologically Compatible Compounds Faculty of Dentistry Street Avicenne 5019 Monastir Tunisia Laboratory of Plant Protection The National Institute for Agricultural Research INRA Tunisia Street Hedi Karray 2049 Ariana Tunisia Laboratory of Biochemistry (UR 07/06) Faculty of pharmacy 5019 Monastir Tunisia Laboratory of Physiology Faculty of Medicine 5019 Monastir Tunisia

Objective To evaluate histopathological alterations of the liver and kidney of female rats exposed to low doses of DM and its potential genotoxic activity. Methods Female Wistar rats were randomly assigned to control （3 groups, 6 rats in each） and treatment groups （3 groups, 6 rats in each）. They were subjected to subcutaneous injections of DM （at doses of 0.003, 0.03, and 0.3 mg/kg bw/d） after 30, 45, and 60 d, respectively. Results Significant alterations were recorded in liver parenchyma induced by hepatic vacuolization, fragmented chromatin in nuclei, dilatation of sinusoids and congestions. Lesions within proximal and distal tubules were observed in the kidneys. Tissue congestions and severe alterations within glomeruli were visible. DM as a pyrethroid insecticide induced significant increase （P〈_O.05） of plasma MDA concentrations after 45 d. A significant increase （P_〈0.05） in plasma ALT （after 45 and 60 d） and AST （after 60 d） concentrations was recorded as compared to controls. During the whole experimental period the toxic agent provoked significant DNA damages （P〈0.05）, especially in the dominance of classes 3 and 4 of obtained comet. Conclusion DM even at a very low dose displays harmful effects by disrupting hepatic and renal function and causing DNA damages in puberscent female rats. Low doses of DM are hepatotoxic and nephrotoxic.

关键词： Deltamethrin Rats Liver Kidney Histopathology Comet assay DNA damage.

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Imidacloprid enhances liver damage in Wistar rats: Biochemical, oxidative damage and histological assessment

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Journal of Coastal Life Medicine 2017年第12期5卷 540-546页

作者： Sana Chakroun intissar grissa Lobna Ezzi Oumaima Ammar Fadoua Neffati Emna Kerkeni Mohamed Fadhel Najjar Zohra Haouas Hassen Ben Cheikh Laboratory of Histology and Cytogenetic(Research Unit of Genetic Genotoxicity and Childhood Illness UR12ES10)Faculty of MedicineUniversity of MonastirStreet AvicenneMonastir 5019Tunisia Laboratory of Biochemistry and Toxicology Fattouma Bourguiba UniversityHospital of MonastirMonastirTunisia

Objective: To investigate the potential adverse effects of imidacloprid on biochemical parameters, oxidative stress and liver damage induced in the rat by oral sub-chronic imidaclopride exposure. Methods: Rats received three different doses of imidacloprid (1/45, 1/22 and 1/10 of LD50) given through gavage for 60 days. Two dozen of male Wistar rats were randomly divided into four experimental groups. Liver damage was determined by measuring aspartate aminotransferase, alanine aminotransferase, alkaline phosphatase and lactate dehydrogenase leakages. The prooxidant-antioxydant status in hepatic tissue homogenate was evaluated by measuring the degree of lipid peroxidation, the antioxidant enzymes activities such as catalase, superoxide dismutase and glutathione peroxidase (GPx). Results: The relative liver weight was significantly higher than that of control and other treated groups at the highest dose 1/10 of LD50 of imidacloprid. Additionally, treatment of rats with imidacloprid significantly increased liver lipid peroxidation (P ≤ 0.05 or 0.01) which went together with a significant decrease in the levels of superoxide dismutase and catalase activities. Parallel to these changes, imidacloprid treatment enhanced liver damage as evidence by sharp increase in the liver enzyme activities of aspartate aminotransferase, alanine aminotransferase, alkaline phosphatase and lactate dehydrogenase. These results were also confirmed by histopathology. Conclusions: In light of the available data, it is our thought that after imidacloprid sub-chronic exposure, depletion of antioxidant enzymes is accompanied by induction of potential oxidative stress in the hepatic tissues that might affect the function of the liver which caused biochemical and histopathological alteration.

关键词： Imidacloprid Biochemical parameters Hepatotoxicity Oxidative stress Neonicotinoids

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