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The neurological damages resulted by endosulfan poisoning is not completely elucidated, especially in cellular organelles such as mitochondria. In the present study, the pro-oxidant effect of endosulfan on brain mitochondria was first investigated. Gavages of endosulfan into rats at the dose of 2 mg/kg induced oxidative stress in this organelle since it provokes a significant reduction of catalase (CAT), superoxide dismutase (SOD), and glutathione (GSH) level. In addition, a significant increase in mitochondria swelling and malondialdehyde (MDA) levels were observed in neuronal mitochondria, indicating clearly an intense peroxidation within mitochondria. Second, the protective effect of quercetin (QE) (10 mg/kg) against endosulfan-induced oxidative stress in mitochondria was also assessed. Indeed, the pretreatment of rats with QE protects brain mitochondria from oxidative stress, lipid peroxidation, and mitochondria swelling induced by endosulfan. The activities of antioxidant enzymes and the mitochondrial content of GSH and MDA were returned to control values. Thus, although endosulfan can have neurotoxic effects in brain rats, this toxicity can be prevented by quercetin.

Les effets antidiabétogène et cytoprotecteur des extraits de flavonoïdes de Ranunculus repens L. et de la quercétine sont étudiés dans le cas du diabète induit par l'alloxane chez les rats Wistar albinos. Ces composés phé-noliques se sont montrés d'un potentiel cytoprotecteur des cellules β et d'une capacité antidiabétogène dans le diabète alloxanique qui déséquilibre le statut redox des cellules pancréatiques au profit du stress oxydatif. L'activité de ces flavonoïdes se traduit par un effet significativement positif sur l'insulinosécrétion des cellules β et la glycémie. Cet effet est dû au pouvoir antioxydant et cytoprotecteur des composés phénoliques porté sur les cellules β intoxiquées par l'alloxane se traduisant par la réduction de la production du MDA en empêchant donc la lipoperoxydation et la normalisation du niveau cytosolique des systèmes antioxydants (SOD, CAT et GSH). Ces effets sont susceptibles de maintenir, par conséquent, un statut redox cellulaire en équilibre après l'administration de l'alloxane en association aux flavonoïdes. Mots clés : Alloxane -Flavonoïdes -Ranunculus repens L. -Quercétine -Effet antidiabétogène -Stress oxydant Antidiabetogenic and cytoprotective effect of butanolic extract of Ranunculus repens L. and quercetin on an experimental model of alloxanic diabetesAbstract: The antidiabetogenic and cytoprotective effects of flavonoid extracts of Ranunculus repens L. and quercetin are studied in the case of diabetes induced by alloxan in Wistar Albino rats. These phenolic compounds have shown cytoprotective potential for β cells and antidiabetogenic capacities for alloxanic diabetes that unbalance the redox status of pancreatic cells for the benefit of oxidant stress. The activity of these flavonoids translates into a significantly positive effect on insulin secretion for β cells and glycaemia. This effect is due to the antioxidant and chemoprotective powers of phenolic compounds brought to bear on β cells intoxicated by alloxan, which thus translates into a reduction in production of MDA by inhibiting lipid peroxidation and normalization of cytosolic levels in antioxidant systems (SOD, CAT and GSH). These effects are hence likely to maintain a balanced cell redox status following administration of alloxan in association with flavonoids.