POSTNATAL ASSESSMENT OF THE ATTENUATION ACTIVITY OF QUERCETIN AND VITAMIN E ON ACCUTANE-INDUCED HIPPOCAMPAL DAMAGE FOLLOWING PRENATAL EXPOSURE IN WISTAR RATS
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Isotretinoin (Accutane), a retinoid widely used for severe acne, has been reported to induce hippocampal toxicity through oxidative stress, apoptosis, and neuroinflammation, which can impair prenatal development. The hippocampus, being particularly vulnerable to oxidative damage, may contribute to learning and memory deficits when exposed to Isotretinoin during gestation. This study evaluates the protective efficacy of Vitamin E, and quercetin against Accutane-induced hippocampal toxicity in prenatal Wistar rats. Four groups were examined in this: control, Accutane only, Accutane + quercetin + vitamin E, and Accutane + vitamin E. Administration was carried out from GD 14-21 of pregnancy. After littering, the neonates were left until PND 31 (postnatal day 31) before sacrifice. Histological analysis of hippocampal integrity, and developmental parameters in offspring (birth weight, neurobehavioral testing) were assessed. Results showed that Accutane exposure led to reduced birth weight and brain weight, along with neuronal degeneration in the hippocampal cells. Co-administration of vitamin E and quercetin significantly improved hippocampal morphology and restored neurobehavioral activity. Neurobehavioral results revealed that Accutane increased transfer latency and reduced exploratory activity, whereas combined antioxidant treatment improved behavioral performance. Offspring from the co-treated group also exhibited higher body weight and brain weights compared to the Accutane-only group. In conclusion, quercetin and vitamin E effectively counteracted Accutane-induced prenatal toxicity in the hippocampus of Wistar rats. The synergistic antioxidant action of both compounds preserved neural architecture and improved developmental outcomes, suggesting their potential as therapeutic agents against retinoid-related neurotoxicity in pregnancy.
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