Abamectin exposure during lactation triggering oxidative stress and expression pattern of Bcl-2 perturbation in rat pups brain
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Abstract
Pesticides, for example, are thought to be essential drivers of brain injury and dysfunction. Abamectin (ABA) is by far the most routinely used pesticide in farming and healthcare, and its toxicity to nontarget organisms has attracted considerable interest. The effect of abamectin pesticide delivered at the postnatal period on the antioxidant defense system was assessed. This study also examined apoptotic gene expression indicators in the brains of rat pups over neonatal weeks. Pregnant Wister rats were split into two groups: G1 received deionized water (control), and G2 received 0.211 mg/L of abamectin. The first day of abamectin exposure was the first day after delivery and continued until the tenth day of lactation. After 10 days (mid lactation) and the lactation period, rat pup brain samples were taken for oxidative biochemistry investigations and apoptotic gene expression (RT–qPCR). In comparison to the control group G1, Abamectin reinforces protein carbonyl levels and glutathione-based enzymes (transferase and peroxidase), whereas superoxide dismutase and glutathione levels are reduced in the pup's brain. Furthermore, Abamectin induced considerable upregulation of proapoptotic (Bax) and antiapoptotic (Bcl-2) mRNA gene expression. Overall, our findings characterize the relationship between brain changes and abamectin administration during lactation periods, even at low doses that are considered safe, and indicate that this abamectin insecticide is harmful to the growing neurological system.
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Article Details
Abamectin, Apoptosis, Brain, Lactation, Oxidative stress
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