Lactational exposure to abamectin induced mortality and adverse biochemical and histopathological effects in suckling pups.

Information about the adverse effects of lactation transfer of abamectin (ABA) is important for human health, especially in the third-world countries where breastfeeding is the only source of nutrition for infants. So, the present study was undertaken to evaluate the adverse effects of breastfeeding exposure to ABA on oxidative damage and liver and kidney dysfunction in suckling rats. Dams were orally administered ABA at a doses 22.10, 11.05, and 2.21 mg a.i./kg b.wt from postnatal day 1 (PND1) until day 20 (PND20). The signs of toxicity and high mortality were recorded in suckling male (67.5%) and female (55.0%) pups whose mother exposed to the ABA at dose 22.1 mg a.i./kg b.wt. ABA induced significantly decrease in body weights of mothers and their male and female pups and significant increase in relative liver weights. It caused oxidative stress in the liver and kidney of mothers and their pups by increasing the level of malondialdehyde (MDA) and decreased activities of superoxide dismutase (SOD) and glutathione-transferase (GST). ABA altered the level of serum liver and kidney dysfunction biomarkers either in the mothers or their male and female pups in a dose-dependent manner. It caused histopathological alterations in the liver and kidney tissues. It can be decided that ABA was accumulated in mother's milk, transferred through breast feeding, and induced mortality in their suckling pups. It caused oxidative stress, lipid peroxidation, and biochemical and histopathological alterations in the liver and kidney of mothers and their suckling pups. The results in the present study add some information about the adverse effect of lactation transfer of ABA, which is important for human health in the third-world countries where breastfeeding may be the only source of nutrition for infants in the first and most critical weeks of life.