Protective effect of amino acid, Glycine in broilers fed on Imidacloprid treated rations

Abstract

Broiler chicks were segregated into three groups. Group 1 fed on a basal diet and served as a control, group 2 was given Imidacloprid (IM) at a dose of 50 mg/kg diet and group 3 was dietary supplemented with 0.5 % Glycine (GLY) and IM (50 mg/kg diet) for 4 weeks. Blood and tissue samples were collected on the 7th, 14th, 21st, and 28th days. The obtained findings revealed that IM residues were beyond the maximum residue limit (MRL) (0.02 ppm) and were significantly higher in muscles ranging from 0.042±0.0039 to 0.073±0.0026 ppm and in liver tissues ranging from 0.466±0.033 to 0.790±0.017 ppm) throughout the experimental time interval in IM-treated chicks. IM induced a significant decline in the total erythrocytic count (TEC), packed cell volume (PCV), mean corpuscular volume (MCV), hemoglobin (Hb), mean corpuscular hemoglobin (MCH), mean corpuscular hemoglobin concentration (MCHC), total leucocytic counts (TLC) and lymphocyte percent. IM-treated chicks exhibited a significant reduction in the levels of serum acetylcholinesterase (AchE). Besides, the hepatic antioxidants activities [(superoxide dismutase (SOD), catalase (CAT) and reduced glutathione (GSH)] were significantly decreased. A significant increase in the levels of serum alanine aminotransferase (ALT), aspartate aminotransferase (AST), alkaline phosphatase (ALP), uric acid, creatinine, hepatic lipid peroxide malondialdehyde (MDA), heterophils and monocyte percent were observed in IM-treated chicks. Furthermore, IM induced a significant histopathological lesions in the liver, kidney and muscles. Conclusively, GLY supplementation inhibited IM accumulation. Therefore, IM residues were not detected in muscles, while ranging from (0.250±0.029 to 0.553±0.023) ppm in liver tissues of GLY and IM-treated chicks. Dietary GLY improved liver and kidney function and ameliorated hematological alterations, neurotoxicity, oxidative stress and histopathological lesions induced by IM.