Lead (Pb) is one of the most toxic metals to human and wildlife. It also had multiple negative influences on birds with physical, neurological and hematological clinical signs. However, the impacts of lead on bird liver lipid metabolism are still unclear. In this study, female Japanese quails were used to examine the effects of chronic lead exposure on liver histology, oxidative stress and AMPK (AMP-activated protein kinase) based lipid metabolism. Quails were randomly divided into 5 groups and each group was respectively fed with 0, 50, 250, 500 and 1000 ppm lead solution for 49 days. The result showed that exposure to 250, 500 and 1000 ppm Pb induced severe histopathological damages characterized by liver lipid vacuoles and accumulation, hepatic cytoplasmic hyalinization and vacuolization, hepatocytes necrosis, hepatic sinusoid congestion, and it also caused ultrastructural alterations featured by swelling and vacuolar mitochondria, the depolymerization of polyribosome, and lipid droplets accumulation. Moreover, significant decrease of activities of GPx (glutathione peroxidase), SOD (superoxide dismutase), CAT (catalase) and level of T-AOC (total antioxidant capacity) while significant increase of MDA (malondialdehyde) content were found in livers of all Pb groups. In addition, the expressions of genes related to fatty synthesis were significantly upregulated in livers of all Pb groups while the expressions of genes related to fatty β-oxidation were significantly downregulated in livers of 250 ppm Pb group. The present study indicated lead exposure does cause bird health damages through inducing liver microstructural and ultrastructural injury, oxidative damages and lipid metabolism disorder.
Keywords: AMPK pathway; Histopathology; Japanese quails; Lead; Lipid metabolism; Oxidative stress.
Copyright © 2019 Elsevier Inc. All rights reserved.