Lead Caused Developmental Cardiotoxicology in Japanese Quail (Coturnix japonica): Histopathological Injury, Oxidative Stress, Cell Apoptosis, and AMPK‐Based Energy Metabolism Disruption

Lead (Pb) is a well‐known environmental toxin that can accumulate in organisms, especially birds, and cause damage to multiple avian organs and systems, among which the heart is the vital target organ. However, the toxicological impacts of Pb on cardiac tissue remain poorly understood, and the specific molecular mechanism has not been fully elucidated. Therefore, the aim of this study was to examine the effects of chronic Pb exposure on avian heart by using a toxicological model animal—Japanese quail ( Coturnix japonica ). One‐week‐old quail chicks were exposed to 0, 50, 500, and 1000 ppm Pb concentrations in drinking water for 5 weeks. The results showed Pb exposure lowered body weight and adenosine triphosphate (ATP) content in the cardiomyocytes of quails. Meanwhile, both microscopic and ultrastructural analyses revealed substantial cardiac tissue damages. In particular, myocardial fiber disarrangement and dissolution were observed. Moreover, mitochondrial swelling, vacuolation, ridge fracture, membrane dissolution, and hyperplasia were also detected. In addition, excessive cardiac oxidative stress caused by Pb exposure can be confirmed by changes in the content and activity of relevant biomarkers. Pb interference also induced abnormal cardiac apoptosis. Moreover, Pb exposure caused glucose and lipid metabolism disorder resulting in insufficient energy supply in the heart through activating adenosine monophosphate‐activated protein kinase (AMPK) pathway. The present study demonstrated that Pb caused cardiotoxicity through structural injury, abnormal apoptosis, oxidative stress, and AMPK signaling activation.