The disruption of mitochondrial metabolism and ion homeostasis in chicken hearts exposed to manganese

Exposure to high levels of manganese (Mn) can result in cardiotoxicity in animals. However, little is known about the effect of excess Mn on poultry hearts. The aim of this study was to investigate the effect of dietary Mn on chicken cardiac injuries and the possible mechanisms of this process. In the present study, 400 fifty-day-old Hy-line brown cocks were randomly divided into four groups, and were fed either a commercial diet (containing 100 mg/kg Mn) or a Mn-supplemented diet containing 600 mg/kg, 900 mg/kg, or 1800 mg/kg Mn for 30, 60 or 90 days, respectively. Next, we examined several biomarkers of cardiac injury, including biochemical blood serum analyses, electrocardiogram assays, histological analyses, ultra-structural assays and apoptosis assays. To investigate the possible mechanisms of Mn-induced cardiotoxicity, we examined the effect of MnCl2 on mitochondrial function and metal ion homeostasis. We found that subchronic MnCl2 exposure induced damage in chicken hearts. Further investigations indicated that possible mechanisms for Mn-induced chicken cardiac injury included the disruption of mitochondrial metabolism and the alteration of ion homeostasis.

► Mn exposure induced the increase of serum CK and cTnT; abnormal electrocardiogram and ultra-structure, and apoptosis in heart of chicken.
► Mn exposure induced the disruption of mitochondrial metabolism in heart.
► Mn exposure induced the alteration of ion homeostasis in heart including Ca, Fe, Cu, Zn.