Effects of aging on mitochondrial hydrogen peroxide emission and calcium retention capacity in rat heart

Abstract

Aging is a risk factor for heart disease and heart failure, which result from a progressive impairment of cardiac functions, including stroke volume, cardiac output, blood flow, and oxygen consumption. Age-re-lated cardiac dysfunction is associated with impaired cardiac struc-tures, such as the loss of myocytes, structural remodeling, altered cal-cium (Ca2+) handling, and contractile dysfunction. However, the mecha-nism by which aging affects mitochondrial function in the heart is poorly understood. The purpose of this study was to determine the effects of aging on mitochondrial function in the rat heart. Male Fischer 344 rats were randomly assigned to very young sedentary (VYS, 1 month), young sedentary (YS, 4 months), middle-aged sedentary (MS, 10 months), and old sedentary (OS, 20 months) groups. mitochondrial complex protein levels and mitochondrial function (e.g., mitochondrial hydrogen perox-ide (H2O2) emission and Ca2+ retention capacity) were analyzed in the left ventricle. Aging was associated with decreased levels of OXPHOS (oxidative phosphorylation) protein expression of complex I to IV in the function of the electron transport chain. Aging increased the mitochon-drial H2O2 emitting potential in the heart. In contrast, mitochondrial Ca2+ retention capacity gradually decreased with age. These data demon-strate that aging impairs mitochondrial function in cardiac muscle, sug-gesting that mitochondrial dysfunction with aging may be a primary factor for aging-induced cardiac dysfunction in the heart.