Astaxanthin Prevents Dysregulation of Mitochondrial Dynamics in Rat Brain Mitochondria Induced under Isoproterenol-Induced Injury

Abstract

Mitochondria are involved in the development of diseases with different etiologies. The use of drugs which can enhance the functional state of mitochondria may turn into a promising therapeutic approach to diseases with different etiologies. Astaxanthin, a keto-carotenoid (xanthophyll) predominantly of marine origin, shows both lipophilic and hydrophilic properties and can penetrate the cell membrane to localize to mitochondria where it prevents mitochondrial dysfunction. This study examined the effect of astaxanthin on the functional state of rat brain mitochondria, investigated the changes in mitochondrial dynamics and mitophagy under isoproterenol-induced injury. In the presence of astaxanthin, mitochondria were more resistant to Ca2+-induced opening of a nonspecific pore, and the activity of complexes I, IV and V of the respiratory chain increased. Moreover, the presence of astaxanthin led to altered mitochondrial fission and fusion as well as mitophagy, in isoproterenol-induced mitochondrial dysfunction. This presumably increased the quantity of rat brain mitochondria and enhanced their functional state. Astaxanthin can be considered as a mitochondria-targeted agent in therapy in pathological conditions associated with oxidative damage and mitochondrial dysfunction caused by acute heart failure. Astaxanthin as a dietary supplement has the potential to provide antioxidant protection to cells in cardiovascular disease.