Astaxanthin Prevents Dysregulation of Mitochondrial Dynamics in Rat Brain Mitochondria Induced by Isoproterenol

Abstract

Mitochondria are involved in diseases of various etiologies. The use of drugs aimed at improving the functional state of mitochondria may be a promising therapeutic approach to diseases of various etiologies. Astaxanthin is a keto-carotenoid (xanthophyll) of predominantly marine origin. It has both lipophilic and hydrophilic properties and can penetrate through the cell membrane, localizing in the mitochondria and preventing mitochondrial dysfunction. In this paper, the effect of astaxanthin on the functional state of rat brain mitochondria, changes in mitochondrial dynamics and mitophagy in isoproterenol-induced damage is studied. Under the action of astaxanthin, mitochondria are more resistant to the Ca²⁺-induced opening of a nonspecific pore and the activity of complexes I, IV, and V of the respiratory chain increases. Moreover, astaxanthin alters the level of markers of mitochondrial fission and fusion, as well as mitophagy in isoproterenol-induced mitochondrial dysfunction, which probably leads to an increase in the number of functional mitochondria of the rat brain and improved their condition. Astaxanthin can be considered as a mitochondria-directed agent in the therapy for pathological conditions associated with oxidative damage and mitochondrial dysfunction caused by heart failure. As a dietary supplement, astaxanthin has the potential for the antioxidant protection of cells in cardiovascular diseases.