2′,3′-Cyclic nucleotide 3′-phosphodiesterase as a messenger of protection of the mitochondrial function during melatonin treatment in aging

The process of aging is considered to be tightly related to mitochondrial dysfunction. One of the causes of aging is an increased sensitivity to the induction of mitochondrial permeability transition pore (mPTP) opening in the inner membrane of mitochondria. Melatonin, a natural antioxidant, is a hormone produced by the pineal gland. The role of melatonin whose level decreases with aging is well understood. In the present study, we demonstrated that long-term treatment of aged rats with melatonin improved the functional state of mitochondria; thus, the Ca2+ capacity was enhanced and mitochondrial swelling was deaccelerated in mitochondria. Melatonin prevented mPTP and impaired the release of cytochrome c and 2′,3′-cyclic nucleotide 3′-phosphodiesterase (CNPase) from mitochondria of both young and aged rats. Our data suggest that melatonin retains СNPase inside mitochondria, thereby providing the protection of the protein against deleterious effects of 2′,3′-cAMP in aging. [Display omitted] •Melatonin is involved in the process improving the mitochondrial function in aging.•Melatonin abolishes the effect of 2′,3′-cAMP on mPTP opening.•Melatonin prevents the cytochrome c release from mitochondria in aging.•Melatonin retains СNPase inside mitochondria to protect cells.