Nitric oxide and apoptosis in white mice heart during aging

Nino Tevzadze, Rusudan Rukhadze

Department of Histology, Cytology and Embryology, Tbilisi State Medical University, Georgia

The process of aging and senescence is associated with a decline in several organ functions and ultimately takes away independence and reduces quality of life. Programmed cell death or apoptosis is highly involved throughout the aging process, from early developmental changes to senescent declines in function. Multiple pathways exist for inducing apoptosis. In recent years, several studies have established that nitric oxide (NO) and its reaction products can either promote or prevent apoptosis in a multitude of settings. The ubiquitous distribution of the NO synthases and the remarkable diffusibility and diverse chemical reactivity of NO in biological systems make this molecule unique among the regulators of apoptosis. This study was designed to investigate the influence of nitric oxide (NO) on cardiomyocyte's apoptosis in white mice during aging. 30 white mice were used. The animals were distributed in three age groups: juveniles, adults and senescents. The animals were killed under ether narcosis. The heart was removed. Apoptotic nuclei were detected by immunomorphological and Flow cytometry assay. Concentration of NO in samples was measured by ESR Study. The results showed, that the increase of apoptosis in cardiomyocytes during aging is accompaned by decrease in NO production. According to our data, it can be considered that the antiapoptotic effect of nitric oxide on cardiomyocytes declines with aging.

Keywords:  cardiomyocyte, aging, nitric oxide, apoptosis