The potential mediation of nitric oxide in the activation of mitochondrion-dependent apoptosis and yak meat tenderness during postmortem aging

Abstract

Nitric oxide (NO) may play a critical role in the regulation of various physiological and pathophysiological processes due to its effect on the apoptosis pathway. However, few reports have studied the effects of NO on apoptosis and yak meat tenderization. The present study was conducted to explore the molecular mechanisms of Ca2+-independent inducible NO synthase isozyme (iNOS)-derived NO in mitochondrial apoptosis and meat tenderization during postmortem aging. Results indicated that the aminoguanidi hydrochloride (AH) significantly reduced iNOS activities and NO production. Moreover, the inhibitory property of iNOS-derived NO dramatically decreased mitochondrial oxidative stress degree, which further reduced the production of mitochondrial Ca2+ and ATP. The inhibitory property of iNOS-derived NO also influenced the Bcl-2 family members, mitochondrial apoptotic cascade reaction, and meat tenderization by protecting against the degradation of myofibrils and the damage of mitochondrial microstructure. These results demonstrated that the iNOS-derived NO possessed a significant role in the mitochondrial apoptosis pathway and yak meat tenderization during aging.