Effect of non-selenium glutathione peroxidase activity of peroxiredoxin 6 on beef tenderness: underlying mechanisms

This study investigated the effect of non-selenium glutathione peroxidase (NSGPx) activity of Peroxiredoxin 6 (Prdx6) on beef tenderness. Longissimus thoracis et lumborum (LTL) muscle from six cattle were obtained at 30 min post-mortem. Samples from each muscle were randomly assigned to each of four treatment groups: being incubated in H2O2 (simulation of oxidative stress), mercaptosuccinic acid (MA; inhibiting NSGPx activity), N-acetyl-L-cysteine (NAC; inhibiting oxidative stress and increasing NSGPx activity), and saline (control), respectively. Results indicated that cells increased the expression of Prdx6 and NSGPx activity to resist oxidative stress. The inhibition of NSGPx activity group (MA) significantly decreased the Warner-Bratzler shear force and increased the degradation of desmin. Moreover, both the H2O2 and the MA treatment significantly increased the Ca2+ concentration in the sarcoplasm, cell apoptotic rate, and caspase 9 and 3 activity. These results demonstrated that inhibiting NSGPx activity of Prdx6 could accelerate beef tenderization by promoting mitochondrial apoptosis. This study investigated that the inhibition of non-selenium glutathione peroxidase (NSGPx) activity of Peroxiredoxin 6 (Prdx6) enhanced the oxidative stress, and there resulted in the increase of cell apoptosis and further accelerated the tenderization process of bovine Longissimus thoracis et lumborum. image