Abstract: To study the relationship between oxidative stress and mitochondrial damage during post-slaughter chilling, M. longissimus dorsi from Tan sheep was treated with the antioxidant N-acetyl-L-cysteine (NAC) solution or physiological saline and stored at 0–4 ℃. After 0, 2, 4, 6 and 8 days, the opening degree of mitochondrial permeability transition pore (MPTP), membrane potential, reactive oxygen species (ROS) content, complex I, II, III and IV activities, the activities of succinate dehydrogenase (SDH), catalase (CAT), superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) and malondialdehyde (MDA) content were determined, and the mitochondrial structure of myoblasts was observed under transmission electron microscopy (TEM). The results showed that the opening degree of MPTP in both the NAC and control groups gradually increased (P < 0.05) during the postmortem maturation process, and so did the ROS and MDA levels (P < 0.05). The mitochondrial membrane potential and the activities of complexes I, II, III and IV, SDH, CAT, SOD and GSH-Px showed a gradual decreasing trend (P < 0.05). It can be concluded that oxidative stress occurred in the muscle tissue of Tan sheep after slaughter, resulting in a significant increase in ROS content. Excessive ROS, exceeding the ability of the antioxidant defense system to scavenge it, could lead to an imbalance in the redox system, which could in turn accelerate the increase of ROS levels, thereby triggering the opening of MPTP and a decrease in the mitochondrial membrane potential, finally resulting in serious mitochondrial damage. However, NAC alleviated this phenomenon. Increased ROS levels impaired the normal operation of the mitochondrial electron transport chain, thus leading to increased mitochondrial damage. In addition, the lipid oxidation product MDA also damaged the function and structure of mitochondria, causing mitochondrial structural damages such as swelling and deformation, and finally leading to biological dysfunctions.

Key words: Tan sheep; oxidative stress; mitochondria; functional impairment