Mitochondrial Degeneration, Depletion of NADH, and Oxidative Stress Decrease Color Stability of Wet-Aged Beef Longissimus Steaks.

Interrelationship between mitochondria and myoglobin function influence beef color. NADH level in postmortem muscle is an important determinant of mitochondrial activity and metmyoglobin reduction. Increased aging time promotes discoloration of steaks; however, the mechanism of this effect is not clear. The objective was to characterize the role of wet-aging in beef longissimus lumborum muscle mitochondrial function and to characterize the global metabolome to determine the mechanism of that can regenerate NADH. Beef longissimus lumborum muscles were randomly assigned to 3, 7, 14, 21, and 28 days aging periods. Surface color, biochemical, mitochondrial, and metabolite profiles were determined at each aging period and at the end of 6-day display. During 6-day display, sections aged for 28 days had 30.4% decrease in redness than sections aged for 3 days. Aging time decreased (P <0.05) muscle oxygen consumption, mitochondrial protein content, and antioxidant capacity. Metabolites such as fumaric acid, creatinine, and fructose, that can take part in glycolytic/TCA cycle and regenerate NADH decreased (P <0.05) with aging and display time. In support, NADH levels also decreased (P <0.05) with aging time, but aging time had no effect (P = 0.44) on NADH-dependent reductase activity. The results suggest that decreased color stability in aged beef can be attributed to increased mitochondrial damage, depletion of metabolites that can regenerate NADH, and increased oxidative stress. PRACTICAL APPLICATION: Beef aging time results in increased discoloration of steaks under retail display. The current research determines the fundamental basis of lower color stability in aged beef. The results indicate that mitochondrial degeneration, depletion of metabolites that produce NADH, and increased oxidative stress can limit shelf-life of aged steaks. Hence, application of post-harvest strategies to minimize mitochondrial damage and oxidative changes may have the potential to increase shelf-life of aged beef.