Lysosomal Fe2+contributes to myofibrillar protein degradation through mitochondrial-dysfunction-induced apoptosis. (May 2021)

• Record Type: Journal Article
• Authors: Chen, Cheng; Guo, Zhaobin; Ma, Guoyuan; Ma, Jibing; Zhang, Zhen; Yu, Qunli; Han, Ling
• Is Part Of: Lebensmittel-Wissenschaft + Technologie =. Volume 143(2021)
• Publication Date: 2021-05
• Subjects: Mitochondrial swelling -- Cytochrome c -- Caspase-3 -- μ-calpain -- Protein degradation; Food industry and trade -- Periodicals; Food -- Composition -- Periodicals; Microbiology -- Periodicals; Nutrition -- Periodicals; 664.005
• DOI: 10.1016/j.lwt.2021.111197
• Languages: English
• ISSNs: 0023-6438

Abstract

Abstract: To verify the role of lysosomal Fe 2+ in mitochondrial-dysfunction-mediated apoptosis and postmortem tenderization of bovine muscles, mitochondrial apoptotic factors, myofibrillar protein degradation, and μ-calpain activity were evaluated in the control group and the iron chelator desferrioxamine (DFO) group. The control group showed 1) increased mitochondrial swelling and lipid peroxidation by 47% and 36% at 72 h, respectively ( P < 0.05), significantly higher than the DFO group at 12–24 h and 72–168 h ( P < 0.05); 2) significantly increased mitochondrial Ca 2+ influx at 12–24 h ( P < 0.01); 3) a 15%, 24%, and 30% lower cytochrome c reduction level than the DFO group at 6–24 h ( P < 0.01, P < 0.05); 4) a significantly increased caspase-3 expression level at 0–120 h ( P < 0.05), where the caspase-3 activity was 30% and 49% higher than that of the DFO group at 12–24 h, respectively ( P < 0.01); 5) an increased μ-calpain activity by 56% at 24–168 h ( P < 0.05), and 6) 75% ( P < 0.01) and 34% ( P < 0.05) higher degradation of desmin and troponin-T than the DFO group at 168 h, respectively. In summary, lysosomal Fe 2+ facilitates postmortem tenderization by promoting the mitochondrial-dysfunction-induced apoptosis of bovine muscle. Highlights: Fe 2+ induces mitochondrial dysfunction by accelerating lipid peroxidation. Fe 2+ increases mitochondrial Ca 2+ accumulation and cytochrome c oxidation level. Fe 2+ promotes upregulation of caspase 3 expression and increases its activity. Mitochondrial dysfunction severs as a trigger for apoptosis of bovine muscle. Fe 2+ -induced mitochondrial apoptotic pathway contributes to meat tenderization.