Effect of mitochondrial calcium homeostasis-mediated endogenous enzyme activation on tenderness of beef muscle based
Zhenjiang Ding1, Chunmei Liu2, Zihan Zhang2
1Beijing Key Laboratory of the Innovative Development of Functional Staple and Nutritional Intervention for Chronic Diseases, China National Research Institute of Food and Fermentation Industries, Beijing 100015, China.
Abstract:
The mitochondrial calcium uniporter (MCU) occupies a noteworthy position in the regulation of mitochondrial calcium uptake. This study investigated the effects of MCU modulator-mediated mitochondrial calcium on mitochondrial dysfunction, oxidative stress, endogenous enzyme activities, and tenderness during postmortem aging. Spermine, as an activator of MCU, resulted in an increase in mitochondrial calcium levels, not only disrupting mitochondrial morphology but also triggering mitochondrial oxidative stress and downregulation of antioxidant factors. Additionally, the spermine group underwent later activation of calpain and earlier activation of caspases, as well as the myofibril fragmentation index was initially lower and then higher compared with control group, indicating that endogenous enzymes played an indispensable role in different aging periods. Interestingly, the results of the Ru360 (an inhibitor of MCU) group were opposite to those aforementioned findings. Our data provide a novel perspective on the regulatory mechanism of mitochondrial calcium homeostasis mediated by MCU on tenderness.
Insights
Mitochondrial calcium uniporter (MCU) modulators impact meat tenderness. Activating MCU increases mitochondrial calcium, causing dysfunction and altering enzyme activity, while inhibiting MCU shows opposite effects on meat aging.
Area of Science:
- Biochemistry
- Cellular Biology
- Food Science
Background:
- Mitochondrial calcium uptake is regulated by the mitochondrial calcium uniporter (MCU).
- Understanding MCU's role in postmortem aging is crucial for meat quality.
- Mitochondrial dysfunction and oxidative stress impact meat tenderness.
Purpose of the Study:
- To investigate the effects of MCU modulators on mitochondrial calcium levels.
- To determine the impact of MCU-mediated calcium changes on mitochondrial dysfunction, oxidative stress, and endogenous enzyme activities.
- To elucidate the relationship between MCU activity and meat tenderness during postmortem aging.
Main Methods:
- Utilized spermine as an MCU activator and Ru360 as an MCU inhibitor.
- Assessed mitochondrial morphology, calcium levels, and oxidative stress markers.
- Measured endogenous enzyme activities (calpain, caspases) and myofibril fragmentation index.
- Evaluated meat tenderness postmortem.
Main Results:
- Spermine (MCU activator) increased mitochondrial calcium, disrupted morphology, induced oxidative stress, and altered antioxidant factors.
- Spermine group showed delayed calpain activation and earlier caspase activation.
- Ru360 (MCU inhibitor) produced opposite effects to spermine.
- Myofibril fragmentation index exhibited a biphasic pattern in the spermine group.
Conclusions:
- MCU plays a significant role in regulating mitochondrial calcium homeostasis.
- MCU-mediated mitochondrial calcium influences mitochondrial dysfunction and oxidative stress.
- Endogenous enzyme activities and subsequent meat tenderness are modulated by MCU activity during postmortem aging.
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