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Melatonin protects hepatic mitochondrial respiratory chain activity in senescence-accelerated mice
Yuji Okatani1, Akihiko Wakatsuki, Russel J Reiter
1Department of Clinical Nursing Science, Kochi Medical School, Nankoku, Japan. okataniy@med.kochi-ms.ac.jp
Abstract:
Mitochondrial oxidative damage from free radicals may be a factor underlying aging, and melatonin, a powerful free radical scavenger, may participate in mitochondrial metabolism. We measured respiratory chain complex I and IV activities in liver mitochondria from a strain of senescence-accelerated prone mice (SAMP8) and a strain of senescence-accelerated resistant mice (SAMR1) at age 3, 6, and 12 months. No age-associated effects were found in either complex I and IV activities, thiobarbituric acid-reactive substances (TBARS), or glutathione peroxidase (GPx) activity in SAMRI. In contrast, SAMP8 showed significant age-associated decreases in complex I and IV activities. While no age effect was found in TBARS in SAMP8, TBARS levels in SAMP8 were significantly more abundant than in SAMRI. GPx activity in SAMP8 decreased significantly by 12 months. Daily oral melatonin administration (2 microg/mL of drinking fluid) beginning when the mice were 7 months old significantly increased complex I and IV activity, decreased TBARS, and increased GPx activities in both SAMRI and SAMP8 at 12 months. The implication of the findings is that melatonin may be beneficial during aging as it reduced the deteriorative oxidative changes in mitochondria and other portions of the cell associated with advanced age.
Insights
Melatonin, a potent antioxidant, may combat aging by protecting mitochondria. This study shows melatonin improves mitochondrial function and reduces oxidative stress in aging mice, suggesting a beneficial role in aging processes.
Area of Science:
- Gerontology
- Mitochondrial Biology
- Oxidative Stress
Background:
- Mitochondrial oxidative damage is implicated in aging.
- Melatonin is a powerful free radical scavenger with potential roles in metabolism.
Purpose of the Study:
- To investigate the effects of aging on mitochondrial function in senescence-accelerated mice.
- To evaluate the impact of melatonin supplementation on mitochondrial oxidative damage and function during aging.
Main Methods:
- Assessed respiratory chain complex I and IV activities, thiobarbituric acid-reactive substances (TBARS), and glutathione peroxidase (GPx) activity in liver mitochondria.
- Used senescence-accelerated prone (SAMP8) and resistant (SAMR1) mice at 3, 6, and 12 months of age.
- Administered oral melatonin to mice starting at 7 months of age.
Main Results:
- Senescence-accelerated prone mice (SAMP8) exhibited age-associated declines in complex I and IV activities and decreased GPx activity.
- SAMP8 mice showed higher levels of TBARS compared to SAMR1 mice.
- Melatonin administration significantly improved complex I and IV activities, reduced TBARS, and increased GPx activity in both mouse strains at 12 months.
Conclusions:
- Aging is associated with mitochondrial dysfunction and increased oxidative stress, particularly in senescence-prone mice.
- Melatonin supplementation effectively counteracted age-related mitochondrial deterioration and oxidative damage.
- Melatonin may be a beneficial intervention to mitigate age-associated cellular damage and support mitochondrial health during aging.