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 round in either complex I and IV activities, thiobarbituric acid-reactive substances (TBARS), or glutathione peroxidase (GPx) activity in SAMR1. In contrast, SAMP8 showed significant age-associated decreases in complex I and IV activities. While no age effect was round in TBARS in SAMP8, TBARS levels in SAMP8 were significantly more abundant than in SAMR1. GPx activity in SAMP8 decreased significantly by 12 months. Daily oral melatonin administration (2 μg/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 SAMR1 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.
- Free radical respiratory chain
- Senescence-accelerated mice
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