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Melatonin protects hepatic mitochondrial respiratory chain activity in senescence‐accelerated mice
Author(s) -
Okatani Yuji,
Wakatsuki Akihiko,
Reiter Russel J.
Publication year - 2002
Publication title -
journal of pineal research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.881
H-Index - 131
eISSN - 1600-079X
pISSN - 0742-3098
DOI - 10.1034/j.1600-079x.2002.1o106.x
Subject(s) - tbars , melatonin , endocrinology , medicine , senescence , glutathione peroxidase , thiobarbituric acid , oxidative stress , mitochondrial respiratory chain , mitochondrion , respiratory chain , biology , chemistry , lipid peroxidation , biochemistry , superoxide dismutase
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 SAMR1. 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 SAMR1. GPx activity in SAMP8 decreased significantly by 12 months. Daily oral melatonin administration (2 μ g/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.