Hepatic mitochondrial dysfunction in senescence-accelerated mice: correction by long-term, orally administered physiological levels of melatonin.

@article{Okatani2002HepaticMD,
  title={Hepatic mitochondrial dysfunction in senescence-accelerated mice: correction by long-term, orally administered physiological levels of melatonin.},
  author={Yuji Okatani and Akihiko Wakatsuki and Russell J Reiter and Yasuyo Miyahara},
  journal={Journal of pineal research},
  year={2002},
  volume={33 3},
  pages={127-33}
}
Mitochondrial oxidative damage from free radicals may be a factor underlying aging. We investigated whether long-term administration of physiological levels of melatonin, a direct free radical scavenger and indirect antioxidant, influences mitochondrial respiratory activity in liver of senescence-accelerated mice (SAM). Liver was obtained in the middle of dark period of the daily light:dark cycle from SAMP8, a strain of mice prone to accelerated senescence, and from SAMR1, a senescence… CONTINUE READING