Energy metabolism abnormality of ultraviolet irradiation sensitive mutant <I>rad-8</I> in <I>C.elegans</I>

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  • 線虫<I>C.elegans</I> における紫外線感受性株<I>rad-8</I>のエネルギー代謝異常

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C. elegans rad-8 has been isolated as an ultraviolet radiation hypersensitive mutant1) and we have also found that this mutant is oxygen hypersensitive2). Reactive Oxygen Species (ROS) as well as radiation cause cellular damages and result in a variety of diseases including cancer and aging. It is well known that most endogenous ROS are produced from mitochondria. Mitochondria are specialized organelles that produce ATP, regulate programmed cell death, or apoptosis and produce the ROS as a byproduct of energy metabolism. In order to know whether oxidative sensitivity of rad-8 mutant is correlated with mitochondrial oxidative stress, we examined, 1) amount of supeoxide anion (O2-) one of ROS, from mitochondria and 2) carbonylated protein as a marker of oxidative stress, 3) apoptosis at embryonic stage, 4) growth rate and 5) energy metabolism. Our results showed that the level of O2- and the carbonylated protein in mitochondria produced by the O2- significantly increased compared to N2 wild type. The apoptosis also increased. On the other hand, the energy metabolisms and growth rate of rad-8 were lower compared to N2. Furthermore, the body size of rad-8 at the adult stage was smaller than N2. These data suggested that the function of rad-8 gene is related with mitochondria. It is assumed that the energy metabolic abnormality in rad-8 mitochondria leads to increase of oxidative stress and apoptosis by the ROS over production.<BR> <BR> References<BR> 1) Hartman PS et al., Genetics 102:157-178, 1982<BR> 2) Ishii N, et al., Mech. Ageing Develop. 68: 1-10, 1993

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