Abstract
Reactive oxygen species (ROS) are toxic substances produced during metabolic processes. ROS increase internal oxidative stress. ROS produced in living organisms are highly reactive and damage lipids, proteins and DNA. ROS-mediated DNA damage contributes to spontaneous mutagenesis. The oxidation of DNA results in various functional disorders, including premature aging and cancer. Recently, the OXR1 gene was identified in human cells and revealed to be involved in protection against oxidative stress. However, its function still remains uncertain. The nematode C. elegans is often used to clarify the mechanisms underlying aging and development. However, any homologs of human OXR1 have not been identified in the nematode. In this study, we first identified the C. elegans homolog CeOXR and examined the roles of CeOXR in protection against oxidative stress. We cloned the CeOXR gene and examined whether this protein could complement the phenotype of the E. coli mutM mutY mutant. The double mutant shows a high mutation frequency. We found that the E. coli mutM mutY mutant expressing the cloned CeOXR protein showed a decreased mutation frequency, indicating that the CeOXR suppress the oxidative stress in C. elegans. Furthermore, we compared the lifespan of C. elegans CeOXR mutant with that of wild-type strain N2. The lifespan of CeOXR mutant was shorter than that of wild-type N2. Thus, CeOXR may have a function to extend lifespan by suppressing the oxidative stress in C. elegans.
