Honda Y, Honda S
Tokyo Metropolitan Institute of Gerontology, 35-2 Sakaecho, Itabashiku, Tokyo, 173-0015 Japan.
J Am Aging Assoc. 2002 Jan;25(1):21-8. doi: 10.1007/s11357-002-0003-2.
Life span could be modified by genetic or environmental perturbations in Caenorhabditis elegans. Here we show that two extensions of life span are associated with oxidative stress resistance and upregulation of the gene expression of antioxidant enzymes. First, mutations in age-1 gene (PI3 kinase homologue)that confer life span extension, display oxidative stress resistance and increase in the gene expression of sod-3, one of two Mn-superoxide dismutases (SOD) and ctl-1, cytosolic catalase. In this study, these traits appear to be regulated by the following genetic pathway: daf-2 (insulin receptor family)-> daf-18 (PTEN homologue)-> age-1-> daf-16 (Fork head transcription factor family), similar to the genetic pathway for the life span extension. Second, we show that short-term exposure to hyperoxia extends life span slightly but significantly. This treatment increases oxidative stress resistance and the gene expression of three types of SOD isoforms. These results suggest that both of these two life span extensions are closely related with increase in the antioxidant defense function.
在秀丽隐杆线虫中,寿命可通过基因或环境扰动进行调节。在此我们表明,两种寿命延长情况与抗氧化应激能力以及抗氧化酶基因表达的上调相关。首先,age-1基因(PI3激酶同源物)的突变可延长寿命,表现出抗氧化应激能力,并使两种锰超氧化物歧化酶(SOD)之一的sod-3以及胞质过氧化氢酶ctl-1的基因表达增加。在本研究中,这些特性似乎受以下遗传途径调控:daf-2(胰岛素受体家族)-> daf-18(PTEN同源物)-> age-1-> daf-16(叉头转录因子家族),这与寿命延长的遗传途径相似。其次,我们表明短期暴露于高氧环境可使寿命稍有但显著延长。这种处理增加了抗氧化应激能力以及三种SOD同工型的基因表达。这些结果表明,这两种寿命延长情况均与抗氧化防御功能的增强密切相关。