MANGANESE SUPEROXIDE DISMUTASE AND IN VIVO AGING

锰超氧化物歧化酶和体内老化

• 批准号: 6084008
• 负责人: ATANU DUTTAROY
• 金额: $ 12.76万
• 依托单位: HOWARD UNIVERSITY
• 依托单位国家: 美国
• 财政年份: 2000
• 资助国家: 美国
• 起止时间: 2000-09-01 至 2004-08-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/6084008
• 关键词: Drosophilidae; aging; enzyme mechanism; manganese; mutant; neuropathology; neurotoxicology; oxidative stress; superoxide dismutase

DESCRIPTION (adapted from the Investigator's abstract): The proposed research will probe into the requirement of manganese-superoxide dismutase [MnSOD] in aging and tissue damages thereof through some unique mutant models in Drosophila. These mutant models will be used to (1) investigate the effect of overexpression of MnSOD in different tissues in a directed fashion, testing the hypothesis that overexpression of MnSOD in specific tissue or cell types extends the life span by offering increased protection against oxidative damage; (2) investigate the effect of loss of MnSOD function in specific tissue or cell types, testing the hypothesis that loss of MnSOD function is associated with increased oxidative stress causing accelerated tissue damages; (3) investigate the effects of missense mutations in MnSOD gene, testing the hypothesis that like in familial amyotrophic lateral sclerosis (FALS) patients, altered MnSOD activity could cause neuropathology and degenerative tissue damages.

描述（改编自研究者的摘要）：拟议的研究 将探讨锰超氧化物歧化酶[MnSOD]的需求 通过一些独特的突变模型来研究衰老及其组织损伤 果蝇。这些突变模型将用于（1）研究 MnSOD 在不同组织中以定向方式过度表达，测试 假设 MnSOD 在特定组织或细胞类型中过度表达 通过提供更强的抗氧化保护来延长使用寿命 损害; (2)研究特定组织中MnSOD功能丧失的影响 或细胞类型，检验与 MnSOD 功能丧失相关的假设 氧化应激增加导致加速组织损伤； (3) 研究 MnSOD 基因错义突变的影响，测试 假设就像家族性肌萎缩侧索硬化症（FALS）患者一样， MnSOD 活性改变可能导致神经病理学和退行性组织 损害。