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相關文獻
- Mutation and Oxidative Damage of Mitochondrial DNA and Defective Turnover of Mitochondria in Human Aging
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頁籤選單縮合
題 名 | Mutation and Oxidative Damage of Mitochondrial DNA and Defective Turnover of Mitochondria in Human Aging=人類老化過程中粒線體DNA的突變及氧化性損傷與粒線體汱換缺陷 |
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作 者 | 李新城; 魏耀揮; | 書刊名 | 臺灣醫學會雜誌 |
卷 期 | 96:10 1997.10[民86.10] |
頁 次 | 頁770-778 |
分類號 | 415.149 |
關鍵詞 | 人類老化; 粒線體DNA; 突變; 氧化性損傷; 粒線體汱換缺陷; Aging; Oxidative damage; Mitochondrial DNA; Mutation; Mitochondrial turnover; |
語 文 | 英文(English) |
英文摘要 | Accumulation of somatic mutations in the mitochondrial DNA (mtDNA) is a major contributor to human aging and degenerative diseases. Rapid progress has been made in unraveling the molecular changes associated with aging. MtDNA mutations are likely early molecular events associated with human aging that may be responsible for the age-dependent decline in mitochondrial respiratory functions. Many types of mutations of the mitochondrial genome impair the function of the respiratory and oxidative phosphorylation systems. This not only results in the agedependent decline in cellular functions, but also increases the generation of reactive oxygen species (ROS) through the respiratory chain. ROS may cause oxidative damage to mtDNA, further impairing cellular functions and thereby increasing the rate of aging. How aging is elicited by the relatively low amount (<5%) of aging- associated mutated mtDAN in human tissues is poorly understood. Protein degradation may be a key mechanism in the formation of lipofuscin and possibly in cellular aging. The thiol proteases, critical for protein turnover and degradation, are particularly susceptible to free radical damage at their active sites. If the degradative pathway in mitochondrai is defective, the mitochondrion-derived degradation intermediates accumulate within secondary lysosomes, leading to the formation of residual bodies. These degradation products may become another "stressor" to tissue cells. We therefore propose that defective mitochondrial turnover is a cause of accumulation of defective mitochondrial constituents and an important contributory factor to human aging. |
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