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作 者:李毅[1] 黄永青[1] 郑民缨[1] 杨海华[1] 徐评议[1] 刘焯霖[1]
机构地区:[1]中山大学第一附属医院神经科,广州510080
出 处:《国际遗传学杂志》2007年第3期190-194,共5页International Journal of Genetics
基 金:国家自然科学基金资助项目(30370509、30570645);留学回国人员基金资助项目(2003-406)
摘 要:近年来线粒体在老化发生发展中所起的作用越来越受重视。当线粒体功能异常时,其内的氧化活性物质(ROS)增多,这可引起线粒体自身与细胞肿胀、膜电位下降、细胞内发生钙超载、大分子活性物质受到破坏、生成异常活性物质等等;同时,mtDNA的突变加剧,也可引起线粒体的功能障碍进一步加重。它们影响着细胞代谢,使生物体在细胞水平、组织水平、器官水平受到损伤,最终导致老化。现就近年来在此方面的进展及其现实意义作一综述。Recently, the attention has been increasingly paid to the role of mitochondria in the process of aging. It was reported that when the mitochondria were impaired, a rise of reactive oxygen species (ROS) occurred inside this organelle, which could cause the swelling of mitochondria and cells, a decrease of membrane potential, the calcium overload within cells, destruction of the macro-molecule active substances, the synthesis of abnormally active substances, and so on. In addition, the accumulation of DNA mutations could aggravate the impairment of mitochondria. All of these had a negative impact on the cellular metabolism, damaging the whole individual not only in the level of cell and tissue, but also in the level of organ, and finally produced the aging. Our review will briefly focus on the latest development in this field and its practical effects.
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