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氧化应激、自由基与骨重塑

Oxidative stress, free radicals and bone remodeling.

作者信息

Banfi Giuseppe, Iorio Eugenio L, Corsi Massimiliano M

机构信息

Laboratory of Cell Culture and Molecular Biology, IRCCS Istituto Ortopedico Galeazzi, Milan, Italy.

出版信息

Clin Chem Lab Med. 2008;46(11):1550-5. doi: 10.1515/CCLM.2008.302.

Abstract

Reactive oxygen species (ROS) are widely considered to be a causal factor in aging and in a number of pathological conditions, such as atherosclerosis, carcinogenesis and infarction. Their role in bone metabolism is dual, considering their effects under physiological or pathological conditions. Under physiological conditions, the production of ROS by osteoclasts helps accelerate destruction of calcified tissue, thus assisting in bone remodeling. In pathological conditions, when a bone fractures, e.g., radical generation is remarkably high. However, though the increases in osteoclastic activity and ROS production are linked in many skeletal pathologies, it remains to be clarified whether increased ROS production overwhelms antioxidant defenses, leaving the individual open to hyperoxidant stress.

摘要

活性氧(ROS)被广泛认为是衰老以及多种病理状况(如动脉粥样硬化、致癌作用和梗死)的一个致病因素。考虑到它们在生理或病理条件下的作用,其在骨代谢中的作用是双重的。在生理条件下,破骨细胞产生的ROS有助于加速钙化组织的破坏,从而协助骨重塑。在病理条件下,例如当骨折时,自由基的产生会显著增加。然而,尽管在许多骨骼疾病中破骨细胞活性增加和ROS产生增加有关联,但ROS产生增加是否会压倒抗氧化防御,使个体易受高氧化应激影响仍有待阐明。

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