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作 者:官志忠[1]
机构地区:[1]贵州医科大学分子生物学重点实验室、附属医院病理科,贵阳500004
出 处:《中华地方病学杂志》2016年第2期79-82,共4页Chinese Journal of Endemiology
基 金:基金项目:国家自然科学基金(81160335);国家科技部科技支撑计划(2013BA105803);贵州省2011协同创新中心([2014106)
摘 要:地方性氟中毒可造成全身性病理损害,其发生机制比较复杂。在所涉及的发病机制学说中.氧化应激是迄今为止较为公认的学说。文中主要涉及地方性(或慢性)氟中毒发生过程中氧化应激常见测定指标的改变,氧化应激与生物膜性脂质、乙酰胆碱能受体、信号转导系统、以及凋亡等方面的关系,抗氧化剂的临床及实验研究结果。文中强调了氧化应激在地方性氟中毒全身病理损伤分子机制中的作用.为临床防治及药物开发提供参考依据。Endemic (chronic) fluorosis causes systemic pathological damages, in which the pathogenesis of the disease is complex. Among those relating mechanisms, oxidative stress is a generally accepted theory so far. The comments made in the present paper mainly concern the changes of conventional examinations for oxidative stress, the correlations between oxidative stress and biological membrane lipids, acetylchoiine receptors, signal translation systems and apoptosis, and the clinic or experimental investigations on anti-oxidants. It is emphasized that oxidative stress plays an important role in the molecular mechanisms of systemic damages resulted from endemic fluorosis, which may provide theoretical evidence for clinical prevention and treatment, as well as drug development to the disease.
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