Rayssiguier Y, Durlach J, Gueux E, Rock E, Mazur A
Centre de Recherche en Nutrition Humaine, Laboratoire des Maladies Métaboliques, INRA, St-Genès-Champanelle, France.
Magnes Res. 1993 Dec;6(4):369-78.
Magnesium status may be compromised with ageing for two reasons: insufficient intake (magnesium deficiency) or alterations in magnesium metabolism (magnesium depletion). There is a large volume of literature suggesting that magnesium deficit contributes to the ageing process and to the vulnerability to age-related diseases. One of the biological changes associated with ageing is an increase in free radical formation with subsequent damage to cellular processes. Prime targets of the more reactive free radicals are unsaturated lipids in cell membranes, amino acids in proteins, and nucleotides in DNA. The accumulation of unrepaired oxidative damage products may be a major factor in cellular ageing. Magnesium-deficient animals show an increased susceptibility to an in vivo oxidative stress and their tissues are more susceptible to in vitro peroxidation. Moreover, the protective properties of various antioxidant drugs and nutrients suggest that free radicals are involved in the injury process of magnesium deficiency. The consequences on stress susceptibility, defective membrane functions and perturbation of intracellular calcium metabolism, inflammation, cardiovascular diseases including atherosclerosis and ischaemia/reoxygenation injury, diabetes, fibrosis, immune dysfunction and other diseases associated with ageing are presented and discussed.
随着年龄增长，镁状态可能会受到影响，原因有两个：摄入不足（镁缺乏）或镁代谢改变（镁耗竭）。大量文献表明，镁缺乏会促进衰老过程，并增加患与年龄相关疾病的易感性。与衰老相关的生物学变化之一是自由基形成增加，随后对细胞过程造成损害。更具反应性的自由基的主要靶点是细胞膜中的不饱和脂质、蛋白质中的氨基酸和DNA中的核苷酸。未修复的氧化损伤产物的积累可能是细胞衰老的一个主要因素。缺镁动物对体内氧化应激的易感性增加，其组织在体外更易发生过氧化。此外，各种抗氧化药物和营养素的保护特性表明，自由基参与了镁缺乏的损伤过程。本文介绍并讨论了镁缺乏对压力易感性、膜功能缺陷、细胞内钙代谢紊乱、炎症、包括动脉粥样硬化和缺血/再灌注损伤在内的心血管疾病、糖尿病、纤维化、免疫功能障碍以及其他与衰老相关疾病的影响。
