Kumar B P, Shivakumar K, Kartha C C
Division of Cellular and Molecular Cardiology, Sree Chitra Tirunal Institute for Medical Sciences and Technology, Trivandrum, India.
Int J Biochem Cell Biol. 1997 Jan;29(1):129-34. doi: 10.1016/s1357-2725(96)00124-0.
Magnesium deficiency is known to produce a cardiomyopathy, characterised by myocardial necrosis and fibrosis. As part of the ongoing investigations in this laboratory to establish the biochemical correlates of these histological changes, the present study probed the extent of lipid peroxidation and alterations in collagen metabolism in the heart in rats fed a magnesium-deficient diet for 28, 60 or 80 days. While lipid peroxidation was measured by the thiobarbituric acid reaction, collagen turnover rates and fibroblast proliferation were assessed using [3H]-proline and [3H]-thymidine, respectively. Tissue levels of magnesium and calcium were determined by atomic absorption spectrophotometry. A 39% increase in the cardiac tissue level of thiobarbituric acid reactive substances was observed on day 60 of deficiency (p < 0.001). A marked drop in collagen deposition rate (59%, p < 0.001%) on day 28 but a significant rise in fractional synthesis rate (12%, p < 0.001) and collagen deposition rate (24%, p < 0.001) on day 60 were observed. A fibroproliferative response in the heart was evident on day 80 but not at earlier time-points. Thus, the present study provides evidence of increased lipid peroxidation and net deposition of collagen in the myocardium in response to dietary deficiency of magnesium. These changes were, however, not directly related to alterations in the tissue levels of Mg. It is suggested that the increase in cardiac collagen synthesis and fibroplasia associated with Mg deficiency may represent reparative fibrogenesis, upon oxidative damage to the cardiac muscle, and is mediated by a mechanism independent of changes in cardiac tissue levels of Mg.
已知镁缺乏会引发一种心肌病，其特征为心肌坏死和纤维化。作为本实验室正在进行的确定这些组织学变化的生化关联研究的一部分，本研究探究了喂食缺镁饮食28天、60天或80天的大鼠心脏中脂质过氧化程度以及胶原代谢的变化。脂质过氧化通过硫代巴比妥酸反应进行测定，胶原周转率和成纤维细胞增殖分别使用[3H]-脯氨酸和[3H]-胸腺嘧啶核苷进行评估。通过原子吸收分光光度法测定组织中的镁和钙水平。在缺镁60天时，观察到心脏组织中硫代巴比妥酸反应性物质水平增加了39%（p < 0.001）。在第28天时，胶原沉积率显著下降（59%，p < 0.001%），但在第60天时，分数合成率显著上升（12%，p < 0.001），胶原沉积率上升（24%，p < 0.001）。在第80天时，心脏出现明显的纤维增生反应，但在更早的时间点未出现。因此，本研究提供了证据，表明饮食中镁缺乏会导致心肌中脂质过氧化增加和胶原净沉积。然而，这些变化与组织中镁水平的改变并无直接关联。提示与镁缺乏相关的心脏胶原合成增加和纤维组织增生可能代表心肌氧化损伤后的修复性纤维生成，并且由一种独立于心脏组织中镁水平变化的机制介导。
