Wutzen J
Pol Tyg Lek. 1989 Apr 10;44(10-11):243-6.
A role of enzyme mediated metabolic processes is discussed. Unfavourable effect of magnesium deficiency on the functioning of various organs may lead to extensive and irreversible morphological changes of focal character. Basing on the results of several experiments and own experience, the author discusses an effect of low-magnesium diet on histological, histochemical, and microscopic lesions to the myocardium, skeletal musculature, liver, and pancreas. Magnesium deficiency predisposes to myocardial necrosis which simulates electrolyte-steroid-cardiomyopathy by necrosis (ESCN). Low-magnesium diet decreases resistance of the animals to various types of stress such as: cooling, immobilization, and noise. Insignificant degree of the lesions to skeletal musculature produced by magnesium deficiency and no progress in these lesions during the experiment may depend upon relatively stable magnesium reserve in the muscles. Low-magnesium diet increases the number of so-called Ito cells in the liver. It is probable that these cells together with hepatocytes contribute to the formation of collagen fibres. Magnesium deficiency may lead to the abnormal digestion of nutrients in the pancreas, interfering with exocytosis of zymogen granules. Supplementation of the diet with magnesium may prevent various organopathies.
本文讨论了酶介导的代谢过程的作用。镁缺乏对各器官功能的不利影响可能导致广泛且不可逆的局灶性形态学改变。基于多项实验结果和自身经验，作者探讨了低镁饮食对心肌、骨骼肌、肝脏和胰腺的组织学、组织化学及微观病变的影响。镁缺乏易引发心肌坏死，其坏死情况类似电解质 - 类固醇 - 心肌病（ESCN）。低镁饮食会降低动物对诸如降温、固定和噪音等各类应激的抵抗力。镁缺乏对骨骼肌造成的损伤程度较轻，且在实验过程中这些损伤无进展，这可能取决于肌肉中相对稳定的镁储备。低镁饮食会增加肝脏中所谓的伊托细胞数量。这些细胞可能与肝细胞共同促成胶原纤维的形成。镁缺乏可能会干扰胰腺中营养物质的正常消化，影响酶原颗粒的胞吐作用。在饮食中补充镁可预防多种器官病变。
