Magnesium deficiency-induced cardiomyopathy: Protection by vitamin E

Freedman, Alan M.; Atrakchi, Aisar; Cassidy, Marie M.; Weglicki, William B.

doi:10.1016/0006-291x(90)90506-i

Cited by 68 publications

(33 citation statements)

References 10 publications

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“…It is well known that magnesium deficiency is associated with myocardial injury, by decreasing the body's antioxidative capacity and tissue resistance to free radicals [22,23]. Thus, magnesium deficiency may be associated with cardiomyopathy [24]. Moreover, magnesium deficiency has also been found to be associated with sudden death [25].…”

Section: Discussionmentioning

confidence: 99%

Magnesium Fortification of Drinking Water Suppresses Atherogenesis in Male LDL-Receptor-Deficient Mice

et al. 1999

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Magnesium, an important cofactor of more than 300 enzymes, has previously been found to modulate blood lipid levels, atherogenesis and atherosclerosis in rabbits, when added to their diet. The aim of this study was to examine whether magnesium fortification of drinking water, without a change in diet content, can affect atherogenesis. The study included six groups of LDL-receptor-deficient mice. The mice received either distilled water or water containing 50 g of magnesium sulfate per liter. In the first (12 weeks) and second (6 weeks) stages of the experiment, the mice received low- and high-cholesterol diets, respectively. At the end of each stage, blood was drawn for the determination of plasma magnesium, calcium and lipid levels. In addition, the extent of atherosclerosis was determined at the aortic sinus. In both males and females, magnesium fortification was associated with higher levels of plasma magnesium (50 and 37% increase, respectively), without any differences in plasma calcium content. The extent of atherosclerosis at the aortic sinus in the male mice that received high levels of magnesium was a third of that of the male mice that received distilled water. However, these differences were not found in the female groups. Surprisingly, the female mice that received water fortified with magnesium had higher levels of cholesterol after stage 2, whereas no differences regarding plasma lipid levels were found among the male mice. These results confirm that magnesium fortification of drinking water is capable of inhibiting atherogenesis in male LDL-receptor-deficient mice. The mechanisms of action are yet to be discovered, and are probably not related to diminished lipid excretion, but possibly to the prevention of calcium influx into vascular smooth muscle cells, elevated antioxidative capacity, or other yet undetermined mechanisms.

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Section: Discussionmentioning

confidence: 99%

Magnesium Fortification of Drinking Water Suppresses Atherogenesis in Male LDL-Receptor-Deficient Mice

et al. 1999

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“…32 Increased oxygen free radical production, which may contribute to several human diseases, 33 is associated with both low plasma GSH/GSSG ratios 10 and low Mg [i] concentrations. 24 Vitamin E has been demonstrated to protect against magnesium deficiency-induced myocardial injury 21,34,35 and magnesium deficiency-associated cerebral vascular damage. 36 Conversely, prior magnesium depletion renders cells more sensitive to oxidative damage.…”

Section: Clinical Characteristic Of Study Subjectsmentioning

confidence: 99%

Effects of Vitamin E and Glutathione on Glucose Metabolism

et al. 1999

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Abstract-Vitamin E is an antioxidant that has been demonstrated to improve insulin action. Glutathione, another natural antioxidant, may also be important in blood pressure and glucose homeostasis, consistent with the involvement of free radicals in both essential hypertension and diabetes mellitus. Our group has recently suggested that the effects of reduced glutathione on glucose metabolism may be mediated, at least in part, by intracellular magnesium levels (Mg [i] ). Recent evidence suggests that vitamin E enhances glutathione levels and may play a protective role in magnesium deficiency-induced cardiac lesions. To directly investigate the effects of vitamin E supplementation on insulin sensitivity in hypertension, in relation to the effects on circulating levels of reduced (GSH) and oxidized (GSSG) glutathione and on Mg [i] , we performed a 4-week, double-blind, randomized study of vitamin E administration (600 mg/d) versus placebo in 24 hypertensive patients and measured whole-body glucose disposal (WBGD) by euglycemic glucose clamp, GSH/GSSG ratios, and Mg [i] before and after intervention. The relationships among WBGD, GSH/GSSG, and Mg [i]

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“…We have previously established in this model that the serum magnesium levels were reduced almost a third, from 4.8±1.0 to 1.8±0.5 meq/1 (/?<0.05), over the 14-day period due to the magnesium-deficient diet. 19 The administration of drugs, although protective to the cardiovascular system, did not result in any measurable changes in either weight or magnesium levels from those of the untreated magnesium-deficient animals.…”

Section: Resultsmentioning

confidence: 99%

“…We proposed that magnesium deficiency may reduce the threshold antioxidant capacity of the cardiovascular system leading to an enhanced susceptibility to free radical injury. We tested this hypothesis with the natural antioxidant vitamin E, 19 which substantially attenuated the development of magnesium deficiency-induced myocardial lesions. In the present study, we demonstrated the protective effects of a sulfhydryl (SH)-containing angiotensin converting enzyme (ACE) inhibitor, captopril, on magnesium deficiency-induced cardiomyopathy.…”

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confidence: 99%

Captopril protects against myocardial injury induced by magnesium deficiency.

1991

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We have previously reported that antioxidant drug intervention protects against magnesium deficiency-induced myocardial lesions. In the present study, Golden Syrian male hamsters were fed either a magnesium-deficient diet or a magnesium-supplemented diet Animals from each group received sulfhydryl-containing angiotensin converting enzyme inhibitors: captopril, epi-captopril (a stereoisomer of captopril), and zofenopril* (arginine blend of zofenopril containing a free SH group); another group of animals received the non-sulfhydryl-containing angiotensin converting enzyme inhibitor enalaprilat The animals were killed after 14 days, and their hearts were isolated for morphological and morphometric analyses. Hematoxylin and eosin-stained sections were examined by a computer image analysis system for a morphometric determination of the severity of myocardial injury. Captopril reduced both the density of lesions, from 0.32 to 0.08 lesions/(mm 2 ) (p<0.01), and the area fraction of lesions, from 7.42xlO" 4 to 2.03 xlO" 4 lesion area/(mm 2 ) (p<0.01), as well as the degree of inflammatory infiltration around the blood vessels. Epi-captopril and zofenopril* were virtually equipotent to captopril, but enalaprilat afforded only slight (nonsignificant) protection. These results indicate that a significant component of the protective effect of captopril in this model was attributable to its sulfhydryl moiety, rather than solely due to the inhibition of the angiotensin converting enzyme. These data further support our previous findings of possible free radical participation in cardiomyopathy due to magnesium deficiency. {Hypertension 1991;18:142-147)

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Magnesium deficiency-induced cardiomyopathy: Protection by vitamin E

Cited by 68 publications

References 10 publications

Magnesium Fortification of Drinking Water Suppresses Atherogenesis in Male LDL-Receptor-Deficient Mice

Magnesium Fortification of Drinking Water Suppresses Atherogenesis in Male LDL-Receptor-Deficient Mice

Effects of Vitamin E and Glutathione on Glucose Metabolism

Captopril protects against myocardial injury induced by magnesium deficiency.

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