Abstract
The authors present evidence for a novel, new hypothesis whereby magnesium deficiency (MgD) acts as a genotoxic agent which probably causes numerous, hertofore, unrecognized consequences, even over a short-term, on the physiological, molecular and biochemical machinery of cardiovascular tissues and cells. The end result of these genotoxic effects of MgD probably plays important roles in the etiology and generation of diverse cardiovascular diseases, atherosclerosis, inflammation, and strokes via alterations in the epigenome of cardiovascular tissues and cells. The importance of adequate water-borne and dietary levels of Mg is emphasized.
Highlights
Over the past two decades, a considerable amount of research has taken place around the globe suggesting that a variety of chemicals and mutagens can produce genotoxic effects in multiple tissues and cells [1,2 ]
Numerous advances are being made about genotoxins, very little is known about the potential mechanisms involved in how genotoxins induce lesions in DNA and how these agents could result in chromosomal abberations
Below, background, evidence, and our reasons for believing that magnesium deficiency(MgD) can result in genotoxicity in cardiovascular tissues and cells which probably play major roles in etiology of cardiac diseases, atherogenesis, inflammation, and stroke heretofore unexplained
Summary
Over the past two decades, a considerable amount of research has taken place around the globe suggesting that a variety of chemicals and mutagens can produce genotoxic effects in multiple tissues and cells [1,2 ]. Genotoxicity conotes in genetics a destructive effect(s) on a cell's genetic material (i.e., DNA, RNA) potentially altering cell integrity, functions, and phenotype [1]. Some of these well-known genotoxins include radiation of different types and chemicals known to damage DNA. The end result of genotoxins result in modification of gene expression. Numerous advances are being made about genotoxins, very little is known about the potential mechanisms involved in how genotoxins induce lesions in DNA and how these agents could result in chromosomal abberations
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