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superoxide dismutase

selenium, and others serve to suppress free radical formation or to promote the synthesis of enzymes that function in the free radical suppression system. Table 3 lists nutrients and their roles in free radical protection.

Whereas the nucleus has a very efficient DNA repair process, the mitochondrion does not. However, there is only one nucleus in each cell, whereas there are many mitochondria in that same cell. If one or two are damaged, there are many in the cell to compensate. Disease develops only when damage occurs to a large majority of the mitochondria. A certain threshold of damage must be reached for such damage to have a physiological effect. Again, nutrients that function as free radical suppressants or that enhance the synthesis of enzymes of the free radical suppression system function to protect mitochondria from free radical damage. In the nucleus, the DNA is protected from free radical attack by histone and nonhistone proteins. Histones are highly basic proteins varying in molecular weight from -11000 to -21000. The histones keep the DNA in a very compact form. In contrast, the mitochon-drial DNA does not have this protective histone coat. It is 'naked' and much more vulnerable to damage. In addition, -90% of oxygen free radicals are generated in the mitochondria, providing the means for such damage should the enzyme superoxide dismutase, a manganese-dependent enzyme found in this compartment, not suppress these radicals. The damage can be quite severe, but because each mitochondrion contains 8-10 copies of its genome and there are many mitochondria in each cell (up to 2000), the effects of this damage may not be apparent. There is another superoxide dismutase found in the cytosol that has a similar function. It is a copper/zinc-dependent enzyme. Again, note the dependence of function on particular nutrients

(manganese, zinc, and copper) that in turn have effects on gene expression in health and disease.

Another way that changing DNA in a single cell can profoundly affect the health of the whole organism involves cancer. In this case, the DNA changes occur in particular genes related to the growth regulatory properties of the cell. Normal homeostatic mechanisms fail and the individual cell multiplies rapidly and therefore has a widespread influence. Nutrition interacts with cancer in a number of ways. It can promote or prevent the initiating mutation. It also will influence the progression of cancer by providing the nutrients required for its growth. The cancer often ultimately influences nutrition by limiting food intake. Another level of complexity is added with chemo- and radiotherapies and their interactions with nutrition.

Throughout this article, examples have been given that illustrate the interactions that occur between nutrients and genes. The ultimate goal of understanding such interactions is to use our knowledge to enhance the expression of genes that sustain good health while suppressing the expression of genes associated with disease. Although it is currently not possible to identify individuals with genetic dispositions to chronic diseases, there is no doubt that such screening tests will be developed and will be used as a basis for recommending nutrient (food) intakes. Optimizing health, after all, is the ultimate goal of good nutrition.

See also: Aging. Antioxidants: Diet and Antioxidant Defense. Cancer: Epidemiology and Associations Between Diet and Cancer; Effects of Nutritional Status. Children: Nutritional Problems. Coronary Heart Disease: Hemostatic Factors; Lipid Theory; Prevention. Diabetes Mellitus: Etiology and Epidemiology.

Folic Acid. Hyperlipidemia: Overview. Inborn Errors of Metabolism: Classification and Biochemical Aspects. Iron. Lactose Intolerance. Nutrient-Gene Interactions: Molecular Aspects. Obesity: Definition, Etiology and Assessment. Vitamin D: Rickets and Osteomalacia. Zinc: Physiology; Deficiency in Developing Countries, Intervention Studies.

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