Effect of selenium, riboflavin, and vitamin E on oxygen radical production and cytotoxic activity of peritoneal macrophages of Balb/c mice



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Texas Tech University


In nutrition science, we learn that many foods that are healthful in reasonable portions can also lead to ill health when eaten in excess. One can eat too much of almost anything. For example, vitamin A as retinol, when consumed in excess, has toxic effects, however, this vitamin is also clearly an essential nutrient for vision (Olson, 1984). When we realize that water is the most essential of the nutrients, since we cannot survive much longer than three days without it, then consider that without oxygen human beings will live less than a few minutes. However, at any level of dietary supplementation meeting essential requirements, oxygen is both toxic and carcinogenic. In this context oxygen demonstrates major toxicity and carcinogenicity at the same levels which are required for support of life.

Oxygen toxicity can cause many cellular dysfunctions, including deactivation of essential enzymes by oxidation, with primary effect on the oxidation of cysteine thiols producing disulfides. It also involve effects of cellular mediators and secretions (Huber and Drath, 1981), and lipid peroxidation (Allen et al., 1973). The toxicity of lipid peroxides by disruption of the cellular membrane is the primary mediators of oxygen toxicity. Therefore, the basic schemata for lipid peroxidation functions as follows.



Selenium, Macrophages, Vitamin B2, Active oxygen in the body, Vitamin E, Mice