Can vitamin E protect humans against the pathological effects of ozone in smog?
Article Abstract:
The 1970 Clean Air Act set limits for six pollutants (ozone, carbon monoxide, nitrogen oxides, sulfur dioxide, lead, and particulates) which are often found in city air. The allowable upper limit for ozone, the most powerful oxidant in smog, was established at 0.12 parts per million (ppm) as a one-hour average. However, most large cities are unable to comply with standards set for ozone, and the maximum levels of ozone exceed permissible levels by two- or three-fold in very polluted areas. Ozone causes adverse effects on the lungs, specifically a stiffening and more rapid aging of lung tissue. Antioxidant defense mechanisms, or methods of counteracting the oxidant effects of ozone, protect humans from oxidative stress. Vitamins with antioxidant effects include vitamins E and C. The effects of vitamin E on ozone's effects in various biological systems, animals, and humans, are reviewed in order to answer the question, can vitamin E protect humans against the pathological effects of ozone in smog? An increased understanding of the chemical reactions involving ozone should contribute to knowledge of mechanisms whereby ozone causes biological damage and vitamin E protects against ozone-induced damage. The interaction between ozone and biological molecules in animal and human studies is discussed. Ozone interacts with polyunsaturated fatty acids to form free radicals, which are highly reactive and potentially damaging elements. Vitamin E was shown to delay this reaction and protect against the adverse effects of ozone; the absence of vitamin E enhances the destructive effects of ozone. The opposite effects of ozone and vitamin E on immune factors suggests that vitamin E can protect against ozone-induced damage. The next question, which will require further investigation, is whether consuming amounts of vitamin E above the recommended dietary allowance offers enhanced protection against the effects of ozone. It is noted that most people are not deficient in vitamin E. (Consumer Summary produced by Reliance Medical Information, Inc.)
Publication Name: American Journal of Clinical Nutrition
Subject: Health
ISSN: 0002-9165
Year: 1991
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Consequences of severe copper deficiency are independent of dietary carbohydrate in young pigs
Article Abstract:
Copper is an essential trace element in human nutrition; it is required for proper function of the cardiovascular system, the nervous system, the immune system, and the skeleton. However, typical Western diets provide only 1.0 to 1.5 milligrams per day of this nutrient, less than the recommended 2 to 3 milligrams. Many individuals are, therefore, at risk for marginal copper deficiency. For this reason, the suspicion that some carbohydrates may exacerbate a copper deficiency is especially alarming. Experiments in rats have shown that a diet deficient in copper has disastrous effects on heart function in combination with sucrose and fructose, but not with cornstarch or glucose. Since it is unethical to evaluate this phenomenon directly in humans, it was decided to study the relationship between carbohydrate intake and copper deficiency in pigs. Pigs resemble humans more closely than rats in many ways, and the first understanding of the dietary importance of copper, in fact, came from pigs. Weanling pigs were fed a diet deficient or adequate in copper for a period of 10 weeks. The diet contained either 59 percent sucrose or 59 percent cornstarch. At the end of the study, the type of carbohydrate was found to have no effect on the consequences of copper deficiency. Therefore, the effect which was discovered in rats could not be demonstrated in pigs. Although it is unclear whether such an effect might be possible in humans, the authors feel that the pig is a better model for the effects of copper deficiency in the human than is the rat. (Consumer Summary produced by Reliance Medical Information, Inc.)
Publication Name: American Journal of Clinical Nutrition
Subject: Health
ISSN: 0002-9165
Year: 1990
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