TEL HASHOMER, Israel & BETHESDA, Md.--Two studies released in the April 29 Proceedings of the National Academy of Sciences (www.pnas.org) implicated antioxidants for two conditions of opposite sides of the human health spectrum. Researchers at the Heller Institute of Medical Research in Israel learned that the body's natural antioxidant defenses may not be able to scavenge the increased free radicals that occur as a result of strenuous exercise, and researchers at the National Cancer Institute determined antioxidants may have chemopreventive effects against breast cancer.
The first study (100, 9:5119-23, 2003) was conducted based on the hypothesis that strenuous exercise leads to an increased metabolic rate, heightened production of reactive oxygen species and a compromised antioxidant defense system. To test this theory, researchers recruited 31 men who followed a six-month training schedule of working out five days a week. Participants also carried 35 kg of weight during two extreme marches, which were separated by a two-week regular training schedule. Only 29 men finished the 50 km march, and 16 completed the 80 km march.
Blood samples taken after the 50 km and 80 km marches showed a respective 25-percent and 37-percent increase in uric acid (the body's tool for expelling metabolic nitrogen; levels too high can cause gout), perhaps due to the increased metabolism. The marches also caused a 10-fold boost in leakage of creatine phosphokinase (an enzyme found in muscle tissue released in increasing amounts when muscle is damaged), and a four-fold increase in plasma levels of aspartate transaminase (a marker of liver injury). Researchers concluded the elevated respiration rate that occurs during exercise leads to the production of more reactive oxygen species than the body's antioxidant system can scavenge.
In the second study (100, 9:5390-5, 2003), researchers at the National Cancer Institute, in cooperation with a team from Seattle's Pacific Northwest Research Institute, found antioxidants may protect against breast cancer. They investigated cell toxicity and mutagenicity of 4-hydroxyestradiol (4-OHE2), an oxidative metabolite of estrogen, in human MCF7 and TK-6 lymphoblast cells.
The cytotoxicity of estrogen increased when there was a deficiency of intracellular glutathione, an antioxidant amino acid compound. However, ascorbate and cysteine (a non-essential amino acid precursor of glutathione) were found to protect against cytotoxicity and decrease mutation induction. Researchers concluded oxidation is necessary to induce the damaging effects of estrogen, and a diet rich in vitamins and synthetic antioxidants could decrease the risks associated with estrogen exposure and perhaps prevent breast cancer.