How Big is the Functional Need for GSH?
GSH is depleted by elimination of reactive chemicals dependent upon abundant GSH transferases. These enzymes increase in response to toxic challenge, and trials have been conducted to determine whether continuous elevation of these enzymes can protect against cancer. In protection against cancer, GSH reacts with cancer-causing chemicals at rates that are faster than the chemical can react with DNA, thereby preventing mutations. To date, however, practical approaches to reduce cancer by increasing GSH transferase have not been established. In addition to cellular activities, GSH transferase is associated with mucus and provides a detoxifying barrier in the small intestines. Animal studies showed that provision of GSH to the GSH transferase associated with the mucus provides a defense mechanism to eliminate ingested toxic chemicals, such as oxidation products from polyunsaturated fatty acids, acrylein, acrylamide, and other reactive chemicals, prior to absorption by the body. This defense depends upon GSH supply outside of the cells, either from the bile, from food, or from a supplement. The finding that oral and pharyngeal cancer is decreased in association with intake of foods high in GSH25 could reflect the function of this mechanism in protection against cancer-causing chemicals or a better function of the immune system. Studies with human cells in culture further show that added GSH protects cells even in the absence of GSH uptake, apparently due to protection of proteins on the surface of cells. Recent studies show that cell surface thiols function as redox sensors, signaling processes such as platelet activation and early events of atherosclerosis. As indicated above, in vitro experiments have demonstrated that addition of GSH to the media improved killing of bacteria by pulmonary macrophages and decreased production of infectious influenza virus by human small airway epithelial cells.
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How Big is the Functional Need for GSH?
In addition to the age-related decline mentioned above, GSH levels are inversely associated with environmental exposures and disease risk. GSH is decreased in the epithelial lining fluid of human lung in individuals who abuse alcohol. This example is illustrative of the hidden risks of low GSH in that these individuals have no apparent lung disease and yet are at considerably increased risk of acute lung injury and death from adult respiratory death syndrome. Oxidation of GSH occurs in association with increased carotid intima media thickness, an indicator of cardiovascular disease risk. GSH redox balance (ie, the GSH/ GSSG ratio) favors oxidation in cigarette smokers and type 2 diabetics. Direct evidence that the decrease and oxidation of GSH occurs due to toxic chemical exposures is available from studies in individuals following chemotherapy. The extensive evidence that GSH status is decreased in association with disease and recognized risk factors for disease implies that maintenance of this protective system could reduce risk of disease development.