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Tuesday, August 18, 2015. An article published online on August 6, 2015, in Cell Reports describes the role of antioxidants in slowing aging of the thymus, a gland responsible for the production of immune cells known as T lymphocytes. The thymus reaches its peak size at adolescence and subsequently begins to atrophy. Decreased T cell production is compensated for by existing T cell duplication; however, this eventually results in memory T cell dominance and a reduction in the ability of the immune system to respond to new pathogens. "The thymus begins to atrophy rapidly in very early adulthood, simultaneously losing its function," explained lead researcher Howard T. Petrie, who is presently affiliated with the University of Texas Health Science Center at San Antonio. "This new study shows for the first time a mechanism for the long-suspected connection between normal immune function and antioxidants."
The research, conducted at the Florida campus of The Scripps Research Institute, examined gene activity in the thymus' stromal (connective tissue) cells and lymphoid cells. Dr Petrie's team discovered that stromal cells were deficient in the body's antioxidant enzyme catalase, making them subject to increased damage from reactive oxygen species. "Thus, stromal catalase deficiency, in the context of prolonged exposure to high-level reactive oxygen species, represented a potential mechanism to explain accelerated thymic atrophy," the authors write.
To help confirm the benefit of antioxidant protection, mice were provided with drinking water enhanced with the antioxidant nutrients N-acetylcysteine or L-ascorbate (vitamin C) from the time of weaning. In comparison with mice that received plain water, thymus glands from mice that received either nutrient were larger after ten weeks than those of control animals of the same age, while other organs did not appear to be affected. In another experiment, mice that were genetically modified to overexpress mitochondrially targeted catalase had thymus glands that were twice as large at six months of age as those of normal control animals.
In their discussion, the authors observe that studies involving calorie restriction have also resulted in reduced atrophy of the thymus, further strengthening the association between thymic atrophy and metabolic damage via free radicals.
"Atrophy resulting from accumulated damage is documented in many organs and tissues as part of the 'normal' aging process and is intimately linked to aerobic metabolism and oxygen radicals," the authors write. "However, these are generally slow, progressive processes that do not become apparent until late in life and, with the notable exception of skeletal muscle, often go mostly unnoticed."
The researchers plan to test the effects of antioxidant supplementation on thymus and immune function in aging animals in hope of developing a treatment for age-related thymus atrophy in humans.
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