Scientists from the Florida campus of Scripps Research Institute (TSRI) have shown how aging affects the immune system as we grow older.
The research focuses on an organ called as thymus. It produces T lymphocytes, which are vital to the immune system and needs to be replenished constantly to respond to new threats.
"The thymus begins to atrophy rapidly in very early adulthood, simultaneously losing its function. This new study shows for the first time a mechanism for the long-suspected connection between normal immune function and antioxidants," said TSRI Professor Howard Petrie.
The researchers developed a computational method for analyzing the activity of stromal and lymphoid cells, which are the two major thymic cells. Researchers examined these cells on mouse tissues. They found a deficiency of an antioxidant enzyme called catalase in stomal cells, which had resulted in high levels of reactive oxygen by-products of metabolism and metabolic damage.
The researchers increased the levels of catalase in animal models to confirm the significant role of the enzyme. They found that it preserved the thymus size for a longer period.
Animals that were given two dietary antioxidants, including vitamin C protected them from age related deterioration of the thymus.
The findings provide support for the "free-radical-theory" of aging, which proposes that reactive oxygen species produced during animal metabolism such as hydrogen peroxide, cause damage to cells that contributes to aging and age-related diseases.
"There's no question that the thymus is remarkably responsive to androgens. But our study shows that the fundamental mechanism of aging in the thymus, namely accumulated metabolic damage, is the same as in other body tissues. However, the process is accelerated in the thymus by a deficiency in the essential protective effects of catalase, which is found at higher levels in almost all other body tissues," said Petrie.
The research is published in the journal Cell
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