How oxidative stress may help extend lifespanMay 29th, 2009 - 4:22 pm ICT by ANI
Washington, May 29 (ANI): Scientists at the University of California, San Diego claim to have identified a mechanism of oxidative stress that prevents cellular damage.
“We may drink pomegranate juice to protect our bodies from so-called ‘free radicals’ or look at restricting calorie intake to extend our lifespan,” said Dr Trey Ideker, chief of the Division of Genetics in the Department of Medicine at UC San Diego’s School of Medicine and professor of bioengineering at the Jacobs School of Engineering.
“But our study suggests why humans may actually be able to prolong the aging process by regularly exposing our bodies to minimal amounts of oxidants,” Ideker added.
Reactive oxygen species (ROS), ions that form as a natural byproduct of the metabolism of oxygen, play important roles in cell signalling. However, due to environmental stress like ultraviolet radiation or heat or chemical exposure the ROS levels can increase dramatically, resulting insignificant damage to cellular damage to DNA, RNA and proteins - cumulating in an effect called oxidative stress.
The scientists claim to have discovered the gene responsible for this effect.
One major contributor to oxidative stress is hydrogen peroxide. While the cell has ways to help minimize the damaging effects of hydrogen peroxide by converting it to oxygen and water, this conversion isn’t 100 percent successful.
During the study, the researchers designed a way to identify genes involved in adaptation to hydrogen peroxide.
To figure out which genes might control this adaptation mechanism, the team ran a series of experiments in which cells were forced to adapt while each gene in the genome was removed, one by one - covering a total of nearly 5,000 genes.
They identified a novel factor called Mga2, which is essential for adaptation.
“This was a surprise, because Mga2 is found at the control point of a completely different pathway than those which respond to acute exposure of oxidative agents,” said Ideker.
“This second pathway is only active at lower doses of oxidation,” Ideker added.
“It may be that adaptation to oxidative stress is the main factor responsible for the lifespan-expanding effects of caloric restriction,” said Ideker.
“Our next step is to figure out how Mga2 works to create a separate pathway - to discover the upstream mechanism that senses low doses of oxidation and triggers a protective mechanism downstream.”
The study is published in PLoS Genetics. (ANI)
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