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THURSDAY, Aug. 2 (HealthDay News) -- New research reveals that mutations to the DNA of the mitochondria cause men to age faster than women -- a finding that may explain why women, on average, outlive men.
The researchers from Monash University in Australia examined male and female fruit flies that carried mitochondria -- the part of the cell that converts food into energy -- of various origin. They found that genetic variation in the mitochondria predicted life expectancy in males, but not in females. The investigators concluded that several mutations within the DNA of mitochondria affect how quickly men age as well as their longevity.
"Intriguingly, these same mutations have no effects on patterns of aging in females. They only affect males," Dr. Damian Dowling, from the Monash School of Biological Sciences, said in a university news release. "All animals possess mitochondria, and the tendency for females to outlive males is common to many different species. Our results therefore suggest that the mitochondrial mutations we have uncovered will generally cause faster male aging across the animal kingdom."
The mutations result from the way mitochondrial genes are passed down from one generation to the next, the study authors noted.
"While children receive copies of most of their genes from both their mothers and fathers, they only receive mitochondrial genes from their mothers. This means that evolution's quality control process, known as natural selection, only screens the quality of mitochondrial genes in mothers," explained Dowling. "If a mitochondrial mutation occurs that harms fathers, but has no effect on mothers, this mutation will slip through the gaze of natural selection, unnoticed. Over thousands of generations, many such mutations have accumulated that harm only males, while leaving females unscathed."
The study authors said they plan to continue their research and explore ways to negate the genetic mutations that negatively affect men's life expectancy.
The study was published Aug. 2 in Current Biology.
-- Mary Elizabeth Dallas
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