A short-lived fish living in inland areas in Africa could hold the secret to longevity.
The turquoise killifish, found only in Zimbabwe and Mozambique, frequently live just a few months because their water holes dry out. To survive, they’ve worked out a way to make their eggs dormant to survive a long wait, sometimes more than one year, for the next rains.
Scientists found that when they lowered the activity of genes controlling energy levels in the cells of young killifish, the fish lived longer.
It’s well known that genetic differences among individuals influence lifespan but a study in the journal Cell Systems suggests that differences in patterns of gene expression in youth may also predict longevity.
Alessandro Cellerino of the Scuola Normale Superiore in Italy and the Leibniz Institute on Aging in Jena, Germany, and his colleagues analysed genes in biopsies from the fins of killifish.
The team discovered that genes responsible for cellular respiration — the process by which mitochondria within cells use oxygen to burn sugar and produce energy — were less active at a young age in the fish that were long-lived.
“Up to the present, it was thought that improving mitochondrial function would improve health in aged people; however, our results indicate a more complex scenario where the partial inhibition of mitochondrial function paradoxically has beneficial effects,” he says.
This may occur because such inhibition produces a small amount of free radicals that do not harm the cells but can stimulate a positive, adaptive response.
“This mechanism of adaptation after stress is called hormesis, and it was recently demonstrated that the positive effects of physical exercise in humans are due to hormesis and are destroyed by treatment with antioxidants,” Cellerino says.
This latest research suggests that the effects of aging on mitochondria may involve a compensatory response rather than one that causes problems.
“This obviously has implications on the development of strategies to improve health in older people and prevent aging-associated diseases,” Cellerino says.
There are drugs that inhibit mitochondrial complex I. Metformin, a drug prescribed for type 2 diabetes, has been shown to extend the lifespan of mice.
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