Scientists may have finally revealed one of life's enduring mysteries- why females of many species live longer lives than their male counterparts.

The new research, published in the journal Current Biology, finds that DNA mutations in the mitochondria, vital energy generating parts of cells that convert food into energy that powers the body, may be the answer to unlocking the mystery of the differences in life expectancy between men and women.

Researchers explain that mitochondria have their own DNA that is separate from the DNA in the nucleus of the cell that is generally thought of as being part of the genome. 

However, in almost all species, the DNA in mitochondria is passed down exclusively from mother to child, with no paternal input. This is the "mother's curse" because any mutations that could harm a female get eliminated by natural selection but any mutations that harm males get passed down.

Researchers explain that this direct line of maternal inheritance may allow harmful mutations to accumulate because it reduces the number of genes screened by the process of natural selection which helps keep harmful mutations to a minimum by ensuring that they are not passed down to the offspring.

Surprisingly, researchers studying fruit flies found evidence of the "Mother's Curse," that the mitochondrial DNA mutation is only dangerous to males and not to females.

Researchers looking to uncover differences in longevity and biological aging between males and females took flies with all the same cellular DNA and inserted mitochondrial DNA from 13 different global fruit-fly populations, and found that there were significant differences in life expectancy between males, but not for females.

However, researchers noted that the "Mother's Curse" suggests that the life expectancy gap between males and females is not determined by just a few genes, but in fact are triggered by a combination of a variety of mutations that team up to shorten the male life span.

Researchers said that the genetic inheritance of mitochondrial DNA is the same across species, so they expect to see the results in people. 

"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 ageing across the animal kingdom," lead author Dr. Damian Dowling of the Monash School of Biological Sciences said in a statement.

While children receive copies of most of their genes from both parents, they only receive mitochondrial genes from their mothers, which means that natural selection, "evolution's quality control process" only screens the quality of mitochondrial genes in mothers, but does not take into account if a mitochondrial mutation that harms fathers, Dowling explained.

Therefore, a mitochondrial mutation that harms males has no effect on females because it has slipped through the screening of the natural selection process.

"Over thousands of generations, many such mutations have accumulated that harm only males, while leaving females unscathed," Dowling added.

Dowling previously also found that maternal mitochondria can sometimes even cause male infertility.

"Together, our research shows that the mitochondria are hotspots for mutations affecting male health. What we seek to do now is investigate the genetic mechanisms that males might arm themselves with to nullify the effects of these harmful mutations and remain healthy," Dowling said.

Researchers say that the fact that men have not yet gone extinct means that there is still hope for men.  He explains that the nuclear genome or the DNA inherited from both mom and dad might compensate for the mitochondrial handicap in men. For example, men who have inherited genes that can counteract the ill effects of mitochondrial mutations may do better and pass on their genes more successfully.