Researchers from Newcastle University in England have found that skin aging is closely associated with a decrease in the activity of the mitochondrial complex II electron transport chain, according to research published online in Journal of Investigative Dermatology (Jan. 29, 2016).
The authors note that the theory that dysfunction of mitochondrial electron transport systems leads to increased free radical production and consequently to cell aging is fairly widely accepted, but the specifics have not been known.
To investigate this the investigators measured the rate of complex II activity per mitochondria in cultured human fibroblasts and keratinocytes from 27 donors, from aged six to 72 years. Samples were taken from a sun-protected area of skin. The authors found that the activity of complex II dropped off significantly with age in fibroblasts (p=0.015), though not in keratinocytes. A specific decrease in the activity of complex II with age in senescent cells was also seen (p=0.029). However, no decrease was seen with age in the activity of another mitochondrial electron transfer complex, complex IV.
“Our study shows, for the first time, in human skin that with increasing age there is a specific decrease in the activity of a key metabolic enzyme found in the batteries of the skin cells,” said lead author Mark Birch-Machin, PhD, professor of molecular dermatology at the university, in a press release Feb. 26, 2016.
“This enzyme is the hinge between the two important ways of making energy in our cells,” said Professor Birch-Machin. “Our research means that we now have a specific biomarker, or a target, for developing and screening anti-ageing treatments and cosmetic creams.”
“There is now a possibility of finding anti-ageing treatments which can be tailored to differently aged and differently pigmented skin, and with the additional possibility to address the ageing process elsewhere in our bodies.”