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HomeAgingPollution Accelerates Aging On A Cellular Level

Pollution Accelerates Aging On A Cellular Level

Hasselt University researchers have discovered finding the answer to whether this accelerated aging can be detected in the cells of healthy individuals would not be easy as pollution affects two hallmarks of aging: mitochondrial DNA content and telomere length.

Mitochondria are important in supplying cells with energy, some pollutants cause mitochondria to release more reactive oxygen species which are charged particles that can damage DNA, fats, and proteins; as ROS damage affects functioning of mitochondria even more ROS are produced.

Telomeres can be found on the ends of chromosomes, acting as protective caps that allow cells to continue to divide; shorter telomeres are characteristics of aging, while abnormally long telomeres can often be seen in cancer cells.

175 adults between the ages of 50-65 who were part of the Flemish Environment and Health Study were involved in this study which was focused on various pollutants in their urine and blood samples. Mitochondrial DNA content and telomere length were assessed from cells in blood samples, and multipollutant models were used to analyze all pollutants simultaneously.

Those with higher levels of urinary copper and serum perfluorohexane sulfonic acid were found to have decreased mitochondrial DNA content and shorter telomeres, and higher urinary copper and serum perfluorooctanoic acid levels were linked with shorter telomeres; however some pollutants were associated with either higher mitochondrial DNA content or longer telomeres.

According to the researchers findings suggest that pollutants could impact molecular hallmarks of aging, but additional research is required to determine the mechanisms and biological effects.

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This article is not intended to provide medical diagnosis, advice, treatment, or endorsement.

https://pubs.acs.org/doi/10.1021/acs.est.8b07141

https://www.uhasselt.be/en

https://www.sciencedaily.com/releases/2019/05/190501082004.htm

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