Mitochondria-targeting antibiotics reduce aging in C. elegans

Aging is a constant degenerative process caused by a progressive decline of cell and tissue functions in an organism. This is prompted by the accumulation of damage affecting normal cellular processes which results in cell death. Scientists have long thought that mitochondria have had a critical role in aging.

Now, a research team (Dr Gloria Bonuccelli, Dr Darren R. Brooks, Sally Shepherd, Dr Federica Sotgia, and Dr Michael P. Lisanti) from the University of Salford, have characterised the involvement of mitochondria in aging using Caenorhabditis elegans (C. elegans) as an organismal model.

The C. elegans were treated with a panel of mitochondrial inhibitors and assessed for survival. The team stated: “In our study, we assessed survival by evaluating worm lifespan, and we assessed aging markers by evaluating the pharyngeal muscle contraction, the accumulation of lipofuscin pigment and ATP levels.” 

The study’s findings showed that treatment of C. elegans with either doxycycline or azithromycin, inhibitors of the small or the large mitochondrial ribosomes respectively, or a combination of both, greatly extended the median lifespan of the worms. It also improved their pharyngeal pumping rate and lowered their lipofuscin content and their energy consumption (ATP levels), compared to the control group of untreated worms. This indicated that these drugs had an aging-avoiding effect.

DPI, an inhibitor of mitochondrial complex I and II, was also able to prolong the median lifespan of treated worms. However, providing worms with vitamin C, a pro-oxidant, did not extend C. elegans lifespan and upregulated its energy consumption, showing an increase in ATP level. 

The team concluded: “Therefore, our longevity study reveals that mitochondrial inhibitors (ie, mitochondria-targeting antibiotics) could abrogate aging and extend lifespan in C. elegans.”

This study was published in Aging.