BUFFALO, NY- November 22, 2023 – A new #researchpaper was #published in Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science) Volume 15, Issue 21, entitled, “Antibiotics that target mitochondria extend lifespan in C. elegans.”

Aging is a continuous degenerative process caused by a progressive decline of cell and tissue functions in an organism. It is induced by the accumulation of damage that affects normal cellular processes, ultimately leading to cell death. It has been speculated for many years that mitochondria play a key role in the aging process. 

In this new study, researchers Gloria Bonuccelli, Darren R. Brooks, Sally Shepherd, Federica Sotgia, and Michael P. Lisanti from the University of Salford aimed to characterize the implications 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. 

“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.” 

Their results show that treatment of worms with either doxycycline, azithromycin (inhibitors of the small and the large mitochondrial ribosomes, respectively), or a combination of both, significantly extended median lifespan of C. elegans, enhanced their pharyngeal pumping rate, reduced their lipofuscin content and their energy consumption (ATP levels), as compared to control untreated worms, suggesting an aging-abrogating effect for these drugs. Similarly, DPI, an inhibitor of mitochondrial complex I and II, was capable of prolonging the median lifespan of treated worms. On the other hand, subjecting worms to vitamin C, a pro-oxidant, failed to extend C. elegans lifespan and upregulated its energy consumption, revealing an increase in ATP level. 

“Therefore, our longevity study reveals that mitochondrial inhibitors (i.e., mitochondria-targeting antibiotics) could abrogate aging and extend lifespan in C. elegans.”

DOI - https://doi.org/10.18632/aging.205229

Corresponding authors - Michael P. Lisanti - m.p.lisanti@salford.ac.uk, and Federica Sotgia - f.sotgia@salford.ac.uk

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Keywords - aging, C. elegans, lifespan, lipofuscin, antibiotics, mitochondria, metabolism, DPI

About Aging-US

Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.

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