Mitochondria-Targeting Antibiotics Extend Lifespan in C. Elegans

11-22-2023

“Our ultimate goal is to find existing FDA-approved drugs and dietary supplements that can not only increase lifespan but also improve healthspan.” 

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BUFFALO, NY- November 22, 2023 – A new research paper 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.”

Read the full study: DOI: https://doi.org/10.18632/aging.205229 

Corresponding Authors: Michael P. Lisanti, Federica Sotgia

Corresponding Emails: m.p.lisanti@salford.ac.uk, f.sotgia@salford.ac.uk 

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

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About Aging-US:

Cancer and aging are two sides of age-related tumorigenesis.

The mission of the journal is to understand the mechanisms surrounding aging and age-related diseases, including cancer as the main cause of death in the modern aged population.

The journal aims to promote 1) treatment of age-related diseases by slowing down aging, 2) validation of anti-aging drugs by treating age-related diseases, and 3) prevention of cancer by inhibiting aging. (Cancer and COVID-19 are age-related diseases.)

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