An Xu at the Hefei Institutes of Physical Science of the Chinese Academy of Sciences have found that a magnetotactic bacterium (MTB) called Magnetospirillum magneticum AMB-1 (AMB-1) can extend healthy lifespan in the Caenorhabditis elegans model. The team also identified the main mechanism behind the effect -- suppression of a form of cell death known as ferroptosis. The findings were published in Free Radical Biology and Medicine.
Aging gradually reduces normal physiological function and raises the risk of many chronic diseases. Researchers have explored drugs and genetic approaches as possible anti-aging strategies, but questions about safety and practical clinical use remain. Magnetotactic bacteria (MTB) offer a very different approach.
These microorganisms contain specialized structures called magnetosomes and have shown good biocompatibility. They have already attracted attention for potential uses including drug delivery and cancer treatment, but their possible influence on aging has received far less study. To investigate that question, the researchers tested the MTB strain AMB-1 in C. elegans, a widely used model organism for aging research.
Worms treated with AMB-1 lived substantially longer. Their average lifespan increased by 43.39%, and the treatment also helped preserve neurological function and intestinal integrity in older worms. The team then examined whether magnetosome production was important to this effect.
Their results indicated that the ability to produce magnetosomes played a major role in extending lifespan. Wild-type AMB-1 produced a stronger longevity effect than reversibly non-magnetotactic RNM-AMB-1. In contrast, non-magnetotactic NM-AMB-1 did not extend lifespan.
Blocking an Aging-Linked Form of Cell Death Further experiments offered clues about how AMB-1 produces its effects. The bacteria reduced iron buildup and lowered lipid peroxidation in the worms, changes that suppressed aging-related ferroptosis. Ferroptosis is a form of cell death associated with iron accumulation and oxidative damage to fats within cells.
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