Protecting host mitochondria with vitamin B3 preserves bioenergetics and thermogenesis during antibiotic treatment

Nicotinamide (NAM) protects mitochondrial respiration and mitochondrial thermogenesis from chloramphenicol (CA)–induced, dose-dependent impairment in Drosophila S2 cells and developing larvae.

• Why it matters: Antibiotics that inhibit bacterial translation can also disrupt host mitochondria, limiting broad-spectrum use due to mitochondrial toxicity and leaving off-target physiology poorly understood.
• What they did: Drosophila S2 cells, human HEK293T cells, and developing Drosophila larvae were exposed to CA, with mitochondrial respiration/thermogenesis measured and metabolomics used to track vitamin B3 metabolism changes.
• The result: NAM showed the strongest protective effect among vitamin B3 vitamers tested, mitigating CA-linked mitochondrial dysfunction and aberrant innate immune activation, and enabling co-supplementation strategies via conserved mitochondrial pathways.

AI summary of the abstract · may contain errors · not medical advice · read the paper.