Lipid droplets buffer hydrogen sulfide-induced redox imbalance.

Chronic low-level hydrogen sulfide exposure (4 to 20 µM) in several human cell lines drives robust lipid droplet carbon sequestration linked to reductive NAD and coenzyme Q shifts.

• Why it matters: Acute sulfide toxicity is known, but how cells adapt to chronic, microbially-derived sulfide—especially in colon-relevant contexts—remains unclear.
• What they did: Cells were exposed to 4 to 20 µM H2S, followed by lipidomics and metabolite profiling of NAD and CoQ pools, glycerol-3-phosphate, and cytidine triphosphate (CTP), plus mitochondrial perturbation using a water-generating NADH oxidase.
• The result: Lipid droplets increased and persisted for 48 h after H2S withdrawal while NAD and CoQ slowly reoxidized; blocking fatty acid synthesis during exposure impaired recovery of respiration.

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