In a new study published in Liver Research, a team of researchers in China discovered that nicotinic acid—a common form of vitamin B3—can dramatically reduce liver damage caused by ischemia-reperfusion injury (IRI), a major complication in liver surgery and transplantation.
"Hepatic IRI occurs when blood flow is temporarily cut off and then restored—common during liver resection or transplant—triggering oxidative stress, mitochondrial dysfunction, and inflammation," explains senior author Jia Yao. "While antioxidants like N-acetylcysteine (NAC) have shown some benefit, effective clinical therapies remain limited."
The team's findings demonstrate that nicotinic acid matches or even exceeds NAC's protective effects by targeting the root cause: damaged mitochondria. In experiments using both mice and primary hepatocytes, pretreatment with nicotinic acid markedly lowered markers of liver injury (ALT, AST, LDH), suppressed inflammation, and reduced cell death driven by ferroptosis, an iron-dependent form of programmed cell death.
Notably, nicotinic acid markedly restored mitochondrial quality. "It did not just act as an antioxidant—it actively promoted mitophagy (the cleanup of broken mitochondria) and mitochondrial biogenesis (the creation of new ones)," says Yao. "This dual action stabilized the mitochondrial permeability transition pore, boosted ATP production, and rebalanced cellular redox status."
The authors noted that given its safety, low cost, and widespread availability, nicotinic acid could be rapidly translated into clinical use—potentially improving outcomes for patients undergoing liver surgery. Human trials are now being planned to confirm these benefits in real-world settings.
