Nicotinamide Riboside Prevents Nerve Damage From Toxic Chemicals: Preclinical Findings
Synopsis
Organophosphate-induced delayed neuropathy (OPIDN) is a serious condition caused by exposure to certain toxic chemicals, leading to nerve degeneration similar to Wallerian degeneration, where damaged nerve fibers break down. In this study, researchers used nerve cells from chicken embryos to model OPIDN and found that the chemical tri-ortho-cresyl phosphate (TOCP) caused severe axon damage, loss of mitochondrial function, and depletion of ATP and NAD+, two key molecules for cellular energy. The damage was linked to reduced levels of NMNAT2, an enzyme vital for NAD+ production. Importantly, supplementing the cells with ATP, NAD+, or its vitamin B3 precursor nicotinamide riboside (NR) restored energy levels and prevented axon degeneration. These findings suggest that boosting NAD+ with NR could help protect nerves from toxic injury and offer a potential treatment for organophosphate-related neuropathy.
Journal
Toxicology Letters