Triclosan exposure exacerbates muscle wasting via senescence and IGF-1 pathway suppression: A combined epidemiological and experimental study

Triclosan, a broad-spectrum bactericide in various consumer products, has become a ubiquitous environmental contaminant, with detectable residues found in aquatic systems and human urine. Although studies demonstrated its potential to impair muscle strength, population-level evidence and mechanistic insights linking triclosan exposure to muscle health remain underexplored. This study leveraged 2878 participants data from NHANES, and suggested that individuals in the highest quartile of urinary creatinine-corrected triclosan levels exhibited a 0.18 kg/m2 reduction in appendicular skeletal muscle mass index (ASMI) [β = −0.18, 95 % CI (−0.35, −0.01)] compared to those in the lowest quartile. Importantly, bilirubin was identified as an oxidative stress mediator, explaining 16.799 % of this adverse association. Experimental evidence determined that triclosan accelerates muscle wasting through oxidative imbalance and muscle senescence. Insulin-like growth factor 1 (IGF-1) served as an essential role in the development of triclosan-induced muscle wasting. Molecular docking and molecular dynamics simulations revealed that triclosan could directly interact with IGF-1. The results of experiments demonstrated that triclosan induces muscle senescence and oxidative stress by inhibiting the IGF-1/Akt/mTOR signaling pathway. Furthermore, administration of IGF-1 protein mitigated muscle wasting by reducing oxidative stress and muscle senescence, offering a potential mechanism for counteracting triclosan-induced muscle wasting. This study not only underscores the detrimental effects of triclosan on muscle health but also establishes a mechanistic link between triclosan exposure and muscle wasting. These findings emphasize the need for environmental and public health policies to alleviate the negative effects of triclosan on muscle health.