Galaxolide, a Synthetic Musk, Disrupts Hepatic Mitochondrial Redox Balance in Mozambique Tilapia

Galaxolide, a synthetic polycyclic musk, is an emerging contaminant of increasing concern due to its potential risks to both human and aquatic health through direct and indirect exposure. The present study examined the acute and subchronic effects of sublethal and environmentally relevant concentrations of galaxolide on hepatic mitochondrial function in the freshwater fish, Oreochromis mossambicus. The 96-h median lethal concentration (LC₅₀-96 h) of galaxolide in O. mossambicus was determined to be 5.5 mg/L. Subsequently, fish were exposed to a sublethal concentration (550 μg/L; 1/10th of LC₅₀) and an environmentally relevant concentration (198 ng/L) for 1, 4, and 7 days (short-term exposure) and 15, 30, and 60 days (long-term exposure), alongside unexposed controls. Galaxolide exposure significantly altered the activities of key antioxidant enzymes, including superoxide dismutase, glutathione reductase, and glutathione peroxidase, along with a decline in total antioxidant capacity, indicating an impaired ability to neutralize reactive oxygen species. Concomitantly, elevated levels of hydrogen peroxide, lipid peroxidation, and protein carbonyls indicated the induction of oxidative stress. Besides, increases in nitrite, nitrate, nitric oxide, and 3-nitrotyrosine levels demonstrated nitrative stress. Histopathological examination of liver tissues revealed severe hepatic lesions, including cytoplasmic vacuolization, nuclear elongation, and vacuolar degeneration. Oxido-nitrative stress responses occurred simultaneously throughout the exposure period, and the resulting redox imbalance contributed to mitochondrial dysfunction and hepatocellular injury in O. mossambicus, underscoring the need for stringent regulation of galaxolide usage and its environmental release.