Diclofenac Sodium/Triclocarban

Triclocarban (TCC) and triclosan (TCS) are broad-spectrum biocides that are extensively utilized frequently contaminate water bodies and have high environmental persistence. However, the safety of TCC and TCS for wild organisms remains largely unknown. Here, we evaluated the potential health risks for black-spotted frogs (Pelophylax nigromaculatus) when exposed to TCC and TCS at concentrations of 1, 10, and 100 μg/L for 21 consecutive days. TCC and TCS significantly disrupted the gut microbiome, specifically phylum Proteobacteria, which resulted in elevated serum levels of lipopolysaccharide (LPS), a bacterial endotoxin. After entering the bloodstream, LPS subsequently passes through the liver, where inflammatory cytokines are stimulated, including interleukin-1 β, interleukin-6, and tumor necrosis factor-alpha. Genes related to the inflammatory processes are also activated. This inflammatory response led to an increase in the activity of superoxide anion radicals and oxidative stress markers in the liver, mainly superoxide dismutase, catalase, glutathione peroxidase, and malondialdehyde. In addition to oxidative stress, damage to the liver has also been reported as elevated concentrations of alanine aminotransferase (ALT) and aspartate aminotransferase (AST). Collectively, these findings suggest that TCC and TCS exert hepatotoxic effects on frogs by disrupting the gut-liver axis, thereby inducing hepatic inflammation and oxidative stress. This study highlights the potential health risks posed by TCC and TCS exposure in wild organisms.

Triclocarban (TCC) and triclosan (TCS) are broad-spectrum antimicrobial agents that are widely distributed in aquatic environments. They pose significant risks to aquatic organisms, but their potential impacts on animal health remain poorly understood. In this study, black-spotted frogs (Pelophylax nigromaculatus) were exposed to TCC or TCS at concentrations of 1, 10, or 100 μg/L for 21 days to investigate the effects of these agents on hepatic lipid metabolism. Exposure to TCC/TCS significantly inhibited the synthesis and transport processes of lipids while accelerating their decomposition, resulting in elevated serum lipid levels and a marked decrease in liver lipid content. Lipidomic analysis revealed substantial alterations in the hepatic lipid profile post-exposure, particularly in glycerophospholipids. Kyoto Encyclopedia of Genes and Genomes pathway analysis demonstrated that TCC/TCS exposure had a targeted impact on the metabolic pathways of glycerophospholipids. Molecular docking results showed that TCC and TCS exhibited strong binding affinity towards peroxisome proliferator-activated receptor α (PPARα), which is a crucial regulator of lipid metabolism. The results of molecular dynamics and fluorescence experiments showed that TCS exhibited stronger PPARα binding ability than TCC. Taken together, our results show that exposure to TCC and TCS significantly disrupts lipid metabolism in the liver of the black-spotted frog. The underlying mechanism involves binding to PPAR, which inhibits lipogenesis and activates lipolysis. These findings provide fresh perspectives on the ecological threats posed by emerging contaminants, particularly TCC and TCS, to aquatic organisms.