Chronic Toxicity And Mechanisms Of Triclocarban On Caenorhabditis Elegans

Triclocarban(TCC)is a broad-spectrum and effective antimicrobial agent that is widely used in many personal care products.However,the degradation efficiency of TCC in the environment is low,and its environmental effects have attracted more and more attention.Nevertheless,reports of chronic toxicity of TCC are still limited and the mechanism of its toxicity is not clear.Therefore,in this study,Caenorhabditis elegans was used as a model organism to evaluate the chronic toxicity of TCC,and the mec hanism of TCC-induced to xicity was investigated from the molecular level.We first examined the effects of TCC on the body length,head swing,body bending,number of offspring,generation time and population size of C.elegans.The results showed that 0.1 and 0.2 mg/L TCC could cause significant changes in body length,head thrash,body bend and generation time.However,the brood size decreased significantly only when TCC was expo sed at a concentration of 0.2 mg/L,suggesting that the brood size may not be a sensitive indicator compared with other detection endpoints.To investigate the mechanism of TCC-induced chronic toxicity in C.elegans,we examined the content of reactive oxygen species(ROS),malondialdehyde(MDA),and lipofuscin accumulation after exposure to different concentrations of TCC for 3 days.It was found that 0.1 and 0.2 mg/L TCC could significantly increase ROS levels in nematodes,which led to significant increases in MDA and lipofuscin contents in nematodes.In addition,co-treatment of TCC with ascorbic acid,a free radical scavenger,could alleviate the inhibition of TCC on the length of nematode and reduce the ROS level in cells,indicating that ROS plays an important role in the chronic toxicity of TCC to C.elegans.In addition,we measured the expression levels of antioxidant genes and SKN-1/Nrf2 pathway genes.It was found that 0.1 and 0.2 mg/L TCC could induce up-regulation of antioxidant genes sod-1,sod-5,ctl-1 and ctl-2 in nematodes,and the expression levels of SKN-1/Nrf2 pathway genes skn-1 and gst-10 were significantly higher than those in the control group.Therefore,it is speculated that the possible mechanism of chronic toxicity of TCC is that TCC enhances oxidative stress response by increasing the expression of oxidative stress-re la ted genes and the production of ROS,thus causing oxidative damage.Finally,we explored the effects of triclocarban and food availability on the trade-off between growth and antioxidant response in C.elegans.By measuring the food uptake,body length,enzyme activities of superoxide dismutase(SOD)and catalase(CAT),we found that low food availability caused smaller body length and higher antioxidant enzyme activities compared to those at high food availability.TCC exposure at low food availability increased the inhibition on body length and stimulation of the antioxidant enzyme activity,suggesting that TCC exposure at low food availability biased trade-off toward antioxidants.Moreover,by detecting reactive oxygen species(ROS),we inferred that the mechanism of trade-off might be related to ROS.