Potential genetic damage to nematode offspring following exposure to triclosan during pregnancy.

Abstract

Triclosan (TCS) is widely used as broad-spectrum antibacterial agent. However, it may threaten the health of human offspring if the mother is exposed to TCS during pregnancy. The present study aimed to identify potential mechanisms behind the toxic effect of TCS on the offspring of Caenorhabditis elegans (C. elegans), using this nematode as a suitable animal model. The results of the current study demonstrated that the locomotory behavior and reproductive capacity of C. elegans offspring was severely affected by prenatal exposure to different concentrations of TCS. A high-throughput gene microarray was performed to investigate molecular alterations in C. elegans offspring following TCS exposure during pregnancy. Microarray results indicated that 113 genes were differentially expressed following TCS treatment compared with the control group. Gene ontology analysis demonstrated that these dysregulated genes were primarily associated with neuron development, muscular strength and reproduction. Pathway analysis results demonstrated that differentially expressed genes participated in several signaling pathways, including arginine, proline, and purine metabolism, progesterone-mediated oocyte maturation and neuroactive ligand-receptor interaction. Finally, 7 TCS toxicity-associated genes were confirmed by reverse transcription-quantitative polymerase chain reaction. The present study indicates that TCS exposure during pregnancy may disturb the locomotory behavior and reproductive capacity of C. elegans offspring, primarily through 7 TCS toxicity-associated genes, which merits further study from an environmental health perspective.