Cadmium-induced serotonergic neuron and reproduction damages conferred lethality in the nematode Caenorhabditis elegans. (December 2018)

• Record Type: Journal Article
• Authors: Wang, Shunchang; Chu, Zhaoxia; Zhang, Kegui; Miao, Guopeng
• Is Part Of: Chemosphere. Volume 213(2018)
• Page Start: 11
• Page End: 18
• Publication Date: 2018-12
• Subjects: Cadmium -- Caenorhabditis elegans -- Mean survival time -- Bagging -- Serotonergic neuron; Pollution -- Periodicals; Pollution -- Physiological effect -- Periodicals; Environmental sciences -- Periodicals; Atmospheric chemistry -- Periodicals; 551.511
• DOI: 10.1016/j.chemosphere.2018.09.016
• Languages: English
• ISSNs: 0045-6535

Abstract

Abstract: Cadmium is a ubiquitous environmental toxicant. The use of Caenorhabditis elegans as a model for monitoring cadmium exposure has revealed several conserved signaling pathways. However, little is known about the killing process during lethality assay. In the present study, we investigated the effects serotonergic neuronal and reproductive damages on cadmium exposure in C. elegans . We found that sterile hermaphrodites, males and worms that passed reproduction span presented high cadmium resistance compared to those of young adults. The results demonstrated that reproduction process other than reproduction capacity conferred cadmium sensitivity. Cadmium exposure resulted in high ratio bagging phenotype, which was a severe reproductive deficit with embryos hatched internally that could cause worms to die early. The mechanism of bagging formation was ascribed to cadmium-induced egg laying deficiency that led embryos to retain and hatch in uterus. The addition of serotonin and imipramine promoted egg laying and thereby increased cadmium resistance. The results demonstrated that vulval muscles responsible for egg laying were still functional, while the serotonergic hermaphrodite specific neurons might be dysfunctional under cadmium exposure. Cadmium exposure resulted in shrinkage of serotonergic neuronal body and reduced expressions of tryptophan hydroxylase, the key enzyme for serotonin synthesis. The protection of serotonergic neuron through transient thermal preconditioning improved survival rate. In conclusion, our study demonstrated that damages of serotonergic neurons and reproduction conferred to cadmium-induced lethality. Graphical abstract: Highlights: Sterile and male C. elegans showed cadmium resistance. Cadmium induced BOW contributed to the killing process. Cadmium induced serotonergic neuron damage conferred to BOW formation. Protection of serotonergic neuron increased cadmium resistance in C. elegans.