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Cadmium-induced serotonergic neuron and reproduction damages conferred lethality in the nematode Caenorhabditis
Shunchang Wang1, Zhaoxia Chu1, Kegui Zhang1
1School of Biological Engineering, Huainan Normal University, Huainan 232038, China.
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.
Insights
Cadmium exposure harms Caenorhabditis elegans by damaging reproductive systems and serotonergic neurons. Protecting these systems enhances survival, revealing key mechanisms of cadmium toxicity.
Area of Science:
- Environmental Toxicology
- Neurobiology
- Developmental Biology
Background:
- Cadmium is a widespread environmental toxin.
- Caenorhabditis elegans models reveal conserved pathways for cadmium exposure.
- Mechanisms of cadmium-induced lethality, particularly the killing process, are not fully understood.
Purpose of the Study:
- Investigate the impact of serotonergic neuronal and reproductive damage on cadmium toxicity in C. elegans.
- Elucidate the role of the reproduction process in cadmium sensitivity.
- Determine the mechanisms underlying cadmium-induced lethality.
Main Methods:
- Comparative cadmium resistance assays across different life stages and reproductive statuses (young adults, sterile hermaphrodites, males, post-reproductive worms).
- Analysis of cadmium-induced "bagging" phenotype (internal embryo hatching) and its relation to egg-laying deficiency.
- Assessment of serotonergic neuron function, including neuronal body size and tryptophan hydroxylase expression.
- Evaluation of interventions like serotonin, imipramine, and thermal preconditioning on survival rates.
Main Results:
- Reproduction process, not just capacity, confers cadmium sensitivity.
- Cadmium exposure causes egg-laying deficiency, leading to internal hatching (bagging) and premature death.
- Serotonergic neurons are damaged (shrinkage, reduced enzyme expression), while vulval muscles remain functional.
- Serotonin, imipramine, and thermal preconditioning enhance cadmium resistance by mitigating neuronal and reproductive damage.
Conclusions:
- Damage to serotonergic neurons and reproductive processes are critical contributors to cadmium-induced lethality in C. elegans.
- The study identifies specific cellular and molecular targets of cadmium toxicity.
- Findings suggest potential therapeutic strategies for mitigating cadmium poisoning.
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