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Updated: Aug 6, 2026
Examining the Effect of Pesticides on Caenorhabditis elegans Neurons
Published on: May 27, 2022
Cyromazine induces neurotoxicity associated with damage to dopamine, serotonin, glutamate, and GABA neuronal systems
Zibo Yin1, Jusong Liu1, Qianmei Pang1
1School of Tropical Agriculture and Forestry, Hainan University, Haikou 570228, China.
Abstract:
Cyromazine (CYR) is a widely used insect growth regulator. Its metabolite, melamine, is classified as a Group 2B carcinogen and has been associated with urinary tract lesions and tumors. While previous toxicological studies have largely focused on high-concentration exposures, the mechanisms of toxicity at environmentally relevant concentrations remain poorly understood. In this study, using Caenorhabditis elegans as a model, we demonstrated that CYR induces dose-dependent neurotoxicity, developmental impairment, reproductive toxicity, and oxidative stress. Transcriptomic analysis revealed disruptions in glutamate, dopamine, GABA, and glutathione metabolic pathways. CYR exposure caused damage to dopaminergic and glutamatergic neurons, decreased levels of several neurotransmitters, and downregulated key genes including dop-3, tph-1, and eat-4, resulting in behavioral deficits such as impaired pharyngeal pumping, body bending, and head thrashing. Parental exposure to CYR significantly elevated reactive oxygen species (ROS) and lipofuscin accumulation, activated the glutathione-mediated antioxidant pathway, and disturbed enzymatic balance, indicating a central role for oxidative stress in CYR-induced neurotoxicity. By systematically elucidating the mechanism of ROS-mediated oxidative stress in neurobehavioral toxicity, this study provides a mechanistic foundation for understanding the broader toxicological profile of CYR, thereby offering critical insights for assessing its comprehensive health risks at environmental levels.
Insights
Cyromazine (CYR) causes neurotoxicity, developmental, and reproductive issues, even at low environmental levels. This study reveals oxidative stress and neurotransmitter pathway disruptions as key mechanisms.
Area of Science:
- Environmental Toxicology
- Neuroscience
- Molecular Biology
Background:
- Cyromazine (CYR) is a common insect growth regulator.
- Its metabolite, melamine, is a potential carcinogen linked to urinary tract issues.
- Mechanisms of CYR toxicity at environmentally relevant concentrations are poorly understood.
Purpose of the Study:
- To investigate the neurotoxic effects of CYR at environmentally relevant concentrations using Caenorhabditis elegans.
- To elucidate the underlying molecular mechanisms, including oxidative stress and neurotransmitter pathway disruptions.
- To assess developmental, reproductive, and behavioral impacts of CYR exposure.
Main Methods:
- Utilized Caenorhabditis elegans as a model organism.
- Performed dose-dependent toxicity assessments (neurotoxicity, developmental, reproductive).
- Conducted transcriptomic analysis to identify affected metabolic pathways.
- Measured neurotransmitter levels, gene expression, reactive oxygen species (ROS), and lipofuscin accumulation.
Main Results:
- CYR induced dose-dependent neurotoxicity, developmental impairment, reproductive toxicity, and oxidative stress.
- Transcriptomic analysis showed disruptions in glutamate, dopamine, GABA, and glutathione pathways.
- CYR damaged dopaminergic and glutamatergic neurons, decreased neurotransmitters, and altered gene expression (dop-3, tph-1, eat-4).
- Parental CYR exposure increased ROS and lipofuscin, activating antioxidant pathways and indicating oxidative stress's role in neurotoxicity.
Conclusions:
- CYR exhibits significant neurotoxic effects, developmental impairment, and reproductive toxicity at environmentally relevant concentrations.
- Oxidative stress, particularly ROS generation, is a key mechanism underlying CYR-induced neurobehavioral toxicity.
- This study provides a mechanistic understanding of CYR toxicity, crucial for assessing its health risks at environmental levels.
