Journal
ECOTOXICOLOGY AND ENVIRONMENTAL SAFETY
Volume 245, Issue -, Pages -Publisher
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.ecoenv.2022.114119
Keywords
Microcystis aeruginosa; Sinocyclocheilus grahami; Embryonic development; Neurotoxicity; Endangered species; Cyanobacterial blooms
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Funding
- National Natural Science Foundation of China (NSFC)-Yunnan Joint Key Grant [U1902202]
- Great Lakes Fishery Commission
- Yunnan Provincial Science and Technology Department Grants [2019FA043, 2018FY001-007, 202003AD150017]
- NSERC
- Canada Research Chair
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This study investigated the neurotoxicity and toxicity mechanisms of Microcystis aeruginosa exudates (MaE) on embryos of the endangered fish Sinocyclocheilus grahami. The results showed that MaE affected the development of fish embryos, leading to malformation and mortality while decreasing fertilization rate. MaE also inhibited fish neurobehavior and affected gene and protein expression of neurotransmitters and receptors.
Cyanobacterial harmful algal blooms (cHABs) pose a risk to exposed aquatic and terrestrial species. Numerous studies have addressed effects of single toxins while much less attention has been devoted to mixtures of cHAB metabolites that are continually released by living cyanobacteria. Neuro-impairment associated with cHABs has been reported in fish, though the mechanism remains unclear. Here we exposed embryos of Sinocyclocheilus grahami, an endangered fish, to Microcystis aeruginosa exudates (MaE) to evaluate neurotoxicity and the toxicity mechanism(s). We found that MaE affected embryonic development by increasing malformation and mortality rates and decreasing the fertilization rate. MaE also inhibited fish neurobehavior including touch response, social frequency, swimming distance, and aggravated light-stimulation response. Neurobehavior suppression resulted from a decrease in excitatory neurotransmitters acetylcholine and dopamine, even though receptors increased. MaE also affected gene and protein expression of neurotransmitters, synthetic and/or degrading enzymes, and receptors. Our findings shed light on specific mechanisms by which MaE induces neurotoxicity in early life stages in fish and contributes to improvement of the conservation strategy for this species.
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