期刊
ECOTOXICOLOGY AND ENVIRONMENTAL SAFETY
卷 236, 期 -, 页码 -出版社
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.ecoenv.2022.113493
关键词
Glyphosate; Zebrafish; Developmental toxicity; Mechanism
资金
- Natural Science Foundation of Henan Province [212300410176]
- Key Research and Development Promotion Project in Henan Province [202102310343]
Glyphosate exposure in zebrafish larvae induces developmental toxicity, characterized by premature hatching, reduced heartbeats, and body deformities. This is likely due to disrupted thyroid function and abnormal expression of growth hormone/insulin-like growth factor axis-related genes. Additionally, glyphosate treatment leads to oxidative damage, endoplasmic reticulum stress, inflammatory reactions, and apoptosis.
Glyphosate (GLY) induces developmental toxicity in fish, but research on the toxicity mechanism is limited. In this study, zebrafish embryos were exposed for 120 hpf to 0.7, 7, and 35 mg L-1 GLY. The results show that GLY treatment induced developmental toxicity in the fish, including premature hatching, reduced heartbeats, pericardial and yolk sac oedema, swim bladder deficiency, and shortened body length, which was possibly due to a significantly decreased triiodothyronine (T3)/thyroxine (T4) ratio and the abnormal expression patterns of hypothalamic-pituitary-thyroid (HPT) (crh, tsh beta, tr alpha, tr beta, and t tr ) and growth hormone/insulin-like growth factor (GH/IGF) axis-related genes (gh, ghr alpha, ghr beta, igf1, igf1r alpha, and igf1r beta) in larvae exposed to GLY. In addition, GLY exposure altered the levels of SOD and CAT, increased ROS, promoted malondialdehyde (MDA) content, and significantly altered the levels of endoplasmic reticulum (ER) stress signalling pathway factors (perk, eif2 alpha, gadd34, atf4, ire1 alpha, xbp1, atf6, hspa5, and chop), suggesting that GLY treatment induced oxidative injury and ER stress in the larvae. Further research showed that treatment with a higher concentration of GLY upregulated the levels of iNOS, IL-1 beta, and TNF-alpha while inhibiting the expression of IL-10 and TGF-beta, suggesting that GLY causes an inflammatory reaction in the larvae. In addition, we also found that apoptosis was induced in the larvae, which was determined by acridine orange staining and abnormal expression of p53, caspase-3,-8, and-9. Taken together, our results demonstrate that GLY exposure altered the T3/T4 ratio, disturbed the expression patterns of HPT and GH/IGF axis-related genes, and induced oxidative and ER stress, inflammatory reactions, and apoptosis in the zebrafish larvae. This investigation contributes to improved understanding of the developmental toxicity mechanism of GLY in fish.
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