PUBLICATION
Microcystin-LR retards gonadal maturation through disrupting the growth hormone/insulin-like growth factors system in zebrafish
- Authors
- Hou, J., Su, Y., Lin, W., Guo, H., Xie, P., Chen, J., Gu, Z., Li, L.
- ID
- ZDB-PUB-170123-1
- Date
- 2017
- Source
- Ecotoxicology and environmental safety 139: 27-35 (Journal)
- Registered Authors
- Chen, Jun, Li, Li
- Keywords
- GH/IGFs axis, Life-cycle exposure, Microcystins, Reproductive development, Retardation
- MeSH Terms
-
- Animals
- Brain/drug effects
- Brain/pathology
- Cyanobacteria
- Environmental Exposure/adverse effects
- Enzyme Inhibitors/toxicity
- Female
- Gonads/drug effects*
- Gonads/physiology
- Growth Hormone/metabolism*
- Insulin-Like Growth Factor I/metabolism
- Life Cycle Stages
- Liver/drug effects
- Liver/pathology
- Male
- Microcystins/toxicity*
- Ovary/drug effects
- Ovary/physiology
- Reproduction/drug effects*
- Somatomedins/metabolism*
- Spermatozoa/drug effects
- Spermatozoa/physiology
- Water Pollutants, Chemical/toxicity*
- Zebrafish/metabolism
- Zebrafish/physiology*
- PubMed
- 28109900 Full text @ Ecotoxicol. Environ. Saf.
Citation
Hou, J., Su, Y., Lin, W., Guo, H., Xie, P., Chen, J., Gu, Z., Li, L. (2017) Microcystin-LR retards gonadal maturation through disrupting the growth hormone/insulin-like growth factors system in zebrafish. Ecotoxicology and environmental safety. 139:27-35.
Abstract
Recent studies have documented that microcystins (MCs) have potential toxic effects on growth and reproduction in fish. However, no systematic data exist on whether MCs cause gonadal development retardation through disrupting the growth hormone/insulin-like growth factors (GH/IGFs) system. To this end, zebrafish hatchlings (5 d post-fertilization) were exposed to 0, 0.3, 3 and 30µg/L microcystin-LR (MC-LR) for 90 d until they reached sexual maturity. Life-cycle exposure to MC-LR caused delayed ovarian maturation and sperm development along with ultrapathological lesions in the brain and liver. Moreover, the retarded gonadal development was accompanied by an inhibition of the GH/IGFs system, which was characterized by significant decreases in the transcriptional levels of brain gh (males only), hepatic igf2a and igf2b as well as gonadal igf1 (males only), igf3 and igf2r. These findings for the first time point to the influence of MC-LR on fish gonadal development via the GH/IGFs system. Also, sex-differential impairments suggested that gonadal development of males is more vulnerable than that of female to MC-LR. Our results provide evidence that MC-LR at environmentally relevant concentrations is able to induce impairments on fish gonadal development.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping