PUBLICATION
Life-cycle exposure to microcystin-LR interferes with the reproductive endocrine system of male zebrafish
- Authors
- Su, Y., Li, L., Hou, J., Wu, N., Lin, W., Li, G.
- ID
- ZDB-PUB-160411-2
- Date
- 2016
- Source
- Aquatic toxicology (Amsterdam, Netherlands) 175: 205-212 (Journal)
- Registered Authors
- Li, Li
- Keywords
- Endocrine-disrupting effect, Hypothalamic-pituitary-gonadal axis, Microcystin-LR, Reproductive toxicity, Sex steroid hormone
- MeSH Terms
-
- Animals
- Endocrine System/drug effects*
- Endocrine System/metabolism
- Enzyme-Linked Immunosorbent Assay
- Estradiol/blood
- Life Cycle Stages
- Liver/drug effects
- Liver/metabolism
- Male
- Microcystins/toxicity*
- RNA, Messenger/metabolism
- Reproduction/drug effects
- Testis/drug effects
- Testis/metabolism
- Testis/pathology
- Testosterone/blood
- Water Pollutants, Chemical/toxicity*
- Zebrafish/physiology
- Zebrafish Proteins/genetics
- Zebrafish Proteins/metabolism
- PubMed
- 27060240 Full text @ Aquat. Toxicol.
Citation
Su, Y., Li, L., Hou, J., Wu, N., Lin, W., Li, G. (2016) Life-cycle exposure to microcystin-LR interferes with the reproductive endocrine system of male zebrafish. Aquatic toxicology (Amsterdam, Netherlands). 175:205-212.
Abstract
Recently, MC-LR reproductive toxicity drew great attention. Limited information was available on endocrine-disrupting effects of MC-LR on the reproduction system in fish. In the present study, zebrafish hatchlings (5 d post-fertilization) were exposed to 0, 0.3, 3 and 30μg/L MC-LR for 90 d until they reached sexual maturity. Male zebrafish were selected, and changes in growth and developmental parameters, testicular histological structure as well as the levels of gonadal steroid hormones were studied along with the related-gene transcriptional responses in the hypothalamic-pituitary-gonadal axis (HPG-axis). The results, for the first time, show a life cycle exposure to MC-LR causes growth inhibition, testicular damage and delayed sperm maturation. A significant decrease in T/E2 ratio indicated that MC-LR disrupted sex steroid hormones balance. The changes in transcriptional responses of HPG-axis related genes revealed that MC-LR promoted the conversion of T to E2 in circulating blood. It was also noted that vtg1 mRNA expression in the liver was up-regulated, which implied that MC-LR could induce estrogenic-like effects at environmentally relevant concentrations and long-term exposure. Our findings indicated that a life cycle exposure to MC-LR causes endocrine disruption with organic and functional damage of the testis, which might compromise the quality of life for the survivors and pose a potent threat on fish reproduction and thus population dynamics in MCs-contaminated aquatic environments.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping