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Effects Of Microcystin-LR On The Reproduction And Offspring Development Of Zebrafish

Posted on:2019-12-21Degree:MasterType:Thesis
Country:ChinaCandidate:H C ChengFull Text:PDF
GTID:2371330545491062Subject:Aquatic biology
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In recent years,cyanobacterial blooms and the produced cyanotoxins pose a serious threat to human health.Microcystins(MCs)are the most widely distributed and most poisonous cyanotoxins,among which microcystin-LR(MCLR)is the most toxic and has been studied in detail.Considering the potential harms caused by MCLR to ecological environment and human beings,zebrafish were selected as a model to investigate the toxicological effects of MCLR.In this study,we investigated the effects of MCLR on zebrafish reproduction and offspring development.The main results and conclusions are as below:Exposure to environmentally relevant concentrations(0,0.5,4 and 32μg/L)of MCLR reduced the egg production of zebrafish.We found that MCLR accumulated in different organs such as liver,brain and gonad.Furthermore,the plasma E2 and T levels were significantly decreased and disturbed the transcription pattern of genes along the hypothalamus-pituitary-gonadal(HPG)after exposure to MCLR.In addition,the reproductive effects of microcystin-LR(MCLR)in the presence of titanium dioxide nanoparticles(n-TiO2)were also detected in this study.The results indicated the egg production was further reduced after coexposure to MCLR and n-TiO2.In comparison with MCLR alone,the plasma E2 and T levels were further decreased and the contents of MCLR in liver,brain and gonad were obviously increased after coexposure to MCLR and n-TiO2.We speculated that the increase accumulation of MCLR may be explained for the further decrease of egg production in zebrafish.Exposure to environmentally relevant concentrations(0,1,5 and 25μg/L)of MCLR decreased the body length of F1 offspring,decreased thyroid hormone(T4 and T3)levels both in F0 and F1 generations,and disturbed the transcription pattern of genes related to thyroid hormone synthesis and metabolism.The results showed that parental exposure to MCLR could cause growth inhibition of F1 larvae.The possible mechanisms may be that(1)MCLR decreases T4 level in F1 offspring by inhibiting the secretion of T4 in maternal,(2)MCLR inhibits T4 level by interfering the transcription of genes along the hypothalamic-pituitary-thyroid(HPT)axis of F1larvae.
Keywords/Search Tags:Microcystin-LR (MCLR), Reproductive toxicity, Developmental toxicity, Endocrine disruption, Coexposure
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