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Effects Of Monocrotophos Pesticide On The Growth And GH/IGF-â…  Axis In Juvenile Nile Tilapia, Oreochromis Niloticus

Posted on:2013-10-12Degree:MasterType:Thesis
Country:ChinaCandidate:Y ZhengFull Text:PDF
GTID:2233330377952262Subject:Ecology
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Monocrotophos (MCP) pesticide has strong neurotoxicity and endocrinedisrupting effects, itswide use and high residual has caused severe water pollution.The MCP in water may affect the fish growth and development, damage the structureand functionand disrupt the behavior and reproduction, resulting in the poor healthstatus of the fish population, and even of the entire aquatic ecosystem. However, theresearch related to the effects of MCP pesticide on fish growth isinfrequent, so itbecomes essential to explore the effects and potential mechanism. For this reason, weinvestigated the effects of exposure to0.0011.000mg·L-1MCP pesticide for21and42days on the growth of “New GIFT” Nile tilapia (Oreochromis niloticus), takingstandard length, body weight and specific growth rate (SGR) as growth indexes.Sincethat the growth of teleost is mainly regulated and controlled by growthhormone/insulin-like growth factor-Ⅰ axis (GH/IGF-Ⅰ axis), we further measured thegene expression level of tilapia pituitary GH, hepatic GHR1/2and IGF-Ⅰ byreal-timePCR, and also the changes of plasma GH, IGF-Ⅰ and IGFBP-3concentrationbyradioimmunoassay (RIA) and immunoradiometric assay (IRMA), with anattempting to understand the endocrinedisturbancemechanism of MCP on fish growth.Our results providedsome basic data for the evaluation on the effects oforganophosphorus pesticide on fish growth.The results showed that:(1) Compaired to control group, the standard length and body weight of juveniletilapia in experimental groups exposed to0.001,0.010,0.100and1.000mg·L-1MCPpesticide for21and42days reduced significantly, and the SGR declined with the riseof MCP pesticide exposure concentration, representing a dose-effect relationship. Itclearly showedthat MCP pesticide remarkably inhibited the growth of juvenile tilapia.(2) Following a21-day exposure to0.0011.000mg·L-1MCP pesticide, pituitaryGH gene expression and plasma GH concentration elevated in accordance with MCP pesticide exposure concentration. However, there was a negative correlation betweenpituitary GHmRNA or plasma GH level and SGR. Considering the IGF-Ⅰ levelchanges testedlater, we suggestedthat GH mightnotbe the direct target of MCP ontilapia growth, and the rise of GH is very probably the result of feedback effect ofhepatic IGF-Ⅰ.(3) Hepatic GHR2mRNA level declinedobservably in groups exposed to MCP,with distinct dose-effect relationship.Hepatic GHR1mRNA level didn’t show evidentchange at lower MCP concentration, but show significant decline at higher MCPconcentration. SinceGHR2possesses much higher affinity with GH than GHR1inliver, and it is the main GH receptor for mediating the synthesis of IGF-Ⅰ, ourresultsimplied that GHR2is probably the main target of MCP, and the decline ofGHR2gene expression blocked the systhesis of IGF-Ⅰ and thus caused the inhibitionon tilapia growth.(4) When exposed to21and/or42days, hepatic IGF-Ⅰ mRNA and plasma IGF-Ⅰlevel declined as the MCP pesticide concentration increasing, showing obviousdose-effect relationship and positive relationship with SGR and hepatic GHR2mRNAlevel. The resultsfurther support our conjecture that GHR2is the main target of MCPpesticide, and the abnormal reduction of plasma IGF-Ⅰ concentration would promotethe synthesis and secretion of pituitary GH through the negative feedback mechanism.Furthermore, IGF-Ⅰ:IGFBP-3ratio of plasma could reflect the level of free bioactiveIGF-Ⅰ. After21-day and42-day exposure of MCP pesticide, the ratio appeareddecreasedwith the increase of MCP concentration, which indicated the decline ofplasma free IGF-Ⅰ, so the low circulating free IGF-Ⅰ mightbe one of the reasons forfishgrowth inhibition.In conclusion, MCP pesticide could suppress the growth of tilapia inadose-dependent manner, and we speculated the mechanism as follows: As the directtarget of MCP pesticide, the hepatic GHR2expression is inhibited by MCP, whichblocked the stimulatory effect of GH on hepatic IGF-Ⅰ synthesis and secretion,leading to the low concentration of plasma IGF-Ⅰ and slow growth rate of tilapia.Moreover, the MCP pesticide also enhanced the synthesis of IGFBP-3and reduced the biologically active circulating free IGF-Ⅰ. Ultimately, the growth of tilapia wasinhibited by MCP pesticide.
Keywords/Search Tags:monocrotophos (MCP) pesticide, Nile tilapia (Oreochromisniloticus), growth, growth hormone (GH), growth hormone receptor (GHR), insulin-like growth factor-â…  (IGF-â… ), IGF binding protein-3(IGFBP-3)
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