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To elucidate the toxicological mechanisms of endocrine disruptor bisphenol A (BPA) on the aquatic animals, endocrine disruptors and its mechanism. The BPA on acute toxicity in zebrafish BPA zebrafish liver damage, and oxidative stress effect, BPA zebrafish gonadal tissue damage as well as reproductive role of impact of BPA zebrafish liver Esr1 (ERα), AhR2,, as well as VTG mRNA expression. The results show that the the zebrafish: BPA has the acute toxic effects of exposure of BPA interested zebrafish liver, gonads produce tissue injury, BPA affects the reproductive role of zebrafish endocrine disruption; BPA zebrafish. 1. The zebra fish BPA acute toxicity experiment of BPA exposure poison 6 h, high concentrations of zebra fish swimming slowly body gradually lose balance, side tour, Yang Yu, sink to the bottom, weak breathing phenomenon. 12 h, exposure to toxic in high concentrations of zebra fish died, the death of the individual pectoral, abdominal abnormal dark red. BPA zebrafish 96h median lethal concentration of 6.3 mg L -1 , zebra fish are more sensitive to BPA, safe concentration of 0.63 mg L -1 . 2.BPA the zebrafish liver damage and oxidative stress role in order to further understand the toxicity of BPA zebrafish as well as the mechanism of toxicity of zebrafish exposed to BPA, used to detect the BPA zebrafish liver damage and timing to take the zebrafish liver oxidative stress effect. 96 h exposure to a concentration-dependent zebrafish liver damage. 0.2 mg L -1 sublethal concentrations of BPA group, 96 h after the exposure, zebrafish minor damage to the liver; 2 mg L -1 sublethal concentrations of BPA group exposed 96 h, zebrafish liver tissue by injury, nucleus atrophy, cell swelling, nuclear pyknosis; exposed for 96 h in 6.1 mg L -1 BPA group, zebrafish liver produce a great deal of damage, cell vacuolization, a large area of ??tissue necrosis produces empty. Exposed 6h various concentrations of SOD activity showed activated energy level higher than that of the control group, in which 0.2 and 2 mg L -1 concentration group activation effect is not obvious (P gt; 0.05), 6.1 mg L -1 concentrations SOD activity was significantly enhanced (P lt; 0.05). 12h after exposure, the SOD activity of the treatment group and the control group compared to no significant change. Exposed for 24 hours, treated SOD activity were lower than the control group. The above results show that case of 96h sublethal concentrations, the SOD vitality and control group difference not (P gt; 0.05); high-dose group (6 mg L -1 BPA) after treatment, SOD activity level increased significantly at 6h, gradually returned to normal levels as the exposure time. Sublethal concentrations of BPA treatment group (0.1,0.6 mg L -1 ), 48h test results show the GPX vitality was induced (P lt; 0.05); high concentration group (6 mg L - 1 BPA) treated zebrafish liver GPX activity was induced. BPA zebrafish liver has a target organ toxicity. The gonadal damage 3.BPA zebrafish in order to understand BPA zebrafish gonadal damage and injury mechanisms, zebrafish different concentrations of BPA exposure 96h. In the group of high concentration (6.3 mg L -1 ), zebrafish testis structural damage, serious follicle atrophy (atresia rate of 35%); at 0.2 mg L -1 sublethal concentration of BPA group, gonadal tissue structure there is no obvious damage to the ovaries in section Ⅲ phase the late and Ⅳ match sub-number ratio increased the single oocyte diameter increase (P lt; 0.05); in 2 mg L -1 sublethal concentrations of BPA group exposed for 96 h, zebrafish the gonadal tissue damage is not obvious, the ovarian phase late first Ⅳ Ⅲ match sub-number ratio increase; 6.1 mg L -1 BPA group exposed to 96 h, zebrafish testis tissue structure to be some damage, the ovarian atrophy found in a large number of cells; BPA gonadal role worthy of further study. The testis sperm head count results show that low concentrations (2 mg L -1 ) and the concentration (6 mg L -1 ) BPA exposure, zebrafish per gram of testis reduce after the first increase in the number of sperm heads, high concentration (8 mg L -1 ) group showed significant inhibition, and a decrease in the number of per gram of testis sperm head. Sperm head count results are consistent with observations of the testis tissue sections. Of 4.BPA in zebrafish endocrine disrupting effects of bisphenol A on zebrafish liver Esr1, AhR2 well VTG1 mRNA expression, which proved BPA possible mechanism of action of zebrafish endocrine disruption in 96h sublethal set up a concentration within the concentration range of drug experiments on male zebrafish exposed group (2 mg L -1 ). The results show that: the male zebrafish BPA exposure the 12h, Esr1 and VTG1 significantly induce a significant difference (P lt; 0.05), compared with the exposure toxicity 0h. Male zebrafish BPA exposure 24 hours, the relative expression level of Esr1 and VTG1mRNA still maintain a very high level, a significant difference (P lt; 0.05) compared with exposure toxicity 0h. Exposed 48h, Esr1 relative expression levels continue to rise. Exposure to 72h, Esr1 and VTG1mRNA relative expression of exposure to less than 12, 24 and 48 h, compared with 0h no significant difference (P gt; 0.05). BPA exposure, AhR2 be induced at 48h 96 hours, mRNA relative expression level 0h of 3.22 times. Exposure process, Esr1 and VTG1mRNA is relative expression amount changes. In this experiment, the BPA exposure concentration to sublethal concentrations of 2 mg L -1 , proved the ability of BPA the male zebrafish Esr1 VTG1mRNA induced strong. On AhR2 having a certain induced, but inducing ability is weak. The results show that the existence of multi-channel process BPA endocrine disruption in zebrafish.
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