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首页> 外文期刊>Physiology & behavior >Selenomethionine reduces visual deficits due to developmental methylmercury exposures.
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Selenomethionine reduces visual deficits due to developmental methylmercury exposures.

机译：硒代蛋氨酸可减少因发育中甲基汞暴露而造成的视力缺陷。

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Developmental exposures to methylmercury (MeHg) have life-long behavioral effects. Many micronutrients, including selenium, are involved in cellular defenses against oxidative stress and may reduce the severity of MeHg-induced deficits. Zebrafish embryos (<4 h post fertilization, hpf) were exposed to combinations of 0.0-0.30 microM MeHg and/or selenomethionine (SeMet) until 24 hpf then placed in clean medium. Fish were tested as adults under low light conditions ( approximately 60 microW/m(2)) for visual responses to a rotating black bar. Dose-dependent responses to MeHg exposure were evident (ANOVA, P<0.001) as evidenced by reduced responsiveness, whereas SeMet did not induce deficits except at 0.3 microM. Ratios of SeMet:MeHg of 1:1 or 1:3 resulted in responses that were indistinguishable from controls (ANOVA, P<0.001). No gross histopathologies were observed (H&E stain) in the retina or optic tectum at any MeHg concentration. Whole-cell, voltage-gated, depolarization-elicited outward K(+) currents of bipolar cells in intact retina of slices adult zebrafish were recorded and outward K(+) current amplitude was larger in bipolar cells of MeHg-treated fish. This was due to the intense response of cells expressing the delayed rectifying I(K) current; cells expressing the transient I(A) current displayed a slight trend for smaller amplitude among MeHg-treated fish. Developmental co-exposure to SeMet reduced but did not eliminate the increase in the MeHg-induced I(K) response, however, I(A) responses increased significantly over MeHg-treated fish to match control levels. Electrophysiological deficits parallel behavioral patterns in MeHg-treated fish, i.e., initial reactions to the rotating bar were followed by periods of inactivity and then a resumption of responses.
机译：甲基汞（MeHg）的发育暴露具有终生行为影响。许多微量营养素，包括硒，都参与了抗氧化应激的细胞防御，并可能降低MeHg引起的缺陷的严重程度。将斑马鱼胚胎（受精后<4 h，hpf）暴露于0.0-0.30 microM MeHg和/或硒代蛋氨酸（SeMet）的组合中，直到24 hpf，然后置于干净的培养基中。鱼在弱光条件下（约60 microW / m（2））作为成年鱼进行测试，以观察其对旋转的黑条的视觉响应。响应性降低证明了对MeHg暴露的剂量依赖性反应（ANOVA，P <0.001），而SeMet除了0.3 microM以外没有引起缺陷。 SeMet：MeHg的比例为1：1或1：3导致响应与对照组没有区别（ANOVA，P <0.001）。在任何MeHg浓度下，在视网膜或视神经顶盖均未观察到总体组织病理学（H＆E染色）。记录成年斑马鱼的完整视网膜中双极细胞的全细胞，电压门控，去极化引起的向外K（+）电流，并且在MeHg处理的鱼的双极细胞中向外K（+）电流幅度更大。这是由于表达延迟整流I（K）电流的细胞强烈反应所致。在MeHg处理的鱼中，表达瞬时I（A）电流的细胞显示出较小幅度较小趋势。对SeMet的发育性共同暴露减少但并未消除MeHg诱导的I（K）反应的增加，但是，与MeHg处理的鱼相比，I（A）反应显着增加，以达到对照水平。在用MeHg处理的鱼中，电生理缺陷与行为模式平行，即对旋转棒的初始反应之后是一段时间的不活动，然后恢复响应。

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