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氯化物对美洲鲟(Acipenser oxyrinchus oxyrinchus)亚硝酸盐诱导高铁血红蛋白血症的影响。

Effect of chloride on nitrite-induced methaemoglobinemia in Atlantic sturgeon, Acipenser oxyrinchus oxyrinchus (Mitchill).

机构信息

Cooperative Oxford Laboratory, Oxford, MD, USA.

出版信息

J Fish Dis. 2012 Dec;35(12):873-85. doi: 10.1111/j.1365-2761.2012.01418.x. Epub 2012 Sep 13.

Abstract

We evaluated the effects of chloride concentration on the clinical pathology in juvenile Atlantic sturgeon, Acipenser oxyrinchus oxyrinchus (Mitchill), following semi-static exposures to 1 mg L(-1) nitrite for 96 h. In spring water naturally low in chloride (5 mg L(-1)), plasma nitrite concentrated to more than 40× environmental levels resulting in a severe methaemoglobinemia characterized by torpid behaviour, 30-fold increase in methaemoglobin fraction, anaemia, leucopenia and hyperkalaemia. Loss of intracellular water and potassium to extracellular space may have resulted in hyperkalaemia and haemodilution. Fish survived nitrite exposure, but 60% of torpid fish died following capture and tissue sampling. Fish acclimated to 10-fold higher chloride content (55 mg L(-1)) did not concentrate nitrite in the plasma above environmental levels or develop methaemoglobinemia, but did exhibit similar haematology and plasma chemistry changes. Plasma nitrite returned to preexposure levels by 14 days following nitrite exposures, but severity of clinical pathology changes persisted or increased, suggesting that Atlantic sturgeon have reduced capacity to recover from methaemoglobinemia. Fish that survive methaemoglobinemia may be susceptible to mortality from the cumulative effects of intoxication, handling and other stresses for two or more weeks following nitrite remediation. Chloride buffering in aquaculture systems reduces the toxic effects of nitrite accumulation.

摘要

我们评估了氯离子浓度对幼龄大西洋鲟(Acipenser oxyrinchus oxyrinchus)(Mitchill)在半静态暴露于 1mg/L 亚硝酸盐 96 小时后的临床病理学的影响。在氯离子天然含量低的泉水(5mg/L)中,血浆中亚硝酸盐浓缩至 40 倍以上环境水平,导致严重的高铁血红蛋白血症,表现为行为迟钝、高铁血红蛋白比例增加 30 倍、贫血、白细胞减少和高钾血症。细胞内水和钾向细胞外空间的流失可能导致高钾血症和血液稀释。鱼能在亚硝酸盐暴露中存活,但 60%行为迟钝的鱼在捕获和组织采样后死亡。适应氯离子含量高 10 倍(55mg/L)的鱼不会将血浆中亚硝酸盐浓缩至环境水平以上或发生高铁血红蛋白血症,但确实表现出类似的血液学和血浆化学变化。亚硝酸盐暴露后 14 天,血浆中亚硝酸盐恢复到暴露前水平,但临床病理学变化的严重程度持续或增加,这表明大西洋鲟从高铁血红蛋白血症中恢复的能力降低。在亚硝酸盐修复后两周或更长时间内,幸存高铁血红蛋白血症的鱼可能容易因中毒、处理和其他压力的累积影响而死亡。水产养殖系统中的氯离子缓冲作用降低了亚硝酸盐积累的毒性影响。

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