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研究钒对淡水生物毒性的作用机制。

Investigating the mechanism of vanadium toxicity in freshwater organisms.

机构信息

Toxicology Centre, University of Saskatchewan, 44 Campus Drive, Saskatoon, SK, S7N 5B3, Canada.

Toxicology Centre, University of Saskatchewan, 44 Campus Drive, Saskatoon, SK, S7N 5B3, Canada; Department of Biology, University of Saskatchewan, 112 Science Place, Saskatoon, SK, S7N 5E2, Canada.

出版信息

Aquat Toxicol. 2020 Dec;229:105648. doi: 10.1016/j.aquatox.2020.105648. Epub 2020 Sep 28.

Abstract

Vanadium (V) could present a risk for aquatic organisms from the Alberta oil sands region, if present in high concentrations. An industry pilot project has used petroleum coke (PC) as a sorbent to remove organic toxicants from oil sands process-affected water (OSPW), but it also caused V to leach from PC into the OSPW, reaching concentrations of up to 7 mg V/L (a level known to be toxic to aquatic organisms). Vanadium is a transition metal with several oxidation states, which could potentially elicit its toxicity through either ion imbalance or oxidative stress. This study investigated the effect of V on Daphnia magna and Oncorhynchus mykiss. Daphinds and O. mykiss were exposed to concentrations of V up to their respective calculated median lethal concentration (LC): 3 mg V/L for D. magna and 7 mg V/L for O. mykiss. For both organisms, the influence of V on sodium flux and whole body sodium was evaluated. Its effect on whole body calcium and the oxidative stress responses in O. mykiss at the gill and liver levels was also studied. Results suggested that 3.1 mg V/L for D. magna and 6.8 mg V/L for O. mykiss caused an overall increase in sodium influx in both the daphnids and rainbow trout. However, concentrations of V ranging between 0.2 and 4 mg V/L for D. magna and 1.8 and 6 mg V/L for O. mykiss reduced whole body sodium in both organisms and whole body calcium in O. mykiss. Concentrations above 3.6 mg V/L caused significant lipid peroxidation in the gills and liver of rainbow trout, while 1.9 mg V/L produced a substantial decrease in the fish gill GSH:GSSG ratio, but no change in the ratio between these thiols in the liver. Concentrations of 6.62 mg V/L sharply increased catalase activity in the liver but not in the gills. Neither liver nor gill superoxide dismutase was altered by V. Overall, results suggest that both ion imbalance and oxidative stress are part of the mechanism of toxicity of V in D. magna and O. mykiss and that further research is warranted to fully elucidate the mechanism(s) of V toxicity in aquatic organisms.

摘要

如果钒(V)在高浓度下存在,它可能会对艾伯塔省油砂地区的水生生物构成风险。一个工业试点项目已经使用石油焦(PC)作为吸附剂,从油砂加工影响水(OSPW)中去除有机有毒物质,但它也导致 V 从 PC 浸出到 OSPW 中,浓度高达 7mgV/L(已知对水生生物有毒)。钒是一种具有多种氧化态的过渡金属,它可能通过离子失衡或氧化应激引发其毒性。本研究调查了 V 对大型溞和虹鳟鱼的影响。Daphinds 和 O. mykiss 暴露于高达各自计算得出的半数致死浓度(LC)的 V 浓度:3mgV/L 用于 D. magna,7mgV/L 用于 O. mykiss。对于这两种生物,评估了 V 对钠离子通量和全身钠离子的影响。还研究了 V 对 O. mykiss 鳃和肝脏水平的全身钙和氧化应激反应的影响。结果表明,对于 D. magna 为 3.1mgV/L,对于 O. mykiss 为 6.8mgV/L,导致两种生物的钠离子内流总体增加。然而,对于 D. magna,V 的浓度在 0.2 至 4mgV/L 之间,对于 O. mykiss,在 1.8 至 6mgV/L 之间,导致两种生物的全身钠离子减少,O. mykiss 的全身钙减少。浓度高于 3.6mgV/L 会导致虹鳟鱼鳃和肝脏的脂质过氧化显著增加,而 1.9mgV/L 会使鱼鳃 GSH:GSSG 比值大幅下降,但肝脏中这些硫醇的比值没有变化。6.62mgV/L 的浓度急剧增加了肝脏中的过氧化氢酶活性,但没有增加鳃中的过氧化氢酶活性。V 既没有改变肝脏也没有改变鳃的超氧化物歧化酶。总体而言,结果表明,离子失衡和氧化应激都是 V 对大型溞和虹鳟鱼毒性的机制的一部分,需要进一步研究以充分阐明 V 对水生生物毒性的机制。

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