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 (LC₅₀): 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.

如果存在高浓度的钒，可能会对来自艾伯塔省油砂地区的水生生物造成危险。一个工业试点项目已使用石油焦（PC）作为吸附剂，从油砂工艺影响的水（OSPW）中去除有机毒物，但也导致V从PC浸出到OSPW中，浓度高达7 mg V / L（已知对水生生物有毒的水平）。钒是一种具有几种氧化态的过渡金属，可能会通过离子不平衡或氧化应激而引起其毒性。本研究考察了V对大型蚤（Daphnia magna）和褐On （Oncorhynchus mykiss）的影响。Daphinds和O.虹鳟暴露到V的浓度达到它们各自的计算中值致死浓度（LC ₅₀）：3毫克V / L为D.蚤和7毫克V / L为O.虹鳟。对于这两种生物，评估了V对钠通量和全身钠的影响。还研究了其对g和肝脏水平下米氏曲霉体内钙和氧化应激反应的影响。结果表明，3.1毫克V / L为D.蚤和6.8毫克V / L为O.虹鳟引起在水蚤和虹鳟鱼既流入钠的整体增加。然而，V的浓度范围毫克0.2和4之间V / L为D.蚤和1.8和6mg V / L为O.虹鳟减少了O. mykiss体内的机体钠和体内的钙。高于3.6 mg V / L的浓度会导致虹鳟鱼的g和肝脏中明显的脂质过氧化，而1.9 mg V / L则使鱼G的GSH：GSSG比值显着降低，但在鱼ls中这些硫醇之间的比值没有变化。肝。浓度为6.62 mg V / L会大大增加肝脏中的过氧化氢酶活性，而not中则没有。V不会改变肝脏和g超氧化物歧化酶。总的来说，结果表明离子失衡和氧化应激均是D. magna和O. mykiss中V毒性机理的一部分，因此有必要进一步研究以充分阐明该机理水生生物的V毒性。