US EPA

7299192 

Journal Article 

Investigating the mechanism of vanadium toxicity in freshwater organisms 

Gillio Meina, E; Niyogi, S; Liber, K 

2020 

Yes 

Aquatic Toxicology
ISSN: 0166-445X
EISSN: 1879-1514 

229 

105648 

English 

33130451 

10.1016/j.aquatox.2020.105648 

WOS:000594707400005 

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.