Investigating the mechanism of vanadium toxicity in freshwater organisms.

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.

Multiple Linear Regression Modeling Predicts the Effects of Surface Water Chemistry on Acute Vanadium Toxicity to Model Freshwater Organisms.

Multiple linear regression (MLR) modeling has been successfully used to predict how water chemistry variables influence the toxicity of cationic metals to aquatic organisms, but no MLR model exists for vanadium (V). Recent research has indicated that an increase in pH (from 6 to 9), or high concentrations of sodium (473 mg Na+ /L), increase V toxicity to Daphnia pulex. In contrast, increases in alkalinity (>100 mg as CaCO3 ) and sulfate (>100 mg SO42- /L) reduce V toxicity. How these variables influence V toxicity to Oncorhynchus mykiss (rainbow trout) was still unknown. Our results show that increasing pH from 6.2 to 8.9 tended to decrease the 96-h median lethal concentration (LC50) for V toxicity to O. mykiss by 9.6 mg V/L. An alkalinity increase from 71 to 330 mg/L as CaCO3 tended to increase the 96-h LC50 by 3.3 mg V/L, whereas when SO42- rose from 150 to 250 mg/L, the LC50 significantly increased by 0.3 mg V/L followed by a significant decrease of 1 mg V/L when SO42- was >250 mg/L. Sodium (between 100 and 336 mg/L) showed no effect on V toxicity to O. mykiss. The toxicity patterns for O. mykiss were similar to those observed for D. pulex, except for that of SO42- , potentially indicating different mechanisms of V uptake or regulation in the 2 species. The LC50s and associated water chemistry were combined to develop an MLR model for O. mykiss and D. pulex. Alkalinity and pH modified V toxicity to both species, whereas SO42- influenced V toxicity to D. pulex. Overall, MLR models should be considered for creating new local benchmarks or water quality guidelines for V. Environ Toxicol Chem 2020;39:1737-1745. © 2020 SETAC.

Mummichog (Fundulus heteroclitus) are less sensitive to 17α-ethinylestradiol (EE2) than other common model teleosts: A comparative review of reproductive effects.

The environmental estrogen 17α-ethinylestradiol (EE2) will depress or completely inhibit egg production in many common model teleosts at low concentrations (≤0.5 ng/L; Runnalls et al., 2015). This inhibition is not seen in the estuarine killifish, or mummichog (Fundulus heteroclitus), even when exposed to 100 ng/L EE2. This relative insensitivity to EE2 exposure indicates species-specific mechanisms for compensating for exogenous estrogenic exposure. This review compares various reproductive responses elicited by EE2 in mummichog to other common model teleosts, such as zebrafish (Danio rerio) and fathead minnow (Pimephales promelas), identifying key endpoints where mummichog differ from other studied fish. For example, EE2 accumulates primarily in the liver/gall bladder of mummichog, which is different than zebrafish and fathead minnow in which accumulation is predominantly in the carcass. Despite causing species-specific differences in fecundity, EE2 has been shown to consistently induce hepatic vitellogenin in males and cause feminization/sex reversal during gonadal differentiation in larval mummichog, similar to other species. In addition, while gonadal steroidogenesis and plasma steroid levels respond to exogenous EE2, it is generally at higher concentrations than observed in other species. In mummichog, production of 17ß-estradiol (E2) by full grown ovarian follicles remains high; unlike other teleost models where E2 synthesis decreases as 17α,20ß-dihydroxy-4-prenen-3-on levels increase to induce oocyte maturation. New evidence in mummichog indicates some dissimilarity in gonadal steroidogenic gene expression responses compared to gene expression responses in zebrafish and fathead minnow exposed to EE2. The role of ovarian physiology continues to warrant investigation regarding the tolerance of mummichog to exogenous EE2 exposure. Here we present a comprehensive review, highlighting key biological differences in response to EE2 exposure between mummichog and other commonly used model teleosts.

Models for the acute and chronic aqueous toxicity of vanadium to Daphnia pulex under a range of surface water chemistry conditions.

Alberta's oil sands petroleum coke (PC) generation has in recent years surpassed 10 million tonnes. Petroleum coke has been proposed as an industrial-scale sorbent to reduce concentrations of organic chemicals in oil sands process-affected water (OSPW). However, PC contains up to 1000 mg of vanadium (V) per kg of PC, and during the treatment it leaches from coke reaching levels of up to 7 mg/L in "treated" OSPW. Little information is available on how common water quality variables affect the toxicity of V to aquatic organisms. Here descriptive relationships are presented to describe how site-specific surface water characteristics representative of the Alberta oil sands region influence the toxicity of V to Daphnia pulex. Results revealed that when D. pulex was exposed to an increase in pH, a threshold relationship was found where acute V toxicity increased from a lethal median concentration (LC50) of 1.7 to 1.2 mg V/L between pH 6 and 7 and then levelled off at around 1 mg V/L. When alkalinity (from 75 to 541 mg/L as CaCO3) and sulphate (from 54 to 394 mg/L) increased, the acute toxicity of V decreased slightly with LC50s changing from 0.6 to 1.6, and from 0.9 to 1.4, respectively. When the length of V exposure was extended (from 2 to 21 d), only an increase of sulphate from 135 to 480 mg/L caused a slight increase in V toxicity from a LC50 of 0.6 to 0.4 mg V/L, the opposite trend seen in the acute exposures. In addition, the influence of two OSPW representative mixtures of increasing sodium and sulphate, and increasing alkalinity and sulphate on V acute toxicity to D. pulex were evaluated; only the mixture of increasing sodium (from 18 to 536 mg/L) and sulphate (from 55 to 242 mg/L) caused a slight decrease in V acute toxicity (LC50 1.0-2.1 mg V/L). Evidence is presented that variations in surface water chemistry can affect V toxicity to daphnids, although only to a small degree (i.e. within a maximum factor of 2 in all cases evaluated here). These relationships should be considered when creating new water quality guidelines or local benchmarks for V.

Effects of 17α-ethinylestradiol (EE2) on reproductive endocrine status in mummichog (Fundulus heteroclitus) under differing salinity and temperature conditions.

Exposure to 17α-ethinylestradiol (EE2), a synthetic estrogen, has previously been shown to decrease reproductive endocrine status and egg production in northern mummichog (Fundulus heteroclitus macrolepidotus). The objective of this study was to evaluate if variations in salinity or temperature conditions of EE2-exposed mummichog modify the effect on whole organism reproductive endocrine status and gonadal steroidogenesis. Mummichog were exposed in vivo for 14 days to 0, 50 and 250 ng/L EE2 in 0, 16 and 32 ppt salinity at 18 °C and to 0 and 250 ng/L EE2 at 10, 18 and 26 °C at 16 ppt. There was a little overall effect of salinity on measured endpoints. In the salinity exposure, 250 ng/L EE2-exposed females had significantly reduced 17ß-estradiol (E2) levels. Increased temperature triggered gonadal growth in both sexes and increased plasma E2 and E2 production and decreased 11-KT (11-ketotestosterone) production. EE2 counteracted the effect of temperature by depressing gonadal growth in males. In both exposures, EE2 effects on testosterone (T) production were variable. The use of steroidogenic precursors (25-OH-cholesterol, and/or pregnenolone and/or testosterone) in the in vitro gonadal incubations indicated decreased E2 production in females and 11-KT production in males were predominately due to suppression of the terminal conversion step between T and E2 or 11-KT. Ovarian aromatase A (cyp19a) gene expression at 16 ppt and 18 °C was not affected by 250 ng/L EE2 (the only treatment combinations tested). Overall, temperature is a factor regulating northern mummichog reproduction; EE2 overrides its effects and disrupts the terminal step of steroidogenesis. Our results should be considered in designing future estuarine fish bioassays and in understanding effects of estrogenic endocrine disruptors in estuaries.