Abstract  The acute toxicities of arsenate, arsenite, cadmium, chromate, copper, mercury, silver, vanadium, and zinc were determined, individually and in two environmentally relevant mixtures, to two life stages of chinook salmon in reconstituted fresh and brackish waters that stimulated potential conditions in the San Joaquin Valley, California. The relative individual toxicities of the elements varied over four orders of magnitude; from most toxic to least toxic, the rank order was cadmium greater than copper greater than mercury greater than zinc greater than vanadium greater than arsenite greater than arsenate greater than chromate (no definitive tests for silver). In general, young fish tested in fresh water were more sensitive to the individual elements and the two mixtures than were advanced fry tested in brackish water. A 13-element mixture simulating concentrations in the San Luis Drain had the same toxicity to fish as the same mixture plus selenate and selenite, thus demonstrating that the presence of selenium at its environmental ratio in the mixture contributed no toxicity in short-term tests. As judged by a comparison of the individual acute values for salmon to the expected environmental concentrations in the San Luis Drain, the margins of uncertainty for cadmium and copper in both waters, zinc in fresh water, and mercury in brackish water were less than 100, whereas for the two environmental mixtures the margins were less than 15 in both test waters. These low margins of uncertainty, especially for the mixtures, indicate a high potential for environmental hazard to chinook salmon in the reconstituted waters tested.

Abstract  Vanadium is widely distributed, occurring in many types of minerals, coal, and petroleum. Anthropogenic sources of vanadium originate from the production, processing, and wastes of these materials. The aquatic toxicity of vanadium to fish species is not well characterized. This study focused on the three-spined stickleback, Gasterosteus aculeatus, a small and widely distributed euryhaline species of fish. The three-spined stickleback is used as an effluent-monitoring species in both Canada and the United States. Five 96-h static renewal acute toxicity tests were performed in moderately hard water with adult fish. The geometric mean and range of the five 96-h LC(50)s based on measured concentrations of total vanadium in the test solution were 3.17 and 2.35-4.07 mg V/L, respectively. A conservative estimation of a safe concentration of vanadium that would not affect survival of adult three-spined sticklebacks over a 96-h exposure period in moderately hard water is approximately 0.30 mg V/L. A comparison with other fish species previously tested suggests that the three-spined stickleback is intermediate in sensitivity to vanadium. Information reported from this study may be useful in effluent toxicity identification evaluations and ecological risk assessments related to vanadium.

Abstract  Vanadium is a metal whose toxicity towards terrestrial and aquatic species has been under-reported to date.. The biochemical responses of vanadium in amphibian species have not been determined. To establish the effects of vanadium (V) on exposed adult Xenopus laevis, acute and chronic exposures were conducted, and biomarker analyses were performed on liver and muscle tissues from exposed frogs. Biomarkers of exposure, such as acetylcholinesterase (AChE) and metallothioneins (MT), were analysed. Biomarkers of effect were also analysed to determine possible increases in reactive oxygen species (ROS), and the effect of the exposure on the energy balance in the organisms. These included superoxide dismutase (SOD), catalase (CAT), reduced glutathione (GSH), protein carbonyls (PC), malondialdehyde (MDA), and cellular energy allocation (CEA) (energy available, energy consumption, lipids, proteins and glucose). In acute exposures, the energy balances in organisms were distinctly affected, possibly due to insulin mimetic properties of V. In chronic exposures, MT, AChE, SOD, CAT and GSH responses were more pronounced. Although AChE is generally inhibited by pollutant exposure, in this study, it was stimulated. There were significant inhibitions of SOD and CAT, previously observed in frog species. PC levels increased in the highest acute exposure concentration, indicating protein damage. The IBR.v2 revealed the biochemical responses of V more effectively than traditional statistical analysis.

Abstract  Vanadium accumulation levels in different tissues (muscle and organs) of the striped mullet Mugil cephalus (Linnaeus, 1758) and possible relationships with blood parameters were evaluated in a Natural Protected Area (Lake Faro, Sicily, Italy), during the winter of 2017. Hematological parameters (red blood cell, RBC; white blood cell, WBC; hemoglobin concentration, Hb; hematocrit, Hct; mean corpuscular volume, MCV; mean corpuscular hemoglobin, MCH; mean corpuscular hemoglobin concentration, MCHC; thrombocytes, TC), biometric indices (weight, total and fork length), and vanadium levels in muscles and organs (gills, liver, stomach and intestine) were determined. Statistical analyses showed significant differences in concentrations of vanadium of the analyzed tissue of M. cephalus and a positive relationship between vanadium concentration in the liver and some hematological parameters (RBC, Hb and Hct) and biometric indices. Our results underline the importance of fish blood parameters as sensitive indicators of toxic impact of environmental factors such as metals. This study, focusing on an ongoing topic, represents a valuable contribution to research concerning the monitoring and prevention of vanadium pollution in aquatic organisms and environments.

Abstract  This study assessed the effect of dietary vanadium (V) and vitamin C (VC) on production performance, egg quality and antioxidant status in laying hens. A total of 360 laying hens (31-week-old) were randomly allotted into a 3 × 3 factorial arrangement treatments (four replicates and 10 chicks per replicate) with three levels of dietary V (0, 5 and 10 mg/kg) and three levels of vitamin C (0, 50 and 100 mg/kg) for 12 weeks. The effect of V and VC did not alter egg production, egg weight, average daily feed intake and feed conversion ratio during 1-12 week. Albumen height and Haugh unit value were linearly decreased (p < 0.001) by addition of V, whereas the effect of 100 mg/kg VC was observed to counteract (p < 0.05) this effect in V-containing treatments during 1-12 week. Hens fed V-containing diet laid lighter (linear effect, p < 0.05) coloured eggs (higher lightness value, lower redness and yellowness value), and the VC exerted no influence on it during 1-12 week. The serum superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GSH-Px) activities, ability to inhibit hydroxyl radical, were significantly decreased, and the malondialdehyde (MDA) and V contents were increased (p < 0.05) by effect of V during 4, 8 and 12 week. The effect of VC alone and the interactive effect between VC and V were shown to increase serum (p < 0.05) SOD activity in 4 week and decrease MAD levels in 12 week. The result indicate that V decreased the egg quality and caused the oxidative stress at level of 5 mg/kg and 10 mg/kg, and the addition of 100 mg/kg vitamin C can alleviate its egg quality reduction effect and can mitigate the oxidative stress to some extent.

Abstract  Diets containing 40% glucose or starch with either 2 ppm chromium (Cr), 2 ppm vanadium (V) or without either supplement were fed to tilapia, Oreochromis niloticus×O. aureus, to investigate the effect of Cr and V on carbohydrate utilization. Each diet was fed to three aquaria with 18 fish/aquarium in a recirculating, filtered rearing system for 8 weeks. Results indicated that weight gain, protein and energy deposition were significantly (P<0.05) higher in fish fed the starch diet than in those fed the glucose diet. Chromium supplementation significantly increased the weight gain, energy deposition and liver glycogen content in fish fed the glucose diet. Delayed plasma glucose plateau and significantly higher body lipid content were observed in fish fed the glucose diet with Cr than in those without the Cr supplementation.

Abstract  Recent studies have shown that vanadium, along with other less well known trace metals, is being introduced into the marine environment in quantities sufficient to allow for a significant bioaccumulation of the metal in the bodies of shellfish (PESCH et al. 1977). In addition, significant amounts are also entering freshwater and estuarine systems (DREHER 1977, JAFFE and WALTERS 1977). JERNELOV (1974), in discussing our present understanding of the environmental implications of anthropogenic inputs of vanadium to marine systems, stated "The extent of man's impact on vanadium concentrations in marine organisms is unknown and so are the biological and ecological effects of vanadium contamination" (p. 812). This same statement holds equally well for frshwater and estuarine systems. Aside from the early, now outdated, work of PROESCHER et al (1917), the only other study of vanadium toxicity in fishes was conducted by TARZWELL and HENDERSON (1960). This study was found to be of limited use in evaluating the toxicity of this element owing to the stated "exploratory" nature of the majority of the results presented. Therefore, as a first consideration in the assessment of the aquatic toxicology of vanadium, a comparative study was undertaken to determine the acute toxicity of four vanadium compounds to two species of frwshwater fishes. The following is a brief report on the principal results of this study.

Abstract  This study evaluated the effect of epigallocatechin-3-gallate (EGCG) alleviating the reduction of antioxidant capacity induced by dietary vanadium (V) in the liver, kidney, and ovary of laying hens. Furthermore, Kelch-like ECH-associated protein 1(Keap1)-nuclear factor erythroid 2-related factor 2 (Nrf2)-small Maf proteins (sMaf) pathway was explored to reveal the molecular mechanism. A total of 768 40-week-old Hyline-Brown laying hens were randomly allocated to 4 groups with 8 pens per group and 24 hens per pen. The experimental groups were as follows: control (basal diet); V15, control + 15 mg/kg V; EGCG150, control + 150 mg/kg EGCG; V15 + EGCG150, V15 + 150 mg/kg EGCG. Our results revealed that dietary EGCG supplementation completely alleviated the V-induced reductions of hen-day egg production, average egg weight, Haugh unit, albumen height, eggshell strength, and eggshell thickness. Dietary EGCG supplementation completely prevented the V-induced reductions of serum follicle-stimulating hormone and luteinizing hormone levels. Besides, dietary EGCG supplementation reversed the V-induced increments of alanine aminotransferase (ALT), aspartate aminotransferase (AST), blood urea nitrogen (BUN), creatinine (Cr), and uric acid (UA). In addition, dietary EGCG supplementation partially alleviated the V-induced reductions of the enzyme activities and gene expressions of superoxidative dismutase (SOD), catalase (CAT), glutathione reductase (GR), and glutathione peroxidase (GSH-Px). Furthermore, dietary EGCG supplementation partially alleviated the V-induced reductions of Nrf2 and sMaf gene expressions, and the increments of Keap1 gene expression. In summary, EGCG partially alleviated V-induced reduction of antioxidant capacity through Keap1-Nrf2-sMaf pathway in the liver, kidney, and ovary of laying hens.

Abstract  Vanadium toxicology is a topic of considerable importance as this metal is widely used in industrial and biomedical fields. However, it represents a potential emerging environmental pollutant because wastewater treatment plants do not adequately remove metal compounds that are subsequently released into the environment. Vanadium applications are limited due to its toxicity, so it is urgent to define this aspect. This metal is associated with sea urchin embryo toxicity as it perturbs embryogenesis and skeletogenesis, triggering several stress responses. Here we investigated its bioaccumulation and the correlation with cellular and molecular developmental pathways. We used cytotoxic concentrations of 1 mM and 500 μM to perform quantitative analyses, showing that vanadium accumulation interferes with calcium uptake during sea urchin development and provokes a disruption in the biomineralization process. At the end of the whole treatment, the accumulation of vanadium was about 14 and 8 μg for embryos treated respectively with 1 mM and 500 μM, showing a dose-dependent response. Then, we monitored the cell signaling perturbation, analyzing key molecular markers of cell survival/cell death mechanisms and the DNA fragmentation associated with apoptosis. This paper clarifies vanadium's trend to accumulate directly into embryonic cells, interfering with calcium uptake. In addition, our results indicate that vanadium can modulate the ERK pathway and activate a cell-selective apoptosis. These results endorse the sea urchin embryo as an adequate experimental model to study metal-related cellular/molecular responses.

Abstract  Larval flannelmouth sucker (Catostomus latipinnis) were exposed to arsenate, boron, copper, molybdenum, selenate, selenite, uranium, vanadium, and zinc singly, and to five mixtures of five to nine inorganics. The exposures were conducted in reconstituted water representative of the San Juan River near Shiprock, New Mexico. The mixtures simulated environmental ratios reported for sites along the San Juan River (San Juan River backwater, Fruitland marsh, Hogback East Drain, Mancos River, and McElmo Creek). The rank order of the individual inorganics, from most to least toxic, was: copper > zinc > vanadium > selenite > selenate > arsenate > uranium > boron > molybdenum. All five mixtures exhibited additive toxicity to flannelmouth sucker. In a limited number of tests, 44-day-old and 13-day-old larvae exhibited no difference in sensitivity to three mixtures. Copper was the major toxic component in four mixtures (San Juan backwater, Hogback East Drain, Mancos River, and McElmo Creek), whereas zinc was the major toxic component in the Fruitland marsh mixture, which did not contain copper. The Hogback East Drain was the most toxic mixture tested. Comparison of 96-h LC50 values with reported environmental water concentrations from the San Juan River revealed low hazard ratios for arsenic, boron, molybdenum, selenate, selenite, uranium, and vanadium, moderate hazard ratios for zinc and the Fruitland marsh mixture, and high hazard ratios for copper at three sites and four environmental mixtures representing a San Juan backwater, Hogback East Drain, Mancos River, and McElmo Creek. The high hazard ratios suggest that inorganic contaminants could adversely affect larval flannelmouth sucker in the San Juan River at four sites receiving elevated inorganics.

Abstract  The cecal tonsil of broiler is known as a secondary lymphoid tissue, which is involved in antigen-specific humoral immune responses. The purpose of this study was to investigate the effects of dietary vanadium on the tissue distribution and quantity of immunoglobulin A-positive (IgA(+)) cell in the cecal tonsil by immunohistochemistry. Simultaneously, the changes in interleukin-6 (IL-6), interleukin-10 (IL-10), interferon gamma (IFN-γ) and tumor necrosis factor-alpha (TNF-α) contents in the cecal tonsil were also quantified by enzyme-linked immunosorbent assay (ELISA). A total of 420 one-day-old avian broilers were divided into six groups and fed on a corn-soybean basal diet (control diet) or the same diet supplemented respectively with 5, 15, 30, 45, and 60 mg/kg of vanadium in the form of ammonium metavanadate for 42 days. The results showed that the population of the IgA(+) cells in the cecal tonsil were significantly lower (p < 0.05 or p < 0.01) in the 45 and 60 mg/kg groups than that in the control group. Meanwhile, IL-10, IFN-γ and TNF-α contents in the cecal tonsil were significantly decreased (p < 0.05 or p < 0.01) in the 30, 45 and 60 mg/kg groups in comparison with those of the control group. However, IL-6 content in the cecal tonsil was only decreased (p < 0.05 or p < 0.01) in 60 mg/kg at 14 and 28 days of age. In conclusion, dietary vanadium in excess of 30 mg/kg reduced the numbers of the IgA(+) cells and changed the contents of the abovementioned cytokines in the cecal tonsil, which may finally impact the function of local mucosal humoral immunity in broilers.

Abstract  Dimethyl sulfoxide (DMSO) is produced in nature and is known to be a source of carbon and sulfur for marine microorganisms. It is currently used in many biological experiments, pharmaceutical preparations, and energy-producing systems such as lithium batteries. Therefore, the toxicity of DMSO has been studied because of its various implications to living organisms; however, such studies are largely limited to measuring individual toxicity whereas the combined toxicity of DMSO with other compounds has rarely been investigated. In the present study, the combined acute toxicity of 0.1% and 0.5% DMSO with vanadium was investigated in zebrafish embryos; the LC50 values of these combinations were 62.0 and 6.38 ppm, respectively. In individual toxicity tests, neither DMSO nor vanadium caused such mortality levels. Therefore, both 0.1% and 0.5% DMSO had a synergistic effect with vanadium, and this result was confirmed using an independent action model. This combined toxicity delayed the development of zebrafish embryos and caused pericardial edema. The synergistic effect of DMSO and vanadium was found to be related to reduced pH and inhibition of cytochrome c oxidase activity. Given its potential synergistic toxicity to aquatic organisms, the introduction of DMSO into the environment should be investigated and routinely monitored.

Abstract  The contribution of decameric vanadate species to vanadate toxic effects in cardiac muscle was studied following an intravenous administration of a decavanadate solution (1mM total vanadium) in Sparus aurata. Although decameric vanadate is unstable in the assay medium, it decomposes with a half-life time of 16 allowing studying its effects not only in vitro but also in vivo. After 1, 6 and 12h upon decavanadate administration the increase of vanadium in blood plasma, red blood cells and in cardiac mitochondria and cytosol is not affected in comparison to the administration of a metavanadate solution containing labile oxovanadates. Cardiac tissue lipid peroxidation increases up to 20%, 1, 6 and 12h after metavanadate administration, whilst for decavanadate no effects were observed except 1h after treatment (+20%). Metavanadate administration clearly differs from decavanadate by enhancing, 12h after exposure, mitochondrial superoxide dismutase (SOD) activity (+115%) and not affecting catalase (CAT) activity whereas decavanadate increases SOD activity by 20% and decreases (-55%) mitochondrial CAT activity. At early times of exposure, 1 and 6h, the only effect observed upon decavanadate administration was the increase by 20% of SOD activity. In conclusion, decavanadate has a different response pattern of lipid peroxidation and oxidative stress markers, in spite of the same vanadium distribution in cardiac cells observed after decavanadate and metavanadate administration. It is suggested that once formed decameric vanadate species has a different reactivity than vanadate, thus, pointing out that the differential contribution of vanadium oligomers should be taken into account to rationalize in vivo vanadate toxicity.

Abstract  The purpose of this 42-day study was to investigate the apoptosis in the bursa of Fabricius induced by different levels of dietary vanadium. A total of 420 1-day-old avian broilers were divided into 6 groups in which there were 7 replicates in each group and 10 broilers in each replicate and fed on a corn-soybean basal diet as control diet (vanadium 0.073 mg/kg) or the same diet amended to contain 5, 15, 30, 45, and 60 mg/kg vanadium supplied as ammonium metavanadate (NH(4)VO(3)). Ultrastructurally, mitochondrial injury and increased numbers of apoptotic cells with condensed nuclei were observed in the 30, 45, and 60 mg/kg groups. As measured by flow cytometry, the percentages of apoptotic lymphocytes were significantly increased in the 15-, 30-, 45-, and 60-mg/kg groups when compared with those of control group. Meanwhile, the terminal deoxynucleotidyl transferase 2'-deoxyuridine 5'-triphosphate nick end-labeling assay showed that there were increased numbers of apoptotic cells in the 30-, 45-, and 60-mg/kg groups. Immunohistochemical tests showed increased numbers of positive cells under Bax and caspase-3 protein detection and decreased Bcl-2 protein in the 15-, 30-, 45-, and 60-mg/kg groups. The vanadium content of the bursa was found to be significantly increased in the 30-, 45-, and 60-mg/kg groups. These results suggested that dietary vanadium in excess of 15 mg/kg could cause lymphocyte apoptosis in the bursa of Fabricius and impact humoral immunity in broilers. Lymphocyte apoptosis in the bursa induced by high levels of dietary vanadium is associated with mitochondrial injury and changes in levels of apoptogenic proteins, such as Bcl-2, Bax, and caspase-3.

Abstract  The purpose of this 42-day study was to investigate the effects of dietary excess vanadium on intestinal immune function by histopathological observation of cecal tonsil and changes of the cecal tonsil T cell subsets by method of flow cytometry. Four hundred twenty 1-day-old avian broilers were divided into six groups and fed on a corn-soybean basal diet as control diet or the same diet amended to contain 5, 15, 30, 45, and 60 mg/kg vanadium supplied as ammonium metavanadate. In comparison with those of control group, lymphocytes in the lymphatic nodule of cecal tonsil were apparently decreased in 45 and 60 mg/kg groups. The percentage of CD(3)(+) T cells was decreased (p < 0.05) in 45 mg/kg group at 28 and 42 days of age and significantly decreased (p < 0.01) in 60 mg/kg group at 28 and 42 days of age. The percentages of CD(3)(+)CD(4)(+) and CD(3)(+)CD(8)(+) T cells were markedly decreased (p < 0.05 or p < 0.01) in 60 mg/kg group from 14 to 28 days of age and were decreased (p < 0.05) in 45 mg/kg group at 28 and 42 days of age. However, changes of the CD(4)(+)/CD(8)(+) ratio were not significant. Meanwhile, the cecal tonsil interleukin-2 (IL-2) contents were decreased (p < 0.05 or p < 0.01) in 45 and 60 mg/kg groups from 14 to 42 days of age. It was concluded that dietary vanadium in excess of 30 mg/kg reduced the percentages of cecal tonsil T cells subsets and IL-2 contents, and caused cecal tonsil lesions, which impaired cecal tonsil function and impacted the local mucosal immune function of the intestines in broilers.

Abstract  The purpose of this 42-day study was to investigate the effects of dietary excess vanadium on immune function by determining changes of the subsets and proliferation function of splenic T cells. Four hundred twenty 1-day-old avian broilers were divided into six groups and fed on a corn-soybean basal diet as control diet or the same diet amended to contain 5, 15, 30, 45, and 60 ppm of vanadium supplied as ammonium metavanadate. When compared with those of the control group, the percentage of CD3+, CD3+CD4+, and CD3+CD8+ of splenic T cells were decreased in the 45 and 60 ppm groups; however, the percentage of CD3+ and CD3+CD4+ were increased in the 5 ppm group, and the CD4+/CD8+ ratios were raised in the 5 and 15 ppm groups at 14 days of age. Meanwhile, the proliferation of splenic T cells were depressed in the 45 and 60 ppm groups but raised in the 5 and 15 ppm groups. Also, the serum interleukin-2 (IL-2) and interleukin-6 (IL-6) contents were decreased in the 45 and 60 ppm groups and increased in the 5 ppm group. It was concluded that dietary vanadium in excess of 30 ppm changed the percentages of splenic T cell subsets and inhibited the proliferation of splenic T cells and reduced the serum IL-2 and IL-6 contents. The cellular immune function was finally impaired in broilers.

Abstract  Vanadium (V) is a trace element which can induce dysfunction of gastro-intestine and egg quality deterioration of laying hens. This study was conducted to determine the effect of tea polyphenols (TP) on intestinal morphology, microflora, and short-chain fatty acid (SCFA) profile of laying hens fed vanadium containing diets. A total of 120 Lohman laying hens (67-week-old) were randomly divided into 4 groups with 6 replicates and 5 birds each for a 35-day feeding trial. The dietary treatments were as follows: (1) control (CON), fed a basal diet; (2) vanadium treatment (V10), CON +10 mg V/kg; (3) TP treatment 1 (TP1): V10 + 600 mg TP/kg; (4) TP treatment 2 (TP2): V10 + 1000 mg TP/kg. Fed 10 mg V/kg diets to laying hens did not affect the cecum flora diversity index (H), degree of homogeneity (EH), and richness (S), but hens fed TP2 diet decreased the H, EH, and S (P < 0.05). The cecum butyrate acid concentration was lower in V10 treatment and higher in TP2 treatment (P < 0.05). Addition of 10 mg/kg V resulted in an increased (P < 0.01) duodenal cell apoptosis rate, and 1000 mg/kg TP supplementation overcame (P < 0.01) this reduction effect induced by vanadium. The results indicated that supplementation of 10 mg/kg vanadium increased duodenal cell apoptosis and reduced cecum butyrate acid content. Addition of 1000 mg/kg TP increased the SCFA production to affect cecum flora ecology and protected the duodenal cell from excess apoptosis caused by vanadium.

Abstract  Seven-day LC50s of vanadium pentoxide for 2.5-g trout showed only a small range, from 1.9 to 6.0 mg V I−1, in tests at all 12 combinations of 30, 100 and 355 mg 1−2 total hardness with pH 5.5, 6.6, 7.7 and 8.8. Toxicity decreased from low to high hardness by an average factor of 1.8, probably because of regulated vanadium intake at the gill membranes. Hardness did not exert a major effect, probably because vanadium is present in water as various anions and does not complex with carbonates and bicarbonates as do most metals which behave as cations. Toxicity was greatest at pH 7.7, and the predominating ion H2VO−4 was apparently the most toxic one. HVO2−4 which prevailed at high pH, was calculated to be 60% as toxic as H2VO−4. Toxicity decreased at pH 6.6 and 5.5, probably because much of the metal was then present as decavanadates, which were found to be half as toxic as H2VO−4 on the basis of vanadium content. Small fish were more resistant to vanadium than larger ones, at least up to 12 g wet wt. However cumulative mortality continued to increase until 2 weeks of exposure, and incipient lethal levels were probably much the same for fish of different size, at about 60–70% of the 7-d LC50s stated in the paper. The toxicity of vanadium is similar to that of zinc except that it does not show a major change with water hardness.

Abstract  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.