Abstract  This study assessed the developmental toxicities of water-soluble carbon black wastes (CBW) extract (1:5, w/v) in zebrafish embryos (Danio rerio). Acute embryonic toxicity was performed following OECD guideline 236. Analysis using ICP-OES revealed that nickel (Ni) and vanadium (V) were predominant in CBW. Embryos exposed to CBW exhibited developmental delay, along with pericardial and yolk sac edemas. Malformed heart chambers were found in the CBW-exposed embryos and heart rates were significantly reduced since 48 h post fertilization (hpf). After RT-qPCR analysis, two cardiac forming-related genes, amhc and nppa responsible for atrial cardiac myofibril assembly and cardiac muscle cell proliferation, were up-regulated after 96 hpf. The increased mortality and delayed yolk-sac development appeared related to CBW-induced decrease in pH to about 5.5. Individual treatments of Ni and V did not cause identical toxic effects as CBW showed. At 100 ppm, V had a pH of approximately 5.5, causing developmental delay and pericardial edema in zebrafish embryos. At the same pH, combined Ni and V induced morphological anomalies and reduced heart rates similar to CBW-exposed embryos. Conclusively, this study demonstrates that environmental runoff is a serious concern, and thus, CBW incineration bottom ash should be treated carefully before disposal in landfills.

Abstract  Engineered nanoparticles (NPs) are emerging contaminants of concern and it is important to understand their environmental behavior and ecological risks to exposed organisms. Despite their ubiquitous presence in the environment, there is little information about the hazards of certain NPs, such as boron (BNPs) and vanadium (VNPs). The aim of the present research was to investigate the effects of commercial BNPs and VNPs (80 to 100 nm) to zebrafish embryos, at different levels of biological organization. A range of nominal concentrations for both NPs (0, 0.01, 0.1, 1, and 10 mg/L) was tested. Due to the presence of triton X-100 in the NPs' stock dispersions, an additional control group was included (0.001% triton X-100). Survival, hatching, and malformations of embryos were assessed for 96 hours (h) exposure. Locomotor behavior was evaluated at 120 h. Furthermore, embryos were exposed to 0, 1, and 10 mg/L of NPs to evaluate a set of biomarker responses after 96 h: cholinesterase (ChE) and glutathione S-transferase (GST) activities, total glutathione (TG) and energy budgets levels. VNPs induced malformations (10 mg/L), hyperactivity (10 mg/L), erratic swimming (0.01 mg/L), altered swimming pattern (>0.01 mg/L), delayed hatching (10 mg/L) and altered biochemical responses involved in antioxidant defense (GST and TG at >1 mg/L), neurotransmission (ChE at 10 mg/L) and energy metabolism (lipids at >1 mg/L and carbohydrates at 10 mg/L). BNPs caused malformations (10 mg/L), affected swimming pattern (>0.01 mg/L), induced erratic swimming (10 mg/L) and decreased TG content and GST activity (>1 mg/L). At the same concentrations, VNPs affected a greater number of endpoints than BNPs, demonstrating a greater toxicity to zebrafish embryos. The present study shows that BNPs and VNPs may affect aquatic organisms, albeit at relatively great non-environmentally relevant concentrations, reinforcing the importance of the risk assessment of different NPs.

Abstract  Vanadium (V) is an ultra-trace element presenting in humans and animals, but excessive V can cause toxic effects. Mitochondrial quality control (MQC) is an essential process for maintaining mitochondrial functions, but the relationship between V toxicity and MQC is unclear. To investigate the effects of excessive V on oxidative stress and MQC in duck hearts, 72 ducks were randomly divided into two groups, including the control group and the V group (30 mg of V/kg dry matter). The cardiac tissues were collected for the histomorphology observation and oxidative stress status evaluation at 22 and 44 days. In addition, the mRNA and protein levels of MQC-related factors were also analyzed. The results showed that excessive V could trigger vacuolar degeneration, granular degeneration, as well as mitochondrial vacuolization and swelling in myocardial cells. In addition, CAT activity was elevated in two time points, while T-SOD activity was increased in 22 days but decreased in 44 days after V treatment. Meanwhile, excessive V intake could also increase the number of Drp1 puncta, the mRNA levels of mitochondrial fission-related factors (Drp1and MFF), and protein (MFF) level, but decrease the number of Parkin puncta and the mitochondrial biogenesis (PGC-1α, NRF-1, and TFAM), mitochondrial fusion (OPA1, Mfn1, and Mfn2), and mitophagy (Parkin, PINK1, P62, and LC3B) related mRNA levels and protein (PGC-1α, Mfn1, Mfn2, PINK1) levels. Collectively, our results suggested that excessive V could induce oxidative stress and MQC disorder in the heart of ducks.

Abstract  OBJECTIVES: The toxic and teratogenic effects of salen (C16H16N2O2) and salen vanadium oxide (VOS) (C16H14N2O3V) were evaluated against chicken embryos along with chicken hepatic and fibroblastic cells in vitro cultures.

METHODS: Salen and VOS complexes were injected in the following concentrations: 5, 10, 20, 40, 80, 160, and 300 μM/egg for salen and 7.5, 15, 75, 120, 150, 240, and 300 μM/egg for VOS. In order to screen for skeletal malformations, the alizarin red clearing and staining method was employed. For studying the cytotoxic effects of these compounds, hepatic and fibroblastic cells were cultured and treated.

RESULTS: Our results show that injecting salen with various concentrations leads to a significant increase in embryonic mortality. Skeletal and morphological malformations resulting from salen injections included ectopic viscera and club foot. Our results show that embryonic mortality increased relative to the control group. In addition, alizarin red staining showed skeletal malformations like deletion of caudal vertebrae.

DISCUSSION: Our comparison showed that salen was a stronger teratogen than VOS, which may be due roles of the vanadium element, whose derivatives show physiological particulars and at low concentrations plays anticancer specifications without toxic effect.

CONCLUSION: Results show that chicken embryos were sensitive to the toxicity of salen and VOS, and these compounds can affect the growth and ossification of the chicken embryos. Moreover, the cytotoxicity of salen and VOS shows that the viability of both salen and VOS-treated cells significantly decreased in a dose-dependent manner.

Abstract  Searching for prospective vanadium-based agents against Trypanosoma cruzi, the parasite causing Chagas disease, four new [VVO(8HQ-H)(L-2H)] compounds, where 8HQ is 8-hydroxyquinoline and L are tridentate salicylaldehyde semicarbazone derivatives L1-L4, were synthesized and characterized in the solid state and in solution. The compounds were evaluated on T. cruzi epimastigotes (CL Brener) as well as on VERO cells, as mammalian cell model. Compounds showed activity against T. cruzi (IC50 6.2-10.5 μM) of the same order than Nifurtimox and 8HQ, and a four- to sevenfold activity increase with respect to the free semicarbazones. For comparison, [VVO2(L-H)] series was prepared and the new [VVO2(L3-H)] was fully characterized. They showed negligible activity and low selectivity towards the parasite. The inclusion of 8HQ as ligand in [VVO(8HQ-H)(L-2H)] compounds led to good activities and increased selectivity towards the parasite with respect to 8HQ. 51V NMR experiments, performed to get insight into the nature of the active species, suggested partial decomposition of the compounds in solution to [VVO2(L-H)] and 8HQ. Depending on the dose, the compounds act as trypanocide or trypanostatic. A high uptake of vanadium in the parasites (58.51-88.9% depending on dose) and a preferential accumulation in the soluble protein fraction of the parasite was determined. Treated parasites do not seem to show a late apoptotic/necrotic phenotype suggesting a different cell death mechanism. In vivo toxicity study on zebrafish model showed no toxicity up to a 25 µM concentration of [VVO(8HQ-H)(L1-2H)]. These compounds could be considered prospective anti-T. cruzi agents that deserve further research.

Abstract  The purpose of this study was to investigate the renal and hepatic oxidative damage and toxicity caused by dietary high vanadium in broilers. A total of 420 one-day-old avian broilers were divided into six groups and fed on a corn-soybean basal diet as control diet (vanadium 0.073 mg/kg), and five high vanadium diets (vanadium 5 mg/kg, high vanadium group I; 15 mg/kg, high vanadium group II; 30 mg/kg, high vanadium group III; 45 mg/kg, high vanadium group IV; and 60 mg/kg, high vanadium group V) throughout the experimental period of 42 days. The results showed that the renal and hepatic superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) activities, ability to inhibit hydroxy radical, and malondialdehyde (MDA), glutathione, and vanadium contents were not significantly changed in high vanadium group I and II when compared with those of the control groups. However, the SOD and GSH-Px activities, ability to inhibit hydroxy radical, and GSH content were significantly decreased, and the MDA and vanadium contents were markedly increased in high vanadium groups III, IV, and V. At the same time, the lesions were also observed in the kidney and liver of high vanadium groups III, IV, and V. The renal tubular epithelial cells showed granular degeneration and vacuolar degeneration, and hepatocytes showed granular degeneration, vacuolar degeneration, and fatty degeneration. It was concluded that dietary vanadium in the range of 30-60 mg/kg could cause oxidative damage and vanadium accumulation, which induced renal and hepatic toxicity and lesions. The renal and hepatic function was finally impaired in boilers.

Abstract  The purpose of this 42-day study was to investigate the effects of dietary excess vanadium on spleen growth and lesions by determining morphological changes and cell cycle of spleen. 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, 60 ppm of vanadium supplied as ammonium metavanadate. When compared with that of control group, the relative weight of spleen was significantly raised in 5- and 15-ppm groups, but depressed in 45- and 60-ppm groups. The gross lesions of spleen showed obvious atrophy with decreased volume and pale color in 45- and 60-ppm groups. Histopathologically, lymphocytes in splenic corpuscle and periarterial lymphatic sheath were variously decreased in number in 30-, 45-, and 60-ppm groups. The percentage of static phase (G0/G1) was significantly decreased, and the percentage of synthesis period (S) phase and the proliferating index (PI) were significantly increased in 5- and 15-ppm groups. The percentage of G0/G1 phase was significantly increased, and the percentage of mitotic phase (G2+M), S phase, and PI significantly decreased in 45- and 60-ppm groups. These results suggested that dietary excess vanadium (45 and 60 ppm) could inhibit growth of spleen and induce lesions in spleen in chicken.

Abstract  The purpose of this 42-day study was to investigate the effects of dietary excess vanadium on immune function by determining the morphological changes and cell cycle of bursa of Fabricius, and the serum Ig contents. A total of 420 one-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 vanadium supplied as ammonium metavanadate. When compared with that of control group, the relative weight of bursa was significantly increased in the 15 ppm group from 14 to 35 days of age and increased in the 5 ppm group at 42 days of age, and significantly decreased in the 60 ppm group from 14 to 42 days of age and decreased in 30 and 45 ppm groups from 35 to 42 days of age. Pathological lesions progressed as the dietary vanadium increased. The gross lesions of bursa showed obvious atrophy with decreased volume and pale color in 45 and 60 ppm groups. Histopathologically, widened cortex and increased number of lymphocytes appeared in 5 and 15 ppm groups, and reduced lymphocytes and connective tissue hyperplasia appeared in 45 and 60 ppm groups. The bursal cells in static phase (G(0)/G(1)) were decreased, and those in the mitotic phase (G(2) + M) and the proliferating index (PI) were increased in 5 and 15 ppm groups. However, bursal cells in the G(0)/G(1) phase were increased, and those in G(2) + M phase, synthesis phase (S) and the PI were decreased in 45 and 60 ppm groups. Also, the serum IgG and IgA contents were increased in 5 and 15 ppm groups, and the serum IgG, IgA, and IgM contents were decreased in 45 and 60 ppm groups. These results suggested that dietary excess vanadium (45 and 60 ppm) could inhibit growth of bursa of Fabricius and impair humoral immunity in chicken.

Abstract  Vanadium, a naturally occurring element widely distributed in soil, water and air, has received considerable interest because its compounds are often used in different applications, from industry to medicine. While the possible medical use of vanadium compounds is promising, its potential harmful effects on living organisms are still unclear. Here, for the first time, we provide a toxicological profile induced by vanadium on Paracentrotus lividus sea urchin embryos, reporting an integrated and comparative analysis of the detected effects reflecting vanadium-toxicity. At the morphological level we found a dose-dependent induction of altered phenotypes and of skeletal malformations. At the molecular levels, vanadium-exposed embryos showed the activation of the cellular stress response, in particular, autophagy and a high degree of cell-selective apoptosis in a dose-dependent manner. The stress response mediated by heat shock proteins seems to counteract the damage induced by low and intermediate concentrations of vanadium while the high cytotoxic concentrations induce more marked cell death mechanisms. Our findings, reporting different mechanisms of toxicity induced by vanadium, contribute to increase the knowledge on the possible threat of vanadium for marine organisms and for both environmental and human health.

Abstract  Five heteroleptic compounds, [VVO(IN-2H)(L-H)], where L are 8-hydroxyquinoline derivatives and IN is a Schiff base ligand, were synthesized and characterized in both the solid and solution state. The compounds were evaluated on epimastigotes and trypomastigotes of Trypanosoma cruzi as well as on VERO cells, as a mammalian cell model. Compounds showed activity against trypomastigotes with IC50 values of 0.29-3.02 μM. IN ligand and the new [VVO2(IN-H)] complex showed negligible activity. The most active compound [VVO(IN-2H)(L2-H)], with L2 = 5-chloro-7-iodo-8-hydroxyquinoline, showed good selectivity towards the parasite and was selected to carry out further biological studies. Stability studies suggested a partial decomposition in solution. [VVO(IN-2H)(L2-H)] affects the infection potential of cell-derived trypomastigotes. Low total vanadium uptake by parasites and preferential accumulation in the soluble proteins fraction were determined. A trypanocide effect was observed when incubating epimastigotes with 10 × IC50 values of [VVO(IN-2H)(L2-H)] and the generation of ROS after treatments was suggested. Fluorescence competition measurements with DNA:ethidium bromide adduct showed a moderate DNA interaction of the complexes. In vivo toxicity study on C. elegans model showed no toxicity up to a 100 μM concentration of [VVO(IN-2H)(L2-H)]. This compound could be considered a prospective anti-T. cruzi agent that deserves further research.

Abstract  The effect of chromium(VI) on the lifespan of laboratory-reared guppies (Poecilia reticulata) has been studied both in the absence and in the presence of the antioxidant D-mannitol, and it has been compared with that produced by vanadium(V). The three substances used as additives exhibited either a weak (D-mannitol), a moderate (chromate) or an acute (vanadate) toxicity to fish. Vanadate, with LC50 (7 days) = 3.84 x 10(-5) mol/L, was about ten times more toxic than chromate, with LC50 (7 days) = 3.42 x 10(-4) mol/L as a single additive and 4.27 x 10(-4) mol/L in the presence of d-mannitol. An increasing effect on the maximum lifespan of males was observed when the additives studied were used at low concentrations, either alone or in a binary combination, following the sequence: vanadate (14%) < D-mannitol (41%) < chromate + D-mannitol (57%) < chromate (69%). Of these substances, only chromate increased also the maximum lifespan of females (72%). The maximum lifespan showed a strong, positive correlation with the concentration of chromate for males (P = 0.00008) and a weaker, positive correlation (P = 0.116) for females. These results suggest the existence of a chemical-hormesis phenomenon that might be subjected to sexual-genre variability. Both the toxicity and the chemical-hormetic effect provoked by chromate were substantially decreased when it was used in combination with d-mannitol, and the possible causes for this double inhibition are briefly discussed.

Abstract  The accumulation, distribution and form of vanadate ions were studied in the mussel Mytilus edulis (L) and the goldfish Carassius auratus. After exposure to increasing doses from 0.5 to 500 μg/l for 4 days, the vanadium content in the mussel increased in all tissues, especially in the byssus which reached 17 μg V/g tissue. This suggests that this tissue could be useful as a marker for vanadium present in the aquatic environment. The vanadium present in the cytosol of the gills was associated with low molecular weight components, whereas in the mantle and hepatopancreas also with high molecular weights. After exposure to 50 μg V/l, Carassius auratus accumulated 0.1% of the dose. Among tissues, the intestine showed the highest concentration, being ∼0.05% of the dose after 4 days exposure. In the cytosol of the fish intestine, vanadium was found associated with low molecular weights, representing an easily available pool to be excreted. The capability of vanadium to be present in marine and freshwater organisms in biochemical form(s) other than the inorganic ones is of particular interest in assessing the exposure of man to environmental vanadium as ingested by food.

Abstract  1. The electrocardiogram was monitored in decerebrate cod and trout after intravenous injection of sodium orthovanadate. 2. Slowing of the heart rate occurred 1 min after injecting 84 μg of Na3VO4 (equivalent to 23 μg elemental V). 3. Heart beat was apparently suppressed for up to 30 min after injecting 168 μg of Na3VO4 and then returned to normal. 4. Significant changes in heart rate and gill ventilation rate did not occur in fish exposed to 10−4 M orthovanadate in the external medium for up to 6 days. 5. Results are discussed in terms of the possible toxicity of environmental vanadium to aquatic species.

Abstract  Several biological studies associate vanadium and cadmium with the production of reactive oxygen species (ROS), leading to lipid peroxidation and antioxidant enzymes alterations. The present study aims to analyse and compare the oxidative stress responses induced by an acute intravenous exposure (1 and 7 days) to a sub-lethal concentration (5 mM) of two vanadium solutions, containing different vanadate n-oligomers (n=1-5 or n=10), and a cadmium solution on the cardiac muscle of the marine teleost Halobatrachus didactylus (Lusitanian toadfish). It was observed that vanadium is mainly accumulated in mitochondria (1.33+/-0.26 microM), primarily when this element was administrated as decameric vanadate, than when administrated as metavanadate (432+/-294 nM), while the highest content of cadmium was found in cytosol (365+/-231 nM). Indeed, decavanadate solution promotes stronger increases in mitochondrial antioxidant enzymes activities (catalase: +120%; superoxide dismutase: +140%) than metavanadate solution. On contrary, cadmium increases cytosolic catalase (+111%) and glutathione peroxidases (+50%) activities. It is also observed that vanadate oligomers induce in vitro prooxidant effects in toadfish heart, with stronger effects induced by metavanadate solution. In summary, vanadate and cadmium are differently accumulated in blood and cardiac subcellular fractions and induced different responses in enzymatic antioxidant defence mechanisms. In the present study, it is described for the first time the effects of equal doses of two different metals intravenously injected in the same fish species and upon the same exposure period allowing to understand the mechanisms of vanadate and cadmium toxicity in fish cardiac muscle.

Abstract  Alevins of brook trout (Salvelinus fontinalis) were less sensitive to vanadium than were yearlings, the 96-h LC50 being 24 and 7 mg V/L, respectively. "Lethal thresholds" were not attained during alevin exposures for 33 days and yearling fish exposures for 12 days. Vanadium solutions were also rendered less toxic by the addition of sulphuric acid and sodium hydroxide, suggesting that a toxic effect of vanadium is an increased loss of electrolytes from membrane surfaces.

Abstract  With tritiated water (THO), we can follow up the diffusional water flow in fish body. Some pollutants may affect the THO flux, which occurs independently of osmotic gradients. The effects of 25 chemicals were determined on the THO influx in 8 species of marine (longchin goby, girella, red sea bream, etc) and fresh water fish (medaka) of small size (0.2-1.5g) for 15 min exposure. Saponins of 2ppm doubled the THO influx ( ?? 100% increase), digitonin and anionic synthetic surfactants (LAS, SDS, Aerosol-OT) had similar effect. Nonionic surfactant Tween 20 (2-20ppm) was less effective ( ?? 40%) and Triton X-100 was barely effective at 80ppm. Except for these surface active agents, the other 18 chemicals were without effect at the concentrations tested. A gill perfusion test with eels, showed saponin to act on gills, the major site for water exchange, but not the skin or oesophagus.

Abstract  Although vanadium is as abundant as nickel and zinc in the earth's crust, it is not a common pollutant. Vanadium does not occur as the free metal, but as relatively insoluble minerals and organo-metallic complexes. Consequently, the concentration of vanadium in natural freshwaters is relatively low, usually less than 20 ug.L -1 (Linstedt and Kruger 1970). A large fraction of vanadium released into the aquatic environment from natural sources originates from erosion of land surfaces by water. However, anthropogenic input has led to a significant enrichment of vanadium in the environment (Goldberg et al. 1979). Vanadium occurs in relatively high concentrations in crude oils and coals and combustion of these fuels constitutes the major source of vanadium emissions to the atmosphere. A large fraction of the anthropogenically derived vanadium-rich atmospheric particles can enter the aquatic environment as particulate fall-out or dissolved in rain. Other possible sources of vanadium contamination are effluent discharges from titanium and uranium processing plants (Jaffe and Walters 1977). Very few vanadium toxicity tests have been conducted with invertebrates. Miramand and Unsal (1978) studied the acute toxicity of vanadium to some marine benthic species. They found 9-day LC50 values of 10, 35 and 65 ppm vanadium for Nereis diversicolor (worm), Carcinus maenas (mussel) and Mytillus galloprovincialis (crab) respectively. There is more information available on the toxic effects of vanadium to fishes. According to Tarzwell and Henderson (1960), 96-h LC50 values for fathead minnow and bluegill in soft and hard waters ranged from 4.8 to 55 ppm vanadium. Knudtson (1979) determined the acute toxicity of various vanadium compounds (V205, VOSO4, N}{4V03 and NaVO3) to goldfish and guppy in relatively soft water. Depending on the compound tested, the S-day LC50 values ranged from 0.s to 4.5 mg V.L -1 for goldfish and 0.12 to 0.65 mg V.L -I for guppy. The 96-h LC50 of vanadium to adult American flagfish was 11.2 mg.L -1 in very hard water while the threshold for chronic toxicity was judged to be about 0.08 mg.L -1 (Holdway and Sprague 1979). Water hardness and pH had only a minor influence on vanadium lethality to rainbow trout (Stendahl and Sprague 1982). The 7-day LC50 values of V205 fell in a small range, from 1.9 to 6.0 mg V.L -1. The aim of this study is to determine the acute and subchronic toxicity of vanadium for various species of freshwater fish. The long-term toxicity and the effect of vanadium on the reproduction of Daplmia magna is also evaluated and compared with the toxicity of other metals.

Abstract  Investigation of developmental molecular events following exposure to environmentally relevant agrochemical mixtures is critical to predicting their potential long-term ecological and human health risks. Here, we sought to uncover transcriptomic changes during zebrafish (Danio rerio) embryonic development following exposure to glyphosate and co-exposure to metals. Glyphosate is widely used globally with an allowable drinking water limit of 700 ppb. We examined effects of glyphosate (10 ppb) alone and when co-exposed to a metal mixture containing low levels of arsenic (4 ppb), lead (5 ppb), cadmium (2 ppb), and vanadium (15 ppb). This mixture was derived based on behavioral and morphological toxicity findings and environmentally relevant concentrations found in agricultural regions where glyphosate and metals are ubiquitously present. Gene expression patterns coupled to a single-cell transcriptomic dataset revealed that developmental exposure (28-72 h post fertilization) to glyphosate dysregulates expression of developmental genes specific to the central nervous system. Subsequent studies indicated significant suppression of larval zebrafish movement with 10 ppb glyphosate exposure. Studies with glyphosate + metals mixture and metals mixture alone showed unique developmental transcriptomic patterns and behavioral changes compared to glyphosate exposure alone. However, some outcomes (e.g., changes in expression of genes involved in epigenetic regulation and extracellular matrix patterning) were common across all three exposures compared to the control. Notably, glyphosate + metals co-exposure distinctly suppresses lysosomal transcripts and targets renal developmental genes. While further studies are required to uncover the precise nature of the interactions between glyphosate and metals, our study shows that glyphosate at very low levels is a behavioral and neurotoxicant that changes when metals are present. Given this herbicide affects distinctive physiological processes, including renal development and lysosomal dysregulation when co-exposed with metals, we conclude that environmental cation levels should be considered in glyphosate toxicity and risk assessment.