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Vanadium Pentoxide (Draft, 2011)

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  • 1.
    The "refereed" or "peer review" status of a journal comes from the Ulrichsweb Global Serials Directory (http://ulrichsweb.serialssolutions.com/), as supplied by the publisher. The term refers to the system of critical evaluation of manuscripts/articles by professional colleagues or peers. The content of refereed publications is sanctioned, vetted, or otherwise approved by a peer-review or editorial board. The peer-review and evaluation system is utilized to protect, maintain, and raise the quality of scholarly material published in serials. Publications subject to the referee process are assumed, then, to contain higher quality content than those that are not.
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    C-H functionalization of tertiary amines by cross dehydrogenative coupling reactions: solvent-free synthesis of α-aminonitriles and β-nitroamines under aerobic condition

    Authors: Alagiri, K; Prabhu, KR
    (2012) Organic and Biomolecular Chemistry 10:835-842.
    Minus Sign. Click to see only selected choices. A solvent-free synthesis of α-aminonitriles and β-nitroamines by oxidative cross-dehydrogenative coupling . . . Plus Sign. Click to expand choices. A solvent-free synthesis of α-aminonitriles and β-nitroamines by oxidative cross-dehydrogenative coupling under aerobic condition is reported. A catalytic amount of molybdenum(vi) acetylacetonoate was found to catalyze cyanation of tertiary amines to form α-aminonitriles, whereas vanadium pentoxide was found to promote aza-Henry reaction to furnish β-nitroamines. Both of these environmentally benign reactions are performed in the absence of solvents using molecular oxygen as an oxidant.
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  • 2.
    The "refereed" or "peer review" status of a journal comes from the Ulrichsweb Global Serials Directory (http://ulrichsweb.serialssolutions.com/), as supplied by the publisher. The term refers to the system of critical evaluation of manuscripts/articles by professional colleagues or peers. The content of refereed publications is sanctioned, vetted, or otherwise approved by a peer-review or editorial board. The peer-review and evaluation system is utilized to protect, maintain, and raise the quality of scholarly material published in serials. Publications subject to the referee process are assumed, then, to contain higher quality content than those that are not.
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    Reprotoxic and genotoxic studies of vanadium pentoxide in male mice

    Authors: Altamirano-Lozano, M; Alvarez-Barrera, L; Basurto-Alcántara, F; Valverde, M; Rojas, E
    (1996) Teratogenesis, Carcinogenesis, and Mutagenesis 16:7-17.
    Minus Sign. Click to see only selected choices. Effects of vanadium pentoxide (V2O5) treatment on reproductive function and testicular DNA in male mice . . . Plus Sign. Click to expand choices. Effects of vanadium pentoxide (V2O5) treatment on reproductive function and testicular DNA in male mice were investigated. These functions were evaluated with fertility rate, implants, resorptions, sperm counts, motility, and morphology. The DNA damage in individual testis cells was analyzed by single-cell gel electrophoresis technique (COMET assay). V2O5 treatment resulted in a decrease in fertility rate, implantations, live fetuses, and fetal weight, and an increase in the number of resorptions/dam. Sperm count, motility, and morphology were impaired with the advancement of treatment. Vanadium treatment induced DNA damage depending on the dose in the testis cells that was expressed and detected as DNA migration in the COMET assay. The distribution of DNA migration among cells, a function of dose, revealed that the majority of cells of treated animals expressed more DNA damage than cells from control animals. It is concluded that vanadium pentoxide was a reprotoxic and genotoxic agent in mice.
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  • 3.
    The "refereed" or "peer review" status of a journal comes from the Ulrichsweb Global Serials Directory (http://ulrichsweb.serialssolutions.com/), as supplied by the publisher. The term refers to the system of critical evaluation of manuscripts/articles by professional colleagues or peers. The content of refereed publications is sanctioned, vetted, or otherwise approved by a peer-review or editorial board. The peer-review and evaluation system is utilized to protect, maintain, and raise the quality of scholarly material published in serials. Publications subject to the referee process are assumed, then, to contain higher quality content than those that are not.
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    Cytogenetic and teratogenic effects of vanadium pentoxide on mice

    Authors: Altamirano-Lozano, M; Alvarez-Barrera, L; Roldán-Reyes, E
    (1993) Medical Science Research 21:711-713.
    Minus Sign. Click to see only selected choices. BIOSIS COPYRIGHT: BIOL ABS. RRM RESEARCH ARTICLE DNA INHIBITION PROTEIN SYNTHESIS INHIBITION DECREASED . . . Plus Sign. Click to expand choices. BIOSIS COPYRIGHT: BIOL ABS. RRM RESEARCH ARTICLE DNA INHIBITION PROTEIN SYNTHESIS INHIBITION DECREASED FETAL BODY WEIGHT GENOTOXIC EFFECT LIMB SHORTENING
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  • 4.
    The "refereed" or "peer review" status of a journal comes from the Ulrichsweb Global Serials Directory (http://ulrichsweb.serialssolutions.com/), as supplied by the publisher. The term refers to the system of critical evaluation of manuscripts/articles by professional colleagues or peers. The content of refereed publications is sanctioned, vetted, or otherwise approved by a peer-review or editorial board. The peer-review and evaluation system is utilized to protect, maintain, and raise the quality of scholarly material published in serials. Publications subject to the referee process are assumed, then, to contain higher quality content than those that are not.
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    Genotoxic studies of vanadium pentoxide (V(2)O(5)) in male mice. II. Effects in several mouse tissues

    Authors: Altamirano-Lozano, M; Valverde, M; Alvarez-Barrera, L; Molina, B; Rojas, E
    (1999) Teratogenesis, Carcinogenesis, and Mutagenesis 19:243-255.
    Minus Sign. Click to see only selected choices. Vanadium pentoxide (V2O5) was tested for its ability to induce genotoxic damage in six different organs . . . Plus Sign. Click to expand choices. Vanadium pentoxide (V2O5) was tested for its ability to induce genotoxic damage in six different organs (liver, kidney, lung, spleen, heart, and bone marrow) of mice by using the alkaline Single Cell Gel Electrophoresis (SCGE) assay. Animals were sacrificed 24 h after i.p. administration of the vanadium pentoxide of 23.0, 11.5, or 5.75 microg/g (corresponding to the LD50, 1/2 LD50 and 1/4 LD50, respectively). In all tissues and organs evaluated (except for bone marrow), V2O5 increased the number of cells with damage. Our results showed that i.p. injection of V2O5 induced DNA damage in different organs and tissues, and that this kind of damage can be observed even 24 h after treatment. The analysis of DNA migration and the distribution of DNA damage showed that there are differences in sensitivity between organs and tissues to this compound. In addition the sensitivity of SCGE assay allows the detection of long term DNA damage and the possibility to compare it in various tissues and target organs.
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  • 5.
    The "refereed" or "peer review" status of a journal comes from the Ulrichsweb Global Serials Directory (http://ulrichsweb.serialssolutions.com/), as supplied by the publisher. The term refers to the system of critical evaluation of manuscripts/articles by professional colleagues or peers. The content of refereed publications is sanctioned, vetted, or otherwise approved by a peer-review or editorial board. The peer-review and evaluation system is utilized to protect, maintain, and raise the quality of scholarly material published in serials. Publications subject to the referee process are assumed, then, to contain higher quality content than those that are not.
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    Sex differences in the effects of vanadium pentoxide administration to prepubertal rats

    Authors: Altamirano, M; Ayala, ME; Flores, A; Morales, L; Dominguez, R
    (1991) Medical Science Research 19:825-826.
    Minus Sign. Click to see only selected choices. Vanadium pentoxide (V sub(2)O sub(5)) is the most toxic form of vanadium for mammals, presumably because . . . Plus Sign. Click to expand choices. Vanadium pentoxide (V sub(2)O sub(5)) is the most toxic form of vanadium for mammals, presumably because of its inhibitory effects on several enzymes. Since puberty is the result of several modifications in the mechanisms controlling gonadotrophin secretion and gonadal reactivity to them, we decided to compare the effects of V sub(2)O sub(5) administered to male and female prepubertal rats.
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  • 6.
    The "refereed" or "peer review" status of a journal comes from the Ulrichsweb Global Serials Directory (http://ulrichsweb.serialssolutions.com/), as supplied by the publisher. The term refers to the system of critical evaluation of manuscripts/articles by professional colleagues or peers. The content of refereed publications is sanctioned, vetted, or otherwise approved by a peer-review or editorial board. The peer-review and evaluation system is utilized to protect, maintain, and raise the quality of scholarly material published in serials. Publications subject to the referee process are assumed, then, to contain higher quality content than those that are not.
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    Role of proto-oncogene activation in carcinogenesis

    Authors: Anderson, MW; Reynolds, SH; You, M; Maronpot, RM
    (1992) Environmental Health Perspectives 98:13-24.
    Minus Sign. Click to see only selected choices. The accumulation of genetic damage in the forms of activated proto-oncogenes and inactivated tumor-suppressor . . . Plus Sign. Click to expand choices. The accumulation of genetic damage in the forms of activated proto-oncogenes and inactivated tumor-suppressor genes is the driving force in the evolution of a normal cell to a malignant cell. For example, both the activation of ras oncogenes and the inactivation of several suppressor genes, including p53, have been observed in the development of human colon and lung tumors. Point mutations in key codons can activate ras proto-oncogenes and inactivate the p53 suppressor gene. Thus, several critical genes for tumorigenesis are potential targets for carcinogens and radiation that can induce point mutations at low doses. The ras proto-oncogenes are targets for many genotoxic carcinogens. Activation of the ras gene is an early event--probably the "initiating" step--in the development of many chemical-induced rodent tumors. ras Oncogenes are observed in more human tumors and at a higher frequency than any other oncogene, and activation of the proto-oncogene may occur at various stages of the carcinogenic process. Numerous proto-oncogenes other than the ras genes have been shown to be activated in human tumors and to a lesser extent in rodent tumors. Mechanisms that induce aberrant expression of proto-oncogenes are gene amplification and chromosomal translocation or gene rearrangement. Amplification of proto-oncogenes and possibly gene overexpression during the absence of gene amplification occur in the development of many human tumors. For a specific tumor type, amplification of any one proto-oncogene may occur at a low frequency, but the frequency of tumors in which at least one proto-oncogene is amplified can be much higher. Proto-oncogene amplification is usually associated with late stages of tumor progression; however, amplified HER2/neu has been observed in early clinical stages of mammary neoplasia. Activation of proto-oncogenes by chromosomal translocation has been detected at a high frequency in several hematopoietic tumors. Non-ras genes have been detected by DNA transfection assays in both human and rodent tumors. For example, ret and trk genes were found to be activated by gene rearrangements in human papillary thyroid carcinomas. Several potentially new types of oncogenes have also been detected by DNA transfection assays. The etiology of the genetic alterations observed in most human tumors is unclear at present. Examples of ras gene activation and those documented for mutations in the p53 gene demonstrate that exogenous conditions can induce oncogenic mutants of normal genes. The genetic alterations observed in most human tumors are probably generated by both spontaneous events and exogenous conditions.
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  • 7.
    The "refereed" or "peer review" status of a journal comes from the Ulrichsweb Global Serials Directory (http://ulrichsweb.serialssolutions.com/), as supplied by the publisher. The term refers to the system of critical evaluation of manuscripts/articles by professional colleagues or peers. The content of refereed publications is sanctioned, vetted, or otherwise approved by a peer-review or editorial board. The peer-review and evaluation system is utilized to protect, maintain, and raise the quality of scholarly material published in serials. Publications subject to the referee process are assumed, then, to contain higher quality content than those that are not.
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    STAT-1 signaling in human lung fibroblasts is induced by vanadium pentoxide through an IFN-beta autocrine loop

    Authors: Antao-Menezes, A; Turpin, EA; Bost, PC; Ryman-Rasmussen, JP; Bonner, JC
    (2008) Journal of Immunology 180:4200-4207.
    Minus Sign. Click to see only selected choices. The inhalation of vanadium pentoxide (V(2)O(5)) results in bronchitis and airway fibrosis. The lung . . . Plus Sign. Click to expand choices. The inhalation of vanadium pentoxide (V(2)O(5)) results in bronchitis and airway fibrosis. The lung fibrotic response to V(2)O(5) partially resolves where fibroblasts first proliferate and deposit collagen, but then undergo growth arrest and apoptosis. STAT-1 mediates fibroblast growth arrest and apoptosis. We previously reported that STAT-1 is a protective factor and mice lacking STAT-1 are more susceptible to lung fibrosis. We also reported that V(2)O(5)-induced STAT-1 phosphorylation in lung fibroblasts requires H(2)O(2) and de novo protein synthesis. In this study, we identified IFN-beta as the protein that mediates STAT-1 activation by V(2)O(5) in normal human lung fibroblasts and identified NADPH and xanthine oxidase systems as sources of H(2)O(2) that drive IFN-beta gene expression. STAT-1 phosphorylation was decreased with neutralizing Abs to IFN-beta as well as an inhibitor of JAK. V(2)O(5) also increased transcription of an IFN-inducible and STAT-1-dependent chemokine, CXCL10. Inhibition of H(2)O(2)-generating enzyme systems NADPH oxidase by apocynin and xanthine oxidase by allopurinol individually reduced STAT-1 phosphorylation. Apocynin and allopurinol also decreased V(2)O(5)-induced IFN-beta mRNA levels and CXCL10 expression. IFN-alpha transcription was inhibited only by allopurinol. Taken together, these data indicate that fibroblasts play a role in the innate immune response to vanadium-induced oxidative stress by synthesizing IFN-beta and activating STAT-1 to cause growth arrest and increase levels of CXCL10, a potent antifibrotic factor. This mechanism is postulated to counterbalance profibrogenic mechanisms that follow V(2)O(5) injury.
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  • 8.
    The "refereed" or "peer review" status of a journal comes from the Ulrichsweb Global Serials Directory (http://ulrichsweb.serialssolutions.com/), as supplied by the publisher. The term refers to the system of critical evaluation of manuscripts/articles by professional colleagues or peers. The content of refereed publications is sanctioned, vetted, or otherwise approved by a peer-review or editorial board. The peer-review and evaluation system is utilized to protect, maintain, and raise the quality of scholarly material published in serials. Publications subject to the referee process are assumed, then, to contain higher quality content than those that are not.
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    Vanadium induced ultrastructural changes and apoptosis in male germ cells

    Authors: Aragon, MA; Ayala, ME; Fortoul, TI; Bizarro, P; Altamirano-Lozano, M
    (2005) Reproductive Toxicology 20:127-134.
    Minus Sign. Click to see only selected choices. Vanadium is a transition metal that is emitted to the atmosphere during combustion of fossil fuels. . . . Plus Sign. Click to expand choices. Vanadium is a transition metal that is emitted to the atmosphere during combustion of fossil fuels. In the environment, vanadium occurs in the (V) oxidized form, but in the body it is found exclusively in the (IV) oxidized form. Vanadium tetraoxide is an inorganic chemical species in the (IV) oxidized form that has been shown to induce toxic effects in vitro and in vivo. The reproductive toxicity of vanadium in males was studied through monitoring germ cell apoptosis during spermatogenesis. We analyzed ultrastructural damage, and testosterone and progesterone concentrations following vanadium tetraoxide administered to male mice for 60 days. Spermatogenesis stages I-III and X-XII frequently showed apoptotic germ cells in control and treated animals; vanadium tetraoxide treatment induced an increase in the number of germ cell apoptosis in stages I-III and XII at 9.4 and 18.8 mg/kg, respectively. Although spermatogenesis is regulated by testosterone, in our study this hormone level was not modified by vanadium administration; thus, germ cell death was not related with testosterone concentration. At the ultrastructural level, we observed inclusion structures that varied as to location and content in the Sertoli and germ cells.
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  • 9.
    The "refereed" or "peer review" status of a journal comes from the Ulrichsweb Global Serials Directory (http://ulrichsweb.serialssolutions.com/), as supplied by the publisher. The term refers to the system of critical evaluation of manuscripts/articles by professional colleagues or peers. The content of refereed publications is sanctioned, vetted, or otherwise approved by a peer-review or editorial board. The peer-review and evaluation system is utilized to protect, maintain, and raise the quality of scholarly material published in serials. Publications subject to the referee process are assumed, then, to contain higher quality content than those that are not.
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    Epigenetics in metal carcinogenesis: Nickel, arsenic, chromium and cadmium

    Authors: Arita, A; Costa, M
    (2009) Metallomics 1:222-228. [Review]
    Minus Sign. Click to see only selected choices. Although carcinogenic metals have been known to disrupt a wide range of cellular processes the precise . . . Plus Sign. Click to expand choices. Although carcinogenic metals have been known to disrupt a wide range of cellular processes the precise mechanism by which these exert their carcinogenic effects is not known. Over the last decade or two, studies in the field of metal carcinogenesis suggest that epigenetic mechanisms may play a role in metal-induced carcinogenesis. In this review we summarize the evidence demonstrating that exposure to carcinogenic metals such as nickel, arsenic, chromium, and cadmium can perturb DNA methylation levels as well as global and gene specific histone tail posttranslational modification marks. We also wish to emphasize the importance in understanding that gene expression can be regulated by both genetic and epigenetic mechanisms and both these must be considered when studying the mechanism underlying the toxicity and cell-transforming ability of carcinogenic metals and other toxicants, and aberrant changes in gene expression that occur during disease states such as cancer.
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  • 10.
    The "refereed" or "peer review" status of a journal comes from the Ulrichsweb Global Serials Directory (http://ulrichsweb.serialssolutions.com/), as supplied by the publisher. The term refers to the system of critical evaluation of manuscripts/articles by professional colleagues or peers. The content of refereed publications is sanctioned, vetted, or otherwise approved by a peer-review or editorial board. The peer-review and evaluation system is utilized to protect, maintain, and raise the quality of scholarly material published in serials. Publications subject to the referee process are assumed, then, to contain higher quality content than those that are not.
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    A review of current toxicological concerns on vanadium pentoxide and other vanadium compounds: gaps in knowledge and directions for future research

    Authors: Assem, FL; Levy, LS
    (2009) Journal of Toxicology and Environmental Health, Part B: Critical Reviews 12:289-306. [Review]
    Minus Sign. Click to see only selected choices. Vanadium pentoxide (V(2)O(5)) and other inorganic vanadium compounds have recently been evaluated by . . . Plus Sign. Click to expand choices. Vanadium pentoxide (V(2)O(5)) and other inorganic vanadium compounds have recently been evaluated by several occupational exposure limit (OEL) setting (occupational exposure limit, OEL) committees and expert groups in response to the publication of several new studies, including the U.S. National Toxicology Program (NTP, 2002) carcinogenicity study of inhaled V(2)O(5) in rats and mice, which concluded that clear evidence of lung tumors was seen in mice of both genders and that there was some evidence of carcinogenicity in male rats. This study reviews the expert evaluations of several OEL committees and expert groups and attempts to understand the strengths and weaknesses in their scientific arguments. This study also evaluates some key studies relating to potential genotoxicity, carcinogenicity, and respiratory effects of vanadium compounds and discusses how they might elucidate the mechanism(s) by which V(2)O(5) induces lung cancer in mice. All expert groups appear to agree that the lung tumors induced in mice in the NTP (2002) study are a site-specific response and, in general, verify that existing in vitro and in vivo studies suggest that tumors were induced by a secondary mechanism (presumably non-genotoxic), which is supported, though not conclusively, by a mechanistic data set. As some vanadium compounds produce a range of DNA and chromosome damage, there is no consensus on which of these changes is critical for the carcinogenic process for V(2)O(5) or whether the findings for the lung tumors seen in mice exposed to V(2)O(5) can be extrapolated to other inorganic vanadium compounds. As such, the various expert committees used the evidence differently, some to read across, i.e., to predict an endpoint for a substance based on the endpoint information of another with similar characteristics (e.g., physicochemical properties [solubility, bioaccessibility, bioavailability], structure, fate [toxicokinetics], and toxicology) for carcinogenicity from V(2)O(5) to other inorganic vanadium compounds. It is noteworthy that the toxicity of metals does not necessarily relate to carcinogenicity in a direct manner; thus, no assumptions should be made a priori when trying to extrapolate from V(2)O(5) to other inorganic vanadium compounds. Recent studies evaluated in this review provided some further insights into possible mechanisms but do not cover all relevant endpoints, address only a limited number of vanadium compounds, and have not established no-effect thresholds for carcinogenicity or respiratory tract irritation. Thresholds need to be established in order for arguments to be made for setting a health-based OEL for non-genotoxic or secondary genotoxic carcinogens. In conclusion, important knowledge gaps preclude confident classification and risk assessment for all vanadium compounds. Evidence suggests that further research that may address some of these critical gaps is needed.
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