Oxidative damage and cell cycle delay induced by vanadium(III) in human peripheral blood cells.

Vanadium (V) is a metal that can enter the environment through natural routes or anthropogenic activity. In the atmosphere, V is present as V oxides, among which vanadium(III) oxide (VO) stands out. Cytogenetic studies have shown that VO is genotoxic and cytostatic and induces DNA damage; however, the molecular mechanisms leading to these effects have not been fully explored.

Vanadium(IV) oxide affects embryonic development in mice.

Vanadium(V) and vanadium(IV) are the predominant redox forms present in the environment, and epidemiological studies have reported that prenatal vanadium exposure is associated with restricted fetal growth and adverse birth outcomes. However, data about the toxic effects of vanadium(IV) oxide (V O ) on the development of mammals are still limited. Therefore, in this work, 4.

Vanadium oxides modify the expression levels of the p21, p53, and Cdc25C proteins in human lymphocytes treated in vitro.

In vitro assays have demonstrated that vanadium compounds interact with biological molecules similar to protein kinases and phosphatases and have also shown that vanadium oxides decrease the proliferation of cells, including human lymphocytes; however, the mechanism, the phase in which the cell cycle is delayed and the proteins involved in this process are unknown. Therefore, we evaluated the effects of vanadium oxides (V O , V O and V O ) in human lymphocyte cultures (concentrations of 2, 4, 8, or 16 μg/ml) on cellular proliferation and the levels of the p53, p21 and Cdc25C proteins. After 24 h of treatment with the different concentrations of vanadium oxides, the cell cycle phases were determined by evaluating the DNA content using flow cytometry, and the levels of the p21, p53 and Cdc25C proteins were assessed by Western blot analysis.

Effect on the offspring of pregnant females CD-1 mice treated with a single thallium(I) application.

Thallium (Tl) is a highly toxic metal for human beings; higher amounts found in diverse fluids of pregnant women are associated with low birth weight and preterm birth. However, experimental data concerning their effects on the embryonic development of mammalian organisms are limited. Hence, in the present work, TI(I) acetate of 0, 4.

Genotoxicity of Casiopeina III-Ea in mouse bone marrow cells.

Casiopeina III-Ea® (Cas III-Ea®) is a chelated copper complex with antineoplastic activity that is capable of reducing tumor size and inducing antiproliferative and apoptotic effects. However, little is known about its in vivo genotoxic effects. Therefore, this study evaluated two cytogenetic and two proliferative parameters 24 h after the administration of Casiopeina III-Ea® to male CD-1 mice.

In vitro DNA damage by Casiopeina II-gly in human blood cells.

A variety of metal ions have biological functions, and many researchers have not actively investigated copper compounds, based on the assumption that endogenous metals might be less toxic. In the present study, we used a dual fluorochrome method and a single cell gel electrophoresis (SCGE) assay at pH > 13 to evaluate the cell viability and DNA damage induced by a copper-based antineoplastic drug, Casiopeina II-gly®, at concentrations of 1.04, 2.

Potential for genotoxic and reprotoxic effects of vanadium compounds due to occupational and environmental exposures: an article based on a presentation at the 8th International Symposium on Vanadium Chemistry, Biological Chemistry, and Toxicology, Washington DC, August 15-18, 2012.

Research on the biological effects of vanadium in humans has shown that acute poisoning in workers can manifest itself in a number of symptoms. There are no reports in humans about reproductive and developmental effects induced by vanadium compounds in humans; however, some studies with rats and mice indicate that vanadium can cross the placental barrier and accumulate in fetal membranes rather than the fetus itself. In this case, probably most consequences of administration of vanadium to pregnant females like reabsorptions, fetal death and reduction in size can be the result of maternal toxicity.

Chromosomal damage induced by vanadium oxides in human peripheral lymphocytes.

Fly ash, the inorganic residue resulting from the combustion of some fuels, may almost exclusively contain vanadium oxides, compounds which exert potential toxic effects on a wide variety of in vitro and in vivo biological systems. Because information related to the oxidation state responsible for inducing genotoxic effects is controversial, the aim of the present study was to evaluate the effects of three vanadium salts in vitro. Human peripheral lymphocyte cultures were exposed to 1, 2, 4, or 8 microg/mL of vanadium(III) trioxide, vanadium(IV) tetraoxide, or vanadium(V) pentoxide (V(2)O(3), V(2)O(4), or V(2)O(5), respectively).

Genotoxic studies of vanadium pentoxide (V(2)O(5)) in male mice. II. Effects in several mouse tissues.

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.

Reprotoxic and genotoxic studies of vanadium pentoxide in male mice.

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).