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. Concerning genetic and related effects in humans exposed to different vanadium compounds, data are controversial. Data on genotoxic effects in workers exposed to vanadium indicate that they can have an increased risk to develop cancer, and DNA instability can give rise to an onset of genetic syndromes, fetal malformations, and cancer. This paper presents materials presented at the 8th International Symposium on Vanadium Chemistry, Biological Chemistry, and Toxicology in a session titled 'Relationship between occupational and environmental exposure to vanadium compounds and the reprotoxic and genotoxic effects'.

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. 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.

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). 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.