Mutagenicity, carcinogenicity and teratogenicity of vanadium compounds

Vanadate Induction of NF-κB Involves IκB Kinase β and SAPK/ERK Kinase 1 in Macrophages

“…A certain degree of additive or synergistic effects may occur between these two signaling axes. This is true in the diseases related to vanadium exposure, in which both mutagenicity and inflammation induced by vanadate have been reported (11,(43)(44)(45). Regarding environmental or occupational PM, in addition to vanadium, other metals and metal-metal interactions may also have some impact on overall PM-induced biological changes.…”

Genotoxic studies of vanadium pentoxide (V2O5) in male mice. II. Effects in several mouse tissues

“…Among metal-induced DNA lesions, single (SSB) and double strand beaks (DSB), DNA-DNA crosslinks, base modification, and SSB, eventually leading to chromosome breakage [7], have been described. Studies on the biological effects of vanadium have increased greatly in recent years due to its potential toxicological [1,8], genotoxic [4][5][6], and reprotoxic [4,[9][10][11] impact on humans and animals, and its possible role as an essential element in mammals in addition to it's potential pharmacological use in the treatment of diabetes [12,13].…”

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

“…At high doses, vanadium compounds can damage a developing organism in the uterus, but, apparently, this effect is mainly due to maternal toxicity. Because vanadium salts are inefficiently transferred to the fetus itself, fetal malformations are found only at very high doses (specific agents and corresponding doses reviewed in Léonard & Gerber, 1998). The available data indicate the necessity for more studies of the effects of vanadium in occupationally-, environmentally-, or pharmacologically-exposed human populations.…”

“…However, if the NaVO 3 is administered via the intraperitoneal route to female mice from days 6-15 of gestation at doses of 4 or 8 mg/kg/day, then an increase occurs in the number of resorptions, dead fetuses, and cleft palates (Gomez et al, 1992). Although the authors of this study reported the presence of maternal toxicity, they postulated that the effect observed in fetuses may be caused by direct contact of vanadium with the tissues from embryos or fetuses and not by maternal toxicity; however, it is likely that most of the effects produced by the administration of vanadium compounds to pregnant females (increased percentage of resorptions, fetal death, and fetal weight reduction) is the result of maternal toxicity caused by high doses of the compounds (Léonard & Gerber, 1998).…”