Transplacental and genotoxicity effects of thallium(I) during organogenesis in mice.

The increased concentration of thallium (Tl) in the environment is a cause for concern because the entire population, including pregnant women, is exposed, and this metal crosses the placenta and reaches the conceptus during development. In biological models such as mice, some abnormalities and delays in ossification occur in the fetuses of mice administered Tl on day 7 of gestation, but exposure to environmental Tl is constant during fetal development; therefore, in this study, the effects of several administrations of TI during organogenesis on the external morphology, skeletal development and genotoxicity of fetuses were evaluated. Four groups of 10 pregnant mice were administered 5.

Oxidative damage to DNA, expression of Mt-1, and activation of repair mechanisms induced by vanadium trioxide in cultures of human lymphocytes.

Vanadium (V) has garnered attention due to its pharmacological properties; however, its toxic effects have also been documented. Among the vanadium compounds that are found in the environment, vanadium trioxide (VO) has attracted interest because of its impact on biomolecules such as DNA, RNA, and proteins. However, its precise mechanism of action remains unclear, although it is suspected to be related to oxidative stress.

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.