Publications by authors named "Mateos-Nava R"

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.

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Photosynthesis is a crucial process supporting life on Earth. However, unfavorable environmental conditions including toxic metals may limit the photosynthetic efficiency of plants, and the responses to those challenges may vary among genotypes. In this study, we evaluated photosynthetic parameters of the chili pepper varieties Jalapeño, Poblano, and Serrano exposed to Cd (0, 5, 10 µM), Tl (0, 6, 12 nM), and V (0, 0.

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Article Synopsis
  • Vanadium is a strategic metal used in various industries, but its production through fossil fuel combustion leads to environmental and health concerns due to toxic waste emissions.
  • Several studies indicate that some vanadium compounds can damage DNA, particularly focusing on vanadium pentoxide.
  • In this study, mouse bone marrow cells were exposed to vanadium(IV) tetraoxide and vanadium(III) trioxide, revealing that both compounds increased chromosomal defects and reduced cell division compared to control treatments.
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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.

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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.

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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.

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Vanadium is a widely distributed metal in the Earth's surface and is released into the environment by either natural or anthropogenic causes. Vanadium (III) oxide (VO) is present in the environment, and many organisms are exposed to this compound; however, its effects at the cellular and genetic levels are still unknown. Therefore, in this study, the ability of VO to induce chromosomal damage and impair cell proliferation was tested on human leukocytes in vitro.

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Introduction: the carcinogenesis may be initiated and promoted by the oxidative DNA damage. The compounds of chrome (Cr [VI]) cause oxidative stress (EOx) and are recognized as carcinogens in humans. In this sense, it is proposed that drinks with a high antioxidative potential, such as red wine, may have protective or modulatory effects on the oxidative DNA damage.

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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.

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Vanadium and vanadium salts cause genotoxicity and elicit variable biological effects depending on several factors. In the present study, we analyzed and compared the DNA damage and repair processes induced by vanadium in three oxidation states. We used human blood leukocytes in vitro and in a single cell gel electrophoresis assay at two pH values.

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