Protective Effects of Dietary Antioxidants against Vanadium-Induced Toxicity: A Review

Vanadium (V) in its inorganic forms is a toxic metal and a potent environmental and occupational pollutant and has been reported to induce toxic effects in animals and people. In vivo and in vitro data show that high levels of reactive oxygen species are often implicated in vanadium deleterious effects. Since many dietary (exogenous) antioxidants are known to upregulate the intrinsic antioxidant system and ameliorate oxidative stress-related disorders, this review evaluates their effectiveness in the treatment of vanadium-induced toxicity. Collected data, mostly from animal studies, suggest that dietary antioxidants including ascorbic acid, vitamin E, polyphenols, phytosterols, and extracts from medicinal plants can bring a beneficial effect in vanadium toxicity. These findings show potential preventive effects of dietary antioxidants on vanadium-induced oxidative stress, DNA damage, neurotoxicity, testicular toxicity, and kidney damage. The relevant mechanistic insights of these events are discussed. In summary, the results of studies on the role of dietary antioxidants in vanadium toxicology appear encouraging enough to merit further investigations

Effects of Sodium Pyruvate on Vanadyl Sulphate-Induced Reactive Species Generation and Mitochondrial Destabilisation in CHO-K1 Cells

Vanadium is ranked as one of the world’s critical metals considered important for economic growth with wide use in the steel industry. However, its production, applications, and emissions related to the combustion of vanadium-containing fuels are known to cause harm to the environment and human health. Pyruvate, i.e., a glucose metabolite, has been postulated as a compound with multiple cytoprotective properties, including antioxidant and anti-inflammatory effects. The aim of the present study was to examine the antioxidant potential of sodium pyruvate (4.5 mM) in vanadyl sulphate (VOSO4)-exposed CHO-K1 cells. Dichloro-dihydro-fluorescein diacetate and dihydrorhodamine 123 staining were performed to measure total and mitochondrial generation of reactive oxygen species (ROS), respectively. Furthermore, mitochondrial damage was investigated using MitoTell orange and JC-10 staining assays. We demonstrated that VOSO4 alone induced a significant rise in ROS starting from 1 h to 3 h after the treatment. Additionally, after 24 and 48 h of exposure, VOSO4 elicited both extensive hyperpolarisation and depolarisation of the mitochondrial membrane potential (MMP). The two-way ANOVA analysis of the results showed that, through antagonistic interaction, pyruvate prevented VOSO4-induced total ROS generation, which could be observed at the 3 h time point. In addition, through the independent action and antagonistic interaction with VOSO4, pyruvate provided a pronounced protective effect against VOSO4-mediated mitochondrial toxicity at 24-h exposure, i.e., prevention of VOSO4-induced hyperpolarisation and depolarisation of MMP. In conclusion, we found that pyruvate exerted cytoprotective effects against vanadium-induced toxicity at least in part by decreasing ROS generation and preserving mitochondrial function

Preliminary studies on the effect of zinc and selenium on vanadium-induced cytotoxicity in vitro

In the present work, we investigated the cytotoxicity of vanadium and the influence of zinc and seleni- um on vanadium-dependent cell damage in the BALB/c 3T3 cell culture. Treatment of cells for 24 hours with medium containing 50, 100 and 200 μ M NaVO 3 caused a significant decrease in the cell viability as measured by MTT test. Furthermore, the assays for reactive oxygen species (NBT reduction and phe- nol red oxidation) demonstrated the increase in superoxide and hydrogen peroxide production. In the cotreatment studies, the cells were exposed to NaVO 3 (50, 100 and 200 μ M) in the presence of nontox- ic concentrations of ZnCl 2 (5 μ M) or Na 2 SeO 3 (0.5 μ M). Following 24 h incubation, the cell viability (assessed in MTT assay) and reactive oxygen species generation were evaluated. Our data suggest that zinc and selenium, in the concentrations mentioned above, provide no protection against adverse actions induced by sodium metavanadate at concentration levels of 50, 100 and 200 μ M. To our knowledge, this is the first report from in vitro studies on interaction between pentavalent vanadium and trace elements that function as antioxidants: zinc and selenium

Identification of Potential Artefacts in In Vitro Measurement of Vanadium-Induced Reactive Oxygen Species (ROS) Production

We investigated vanadium, i.e., a redox-active heavy metal widely known for the generation of oxidative stress in cultured mammalian cells, to determine its ability to interfere with common oxidative stress-related bioassays in cell-free conditions. We first assessed the prooxidant abilities (H2O2 level, oxidation of DHR 123, and DCFH-DA dyes) and antioxidant capacity (ABTS, RP, OH, and DPPH methods) of popular mammalian cell culture media, i.e., Minimal Essential Medium (MEM), Dulbecco’s Minimal Essential Medium (DMEM), Dulbecco’s Minimal Essential Medium-F12 (DMEM/F12), and RPMI 1640. Out of the four media studied, DMEM has the highest prooxidant and antioxidant properties, which is associated with the highest concentration of prooxidant and antioxidant nutrients in its formulation. The studied vanadium compounds, vanadyl sulphate (VOSO4), or sodium metavanadate (NaVO3) (100, 500, and 1000 µM), either slightly increased or decreased the level of H2O2 in the studied culture media. However, these changes were in the range of a few micromoles, and they should rather not interfere with the cytotoxic effect of vanadium on cells. However, the tested vanadium compounds significantly stimulated the oxidation of DCFH-DA and DHR123 in a cell-independent manner. The type of the culture media and their pro-oxidant and antioxidant abilities did not affect the intensity of oxidation of these dyes by vanadium, whereas the vanadium compound type was important, as VOSO4 stimulated DCFH-DA and DHR oxidation much more potently than NaVO3. Such interactions of vanadium with these probes may artefactually contribute to the oxidation of these dyes by reactive oxygen species induced by vanadium in cells

The physiological levels of epigallocatechin gallate (EGCG) enhance the Cd-induced oxidative stress and apoptosis in CHO-K1 cells

Abstract Currently, the increasing pollution of the environment by heavy metals is observed, caused both by natural factors and those related to human activity. They pose a significant threat to human health and life. It is therefore important to find an effective way of protecting organisms from their adverse effects. One potential product showing a protective effect is green tea. It has been shown that EGCG, which is found in large amounts in green tea, has strong antioxidant properties and can therefore protect cells from the adverse effects of heavy metals. Therefore, the aim of the study was to investigate the effect of EGCG on cells exposed to Cd. In the study, CHO-K1 cells (Chinese hamster ovary cell line) were treated for 24 h with Cd (5 and 10 µM) and EGCG (0.5 and 1 µM) together or separately. Cell viability, ATP content, total ROS activity, mitochondrial membrane potential and apoptosis potential were determined. The results showed that, in tested concentrations, EGCG enhanced the negative effect of Cd. Further analyses are needed to determine the exact mechanism of action of EGCG due to the small number of publications on the subject and the differences in the results obtained in the research

Wpływ metod leczenia na jakość życia pacjentów z cukrzycą typu 1

Cukrzyca typu 1 jest chorobą przewlekłą, niosącą za sobą ryzyko rozwoju szeregu powikłań wpływających na jakość życia (JŻ). Celem pracy była ocena wpływu stosowanych metod leczenia na jakość życia pacjentów z cukrzycą typu 1. Materiał i metody: Badaniem objęto 90 pacjentów z cukrzycą typu 1 (64,4 % kobiet, wiek od 18 do 65 lat), których podzielono na dwie grupy badawcze: 45 osób leczonych za pomocą osobistej pompy insulinowej (OPI) oraz 45 osób leczonych metodą intensywnej insulinoterapii (IT). Do oceny JŻ wykorzystano kwestionariusz WHOQOL- -Bref. Wyniki: Pacjenci leczeni za pomocą pompy insulinowej deklarują większy stopień zadowolenia z jakości swojego życia aniżeli leczeni intensywną insulinoterapią (odpowiednio 68,9% vs 37,8%, p<0.05). 46,7% pacjentów leczonych OPI było zadowolonych lub bardzo zadowolonych ze swojego stanu zdrowia, w grupie IT odsetek ten sięgał 31.1%, różnice te jednak nie osiągnęły poziomu istotności statystycznej. Pacjenci leczeni OPI wyżej ocenili JŻ w zakresie podskali fizycznej (p<0.001), psychologicznej (p<0.001), relacji społecznych (p<0.001) i środowiskowej (p<0.001). Wnioski: Stosowana metoda leczenia ma wpływ na ocenę jakości życia pacjentów z cukrzycą typu 1. Osoby leczone za pomocą pompy insulinowej znacząco lepiej oceniają jakość swojego życia we wszystkich dziedzinach. Badane grupy pacjentów z cukrzycą typu 1 podobnie oceniają stan swojego zdrowia, niezależnie od metody leczenia. Czas trwania choroby oraz wiek koreluje ujemnie z jakością życia badanych, natomiast płeć nie ma wpływu na ocenę jakości życia