Increased Cytotoxicity of Vanadium to CHO-K1 Cells in the Presence of Inorganic Selenium

Zwolak, Iwona

doi:10.1007/s00128-015-1615-4

Cited by 17 publications

(14 citation statements)

References 39 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In addition, laboratory-based studies conducted in animal models or cell cultures found that vanadium exposure can induce a variety of toxic effects such as cardiovascular effects (e.g., vascular endothelial dysfunction [30] and arterial hypertension [31]), immune toxicity (e.g., damage to the spleen [32] and thymus [33]), neurotoxicity (e.g., hippocampal alterations [34] and memory loss [35]), developmental disturbances (e.g., increased embryolethality and skeletal defects [36]), and pulmonary toxicity [37]. It should be added that, besides the dose of vanadium and the route of vanadium exposure, many other factors such as the form of vanadium (inorganic versus organic forms) and interactions with other elements such as selenium [38,39] or magnesium [40] can also influence vanadium toxicity (depicted in Figure 1).…”

Section: Overview Of Vanadiummentioning

confidence: 99%

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

Zwolak

2020

Oxidative Medicine and Cellular Longevity

Self Cite

View full text Add to dashboard Cite

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.

show abstract

Section: Overview Of Vanadiummentioning

confidence: 99%

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

Zwolak

2020

Oxidative Medicine and Cellular Longevity

Self Cite

View full text Add to dashboard Cite

show abstract

“…Sodium orthovanadate also inhibits oral squamous, colon and kidney cancer cell proliferation and triggers apoptosis with similar concentrations as the one we report (Khalil & Jameson, ; Klein et al, ) in a manner similar to sodium metavanadate; nevertheless, these reports only mention as possible cause the crosstalk between different signaling phosphoproteins, possibly p53 through the ATM pathway (Suzuki et al, ). Their effect on disruption of cell signaling transduction pathways, cell cycle arrest and apoptosis seem to be valence dependent (Paulpandiyan & Raman, ; Tian et al, ; Wu et al, ; Wu et al, ; Zwolak, ) but the precise cytotoxic mechanism of vanadium compounds remains undetermined (Taddei, Giannoni, Fiaschi, & Chiarugi, ). Therefore, we investigated the mechanisms responsible for NaVO 3 and VOSO 4 cytotoxic activity as each one is representative of biologically important valences of vanadium (Al‐Majed, ; Duprez, Wirawan, Vanden Berghe, & Vandenabeele, ; Kordowiak, Klein, Goc, & Dabros, ; Zwolak, ).…”

Section: Discussionmentioning

confidence: 99%

“…Their effect on disruption of cell signaling transduction pathways, cell cycle arrest and apoptosis seem to be valence dependent (Paulpandiyan & Raman, 2017;Tian et al, 2016;Wu et al, 2014;Wu et al, 2016;Zwolak, 2015) but the precise cytotoxic mechanism of vanadium compounds remains undetermined (Taddei, Giannoni, Fiaschi, & Chiarugi, 2012). Therefore, we investigated the mechanisms responsible for NaVO 3 and VOSO 4 cytotoxic activity as each one is representative of biologically important valences of vanadium (Al-Majed, Duprez, Wirawan, Vanden Berghe, & Vandenabeele, 2009;Kordowiak, Klein, Goc, & Dabros, 2007;Zwolak, 2016).…”

Section: Discussionmentioning

confidence: 99%

“…However, the majority of them exhibit insulin-like effects (Niu et al, 2016), but most significantly, several vanadium compounds prevent and inhibit the growth of various types of cancer in multiple in vitro and in vivo assays (Kowalski, Hac, Wyrzykowski, Zauszkiewicz-Pawlak, & Inkielewicz-Stepniak, 2017;Leon et al, 2015). Their cytotoxic effect (Rivadeneira et al, 2010;Zwolak, 2015), disruption of cellular signal transduction pathways, cell cycle arrest and apoptosis effect is apparently mediated by the generation of reactive oxygen species (ROS); however, these effects are valence dependent (Liao et al, 2013;Rozzo et al, 2017;Wu et al, 2014). Therefore, a better understanding of the mechanism of action of vanadium compounds is required.…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Vanadium compounds and cellular death mechanisms in the A549 cell line: The relevance of the compound valence

Guerrero-Palomo

Rendón-Huerta

Montaño

et al. 2018

J of Applied Toxicology

View full text Add to dashboard Cite

Non‐small lung cell carcinoma has a high morbidity and mortality rates. The elective treatment for stage III and IV is cisplatinum that conveys serious toxic side effects. Vanadium compounds are metal molecules with proven antitumor activity that depends on its valence. Therefore, a better understanding of the mechanism of action of vanadium compounds is required. The aim of our study was to investigate the mechanisms of cell death induced by sodium metavanadate (NaVO3 [V(+5)]) and vanadyl sulfate (VOSO4 [(+4)]), both of which have reported apoptotic‐inducing activity. We exposed the A549 cell line to various concentrations (0‐100 μM) and to different exposure times to each compound and determined the cell viability and expression of caspases, reactive oxygen species (ROS) production, Bcl2, Bax, FasL and NO. Our results showed that neither compounds modified the basal expression of caspases or pro‐ and anti‐apoptotic proteins. The only change observed was the 12‐ and 14‐fold significant increase in ROS production induced by NaVO3 and VOSO4, respectively, at 100 μm concentrations after 48 hours. Our results suggest that classical apoptotic mechanisms are not related to the cell death induced by the vanadium compounds evaluated here, and showed that the higher ROS production was induced by the [(+4)] valence compound. It is possible that the difference will be secondary to its higher oxidative status and thus higher ROS production, which leads to higher cell damage. In conclusion, our results suggest that the efficacy of the cell death mechanisms induced by vanadium compounds differ depending on the valence of the compound.

show abstract

“…However, it has to be used carefully as, at high concentrations, selenium can display pro-oxidant properties and generate ROS (Lee & Jeong, 2012). Concentrations of selenium below 1 µM have been shown to be safe for CHO-K1 cells and are often included in cell culture medium (Zhang, Robinson, & Salmon, 2006;Zwolak, 2015). However, toxic concentrations of selenium have to be determined for each cell line.…”

Section: Trace Elements and Chelatorsmentioning

confidence: 99%

Oxidative stress‐alleviating strategies to improve recombinant protein production in CHO cells

Chevallier

Andersen

Malphettes

2019

Biotech & Bioengineering

View full text Add to dashboard Cite

Large scale biopharmaceutical production of biologics relies on the overexpression of foreign proteins by cells cultivated in stirred tank bioreactors. It is well recognized and documented fact that protein overexpression may impact host cell metabolism and that factors associated with large scale culture, such as the hydrodynamic forces and inhomogeneities within the bioreactors, may promote cellular stress. The metabolic adaptations required to support the high‐level expression of recombinant proteins include increased energy production and improved secretory capacity, which, in turn, can lead to a rise of reactive oxygen species (ROS) generated through the respiration metabolism and the interaction with media components. Oxidative stress is defined as the imbalance between the production of free radicals and the antioxidant response within the cells. Accumulation of intracellular ROS can interfere with the cellular activities and exert cytotoxic effects via the alternation of cellular components. In this context, strategies aiming to alleviate oxidative stress generated during the culture have been developed to improve cell growth, productivity, and reduce product microheterogeneity. In this review, we present a summary of the different approaches used to decrease the oxidative stress in Chinese hamster ovary cells and highlight media development and cell engineering as the main pathways through which ROS levels may be kept under control.

show abstract

Increased Cytotoxicity of Vanadium to CHO-K1 Cells in the Presence of Inorganic Selenium

Cited by 17 publications

References 39 publications

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

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

Vanadium compounds and cellular death mechanisms in the A549 cell line: The relevance of the compound valence

Oxidative stress‐alleviating strategies to improve recombinant protein production in CHO cells

Contact Info

Product

Resources

About