Vanadate-Induced Cell Growth Regulation and the Role of Reactive Oxygen Species

Zhang, Zhuo; Huang, Chuanshu; Li, Jingxia; Leonard, Stephen S.; Lanciotti, Robert S.; Butterworth, Leon; Shi, Xianglin

doi:10.1006/abbi.2001.2464

Cited by 122 publications

(86 citation statements)

References 51 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…In rat alveolar macrophages, 12-otetradecanoyl phorbol-13-acetate stimulates ROS from mitochondrial sources, mainly at complexes I and III (42). In A549 cells, vanadate stimulates the production of ROS (mainly hydrogen peroxide) from mitochondria, which produces growth arrest (52). The present study and a previous study from this laboratory (3) have further shown in human AM that ROFA stimulates ROS production from mitochondria.…”

Section: Discussionsupporting

confidence: 75%

Mitochondrial oxidant production by a pollutant dust and NO-mediated apoptosis in human alveolar macrophage

Huang

Soukup

Harder

et al. 2003

American Journal of Physiology-Cell Physiology

View full text Add to dashboard Cite

Residual oil fly ash (ROFA) is a pollutant dust that stimulates production of reactive oxygen species (ROS) from mitochondria and apoptosis in alveolar macrophages (AM), but the relationship between these two processes is unclear. In this study, human AM were incubated with ROFA or vanadyl sulfate (VOSO4), the major metal constituent in ROFA, with or without nitro-l-arginine methyl ester (l-NAME), diphenyleneiodonium (DPI), and mitochondrial electron transport inhibitors. Interactions among production of ROS, nitric oxide (NO), and apoptosis of AM were determined. ROFA-stimulated ROS production was attenuated by DPI, rotenone, antimycin, and NaN3, but not by l-NAME, a pattern mimicked by VOSO4. ROFA-induced apoptosis was inhibited byl-NAME and a caspase-3-like protease inhibitor, but not by mitochondrial inhibitors. ROFA enhanced NO-mediated increase in caspase-3-like activity. VOSO4 had minor effects on apoptosis. Thus ROFA-stimulated production of ROS from mitochondria was independent of apoptosis of AM, which was mediated by activation of caspase-3-like proteases and NO. The pro-oxidant effect but not the proapoptotic effect of ROFA was mediated by vanadium.

show abstract

Section: Discussionsupporting

confidence: 75%

Mitochondrial oxidant production by a pollutant dust and NO-mediated apoptosis in human alveolar macrophage

Huang

Soukup

Harder

et al. 2003

American Journal of Physiology-Cell Physiology

View full text Add to dashboard Cite

show abstract

“…1). Since GSH was found to be involved in vanadate bioreduction [10][11][12][13][14][15], the levels of GSH should be affected when vanadate is administered. Indeed, it has been reported that the GSH pool is enhanced in the presence of vanadate [23,39].…”

Section: Resultsmentioning

confidence: 99%

“…The overall rate of ROS production in hepatic tissue homogenates was calculated from the kinetics of increase of fluorescence (k exc = 495 nm, k em = 520 nm) using dichlorodihydrofluorescein diacetate (H 2 DCFDA) as probe [14,28]. Fluorescence measurements were carried out under continuous stirring at 25°C with a Perkin-Elmer 650-40 Fluorescence Spectrophotometer (Perkin-Elmer, Foster City, CA, USA).…”

Section: Methodsmentioning

confidence: 99%

“…Vanadium can induce the formation of reactive oxygen species (ROS) in biological systems through: (i) Fenton-like reactions [9]; (ii) vanadate bioreduction mediated by reduced glutathione (GSH), flavoenzymes or NAD(P)H oxidases with ROS as a by-product [10][11][12][13][14][15]; (iii) and recent evidences point out to an indirect promotion of ROS production, probably by interacting with mitochondria [16]. Moreover, vanadium toxicological effects in several cell types have been related with ROS production [16][17][18][19].…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Vanadate oligomers: In vivo effects in hepatic vanadium accumulation and stress markers

Gândara

Soares

Martins

et al. 2005

Journal of Inorganic Biochemistry

View full text Add to dashboard Cite

The formation of vanadate oligomeric species is often disregarded in studies on vanadate effects in biological systems, particularly in vivo, even though they may interact with high affinity with many proteins. We report the effects in fish hepatic tissue of an acute intravenous exposure (12, 24 h and 7 days) to two vanadium(V) solutions, metavanadate and decavanadate, containing different vanadate oligomers administered at sub-lethal concentration (5 mM; 1 mg/kg). Decavanadate solution promotes a 5-fold increase (0.135 ± 0.053 lg V À1 dry tissues) in the vanadium content of the mitochondrial fraction 7 days after exposition, whereas no effects were observed after metavanadate solution administration. Reduced glutathione (GSH) levels did not change and the overall reactive oxygen species (ROS) production was decreased by 30% 24 h after decavanadate administration, while for metavanadate, GSH levels increased 35%, the overall ROS production was depressed by 40% and mitochondrial superoxide anion production decreased 45%. Decavanadate intoxication did not induce changes in the rate of lipid peroxidation till 12 h, but later increased 80%, which is similar to the increase observed for metavanadate after 24 h. Decameric vanadate administration clearly induces different effects than the other vanadate oligomeric species, pointing out the importance of taking into account the different vanadate oligomers in the evaluation of vanadium(V) effects in biological systems.

show abstract

“…Cyclin B1 is able to form a complex with Cdc2 (Taylor and Stark, 2001) and patched1 (ptc1), a tumor suppressor associated with basal cell carcinoma (Barnes et al, 2001) to adjust the rate of cell cycle progression. In addition, Cyclin B1 and the phosphorylated Cdc2 are activated by oxidative stress to regulate cell cycle control (Zhang et al, 2001). From a gene expression profile of MCF-7 breast cancer cells treated with IR, upregulated Cyclin B1 was found to be one of the essential elements for IR-induced radioresistance in MCF-7 cells .…”

Section: Discussionmentioning

confidence: 99%

Expression of ErbB2 enhances radiation-induced NF-κB activation

et al. 2004

View full text Add to dashboard Cite

Her-2/neu (ErbB2) oncogene, the second member of the epidermal growth factor receptor (EGFR) family, encodes a transmembrane tyrosine kinase receptor in Her-2-positive tumors. Accumulating evidences demonstrate that signaling networks activated by EGFR and transcription factor NFjB are associated with cell response to ionizing radiation (IR). The present study shows that overexpression of ErbB2 enhanced NF-jB activation induced by IR in human breast carcinoma MCF-7 cells transfected with ErbB2 genes (MCF-7/ErbB2). Stable transfection of dominantnegative mutant IjB (MCF-7/ErbB2/mIjB) or treatment with anti-ErbB2 antibody, Herceptin, inhibited NF-jB activation and radiosensitized MCF-7/ErbB2 cells. Consistent with NF-jB regulation, basal and IR-induced Akt, a kinase downstream of ErbB2, was activated in MCF-7/ ErbB2 cells and inhibited by Herceptin. To identify specific genes affected by ErbB2-mediated NF-jB activation, a group of IR-responsive elements Cyclin B1, Cyclin D1, Bcl-2, Bcl/XL, BAD and BAX were evaluated. Basal levels of prosurvival elements Cyclin B1, Cyclin D1, Bcl-2 and Bcl/XL but not apoptotic BAD and BAX were upregulated in MCF-7/ErbB2 cells with striking enhancements in Bcl-2 and Bcl/XL. IR further induced Cyclin B1 and Cyclin D1 expression that was reduced by Herceptin. Bcl-2 kept a high steady level after Herceptin þ IR treatment and, in contrast to control MCF-7/Vector cells, Bcl/XL was inhibited in MCF-7/ErbB2 cells by Herceptin þ IR treatment. However, all four prosurvival proteins were downregulated by inhibition of NF-jB in MCF-7/ErbB2/mIjB cells. These results thus provide evidence suggesting that overexpression of ErbB2 is able to enhance NF-jB response to IR, and that a specific prosurvival network downstream of NF-jB is triggered by treatments using anti-ErbB2 antibody combined with radiation.

show abstract

Vanadate-Induced Cell Growth Regulation and the Role of Reactive Oxygen Species

Cited by 122 publications

References 51 publications

Mitochondrial oxidant production by a pollutant dust and NO-mediated apoptosis in human alveolar macrophage

Mitochondrial oxidant production by a pollutant dust and NO-mediated apoptosis in human alveolar macrophage

Vanadate oligomers: In vivo effects in hepatic vanadium accumulation and stress markers

Expression of ErbB2 enhances radiation-induced NF-κB activation

Contact Info

Product

Resources

About