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Cardiovascular Toxicology

Erschienen in:

01.09.2010

Arsenic Induces Apoptosis of Human Umbilical Vein Endothelial Cells Through Mitochondrial Pathways

verfasst von: Yanfen Shi, Yudan Wei, Shanshan Qu, Yang Wang, Yulin Li, Ronggui Li

Erschienen in: Cardiovascular Toxicology | Ausgabe 3/2010

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Abstract

To clarify the molecular mechanisms through which arsenic causes injuries to blood vessels, we analyzed the effects of sodium arsenite (NaAsO₂) on the apoptosis of human umbilical vein endothelial cells (HUVECs), mitochondrial membrane potential (ΔΨm), intracellular reactive oxygen species (ROS), and the expression of the related genes. HUVECs apoptosis increased and ΔΨm decreased in a dose-dependent manner following arsenic treatment. Intracellular ROS showed 2 phase alterations: a slight decrease with low levels of arsenic (5 and 10 μM) treatment; but a sharp increase at higher concentrations (≧20 μM). The arsenic-induced cell apoptosis and intracellular ROS were blocked by the addition of the antioxidant N-acetyl-l-cysteine (NAC). The mRNAs of superoxide dismutase 2 (SOD2) and NAD(P)H:quinone oxidoreductase 1 (NQO1) increased strikingly when cells were treated with a low concentration of NaAsO₂ (5 μM) and the level of induction was decreased with higher concentrations of arsenic treatment. Based on the results, we suggest that the decrease of ΔΨm caused by arsenic and the resulting cell apoptosis may contribute to the injuries of blood vessel in arsenism. The decrease in intracellular ROS and the increase in SOD2 and NQO1 expressions observed when HUVECs were treated with low concentration of NaAsO₂, suggest the role of the two enzymes in protecting HUVECs from injuries of arsenic exposure.

Rahman, M. M., Naidu, R., & Bhattacharya, P. (2009). Arsenic contamination in groundwater in the Southeast Asia region. Environmental Geochemistry and Health, 31(Suppl 1), 9–21.CrossRefPubMed

Yu, G., Sun, D., & Zheng, Y. (2007). Health effects of exposure to natural arsenic in groundwater and coal in China: An overview of occurrence. Environmental Health Perspectives, 115, 636–642.CrossRefPubMed

Sun, G. (2004). Arsenic contamination and arsenicosis in China. Toxicology and Applied Pharmacology, 198, 268–271.CrossRefPubMed

Mukherjee, A., Sengupta, M. K., Hossain, M. A., Ahamed, S., Das, B., Nayak, B., et al. (2006). Arsenic contamination in groundwater: A global perspective with emphasis on the Asian scenario. Journal of Health, Population, and Nutrition, 24, 142–163.PubMed

Wu, M. M., Kuo, T. L., Hwang, Y. H., & Chen, C. J. (1989). Dose-response relation between arsenic concentration in well water and mortality from cancers and vascular diseases. American Journal of Epidemiology, 130, 1123–1132.PubMed

Chang, C. C., Ho, S. C., Tsai, S. S., & Yang, C. Y. (2004). Ischemic heart disease mortality reduction in an arseniasis-endemic area in southwestern Taiwan after a switch in the tap-water supply system. Journal of Toxicology and Environmental Health: Part A, 67, 1353–1361.CrossRef

Navas-Acien, A., Silbergeld, E. K., Pastor-Barriuso, R., & Guallar, E. (2008). Arsenic exposure and prevalence of type 2 diabetes in US adults. Jama, 300, 814–822.CrossRefPubMed

Coronado-Gonzalez, J. A., Del Razo, L. M., Garcia-Vargas, G., Sanmiguel-Salazar, F., & Escobedo-de la Pena, J. (2007). Inorganic arsenic exposure and type 2 diabetes mellitus in Mexico. Environmental Research, 104, 383–389.CrossRefPubMed

Chiu, H. F., Chang, C. C., Tsai, S. S., & Yang, C. Y. (2006). Does arsenic exposure increase the risk for diabetes mellitus? Journal of Occupational and Environmental Medicine, 48, 63–67.CrossRefPubMed

10.

Tseng, C. H., Chong, C. K., Chen, C. J., & Tai, T. Y. (1997). Lipid profile and peripheral vascular disease in arseniasis-hyperendemic villages in Taiwan. Angiology, 48, 321–335.CrossRefPubMed

11.

Tseng, C. H., Huang, Y. K., Huang, Y. L., Chung, C. J., Yang, M. H., Chen, C. J., et al. (2005). Arsenic exposure, urinary arsenic speciation, and peripheral vascular disease in blackfoot disease-hyperendemic villages in Taiwan. Toxicology and Applied Pharmacology, 206, 299–308.CrossRefPubMed

12.

Tseng, C. H., Chong, C. K., Chen, C. J., Lin, B. J., & Tai, T. Y. (1995). Abnormal peripheral microcirculation in seemingly normal subjects living in blackfoot-disease-hyperendemic villages in Taiwan. International Journal of Microcirculation, Clinical and Experimental, 15, 21–27.CrossRefPubMed

13.

Tseng, C. H., Chong, C. K., Chen, C. J., & Tai, T. Y. (1996). Dose-response relationship between peripheral vascular disease and ingested inorganic arsenic among residents in blackfoot disease endemic villages in Taiwan. Atherosclerosis, 120, 125–133.CrossRefPubMed

14.

Tseng, C. H., Chong, C. K., Tseng, C. P., & Centeno, J. A. (2007). Blackfoot disease in Taiwan: Its link with inorganic arsenic exposure from drinking water. Ambio, 36, 82–84.CrossRefPubMed

15.

Balakumar, P., & Kaur, J. (2009). Arsenic exposure and cardiovascular disorders: An overview. Cardiovascular Toxicology, 9, 169–176.CrossRefPubMed

16.

Tseng, C. H. (2008). Cardiovascular disease in arsenic-exposed subjects living in the arseniasis-hyperendemic areas in Taiwan. Atherosclerosis, 199, 12–18.CrossRefPubMed

17.

Mannarino, E., & Pirro, M. (2008). Endothelial injury and repair: A novel theory for atherosclerosis. Angiology, 59, 69S–72S.CrossRefPubMed

18.

Kao, Y. H., Yu, C. L., Chang, L. W., & Yu, H. S. (2003). Low concentrations of arsenic induce vascular endothelial growth factor and nitric oxide release and stimulate angiogenesis in vitro. Chemical Research in Toxicology, 16, 460–468.CrossRefPubMed

19.

Woo, S. H., Park, M. J., An, S., Lee, H. C., Jin, H. O., Lee, S. J., et al. (2005). Diarsenic and tetraarsenic oxide inhibit cell cycle progression and bFGF- and VEGF-induced proliferation of human endothelial cells. Journal of Cellular Biochemistry, 95, 120–130.CrossRefPubMed

20.

Ramanathan, K., Anusuyadevi, M., Shila, S., & Panneerselvam, C. (2005). Ascorbic acid and alpha-tocopherol as potent modulators of apoptosis on arsenic induced toxicity in rats. Toxicology Letters, 156, 297–306.CrossRefPubMed

21.

Engel, R. H., & Evens, A. M. (2006). Oxidative stress and apoptosis: A new treatment paradigm in cancer. Frontiers in Bioscience, 11, 300–312.CrossRefPubMed

22.

Nohl, H., Gille, L., & Staniek, K. (2005). Intracellular generation of reactive oxygen species by mitochondria. Biochemical Pharmacology, 69, 719–723.CrossRefPubMed

23.

Liu, S. X., Athar, M., Lippai, I., Waldren, C., & Hei, T. K. (2001). Induction of oxyradicals by arsenic: Implication for mechanism of genotoxicity. Proceedings of the National Academy of Sciences of the United States of America, 98, 1643–1648.CrossRefPubMed

24.

Perez, M. J., & Cederbaum, A. I. (2003). Adenovirus-mediated expression of Cu/Zn- or Mn-superoxide dismutase protects against CYP2E1-dependent toxicity. Hepatology, 38, 1146–1158.CrossRefPubMed

25.

Epperly, M. W., Bernarding, M., Gretton, J., Jefferson, M., Nie, S., & Greenberger, J. S. (2003). Overexpression of the transgene for manganese superoxide dismutase (MnSOD) in 32D cl 3 cells prevents apoptosis induction by TNF-alpha, IL-3 withdrawal, and ionizing radiation. Experimental Hematology, 31, 465–474.CrossRefPubMed

26.

Faraci, F. M., & Didion, S. P. (2004). Vascular protection: Superoxide dismutase isoforms in the vessel wall. Arteriosclerosis, Thrombosis, and Vascular Biology, 24, 1367–1373.CrossRefPubMed

27.

Gaikwad, A., Long, D. J., 2nd, Stringer, J. L., & Jaiswal, A. K. (2001). In vivo role of NAD(P)H:Quinone oxidoreductase 1 (NQO1) in the regulation of intracellular redox state and accumulation of abdominal adipose tissue. J Biol Chem, 276, 22559–22564.CrossRefPubMed

28.

Joseph, P., Xie, T., Xu, Y., & Jaiswal, A. K. (1994). NAD(P)H:Quinone oxidoreductase1 (DT-diaphorase): Expression, regulation, and role in cancer. Oncology Research, 6, 525–532.PubMed

29.

Ross, D., Kepa, J. K., Winski, S. L., Beall, H. D., Anwar, A., & Siegel, D. (2000). NAD(P)H:Quinone oxidoreductase 1 (NQO1): Chemoprotection, bioactivation, gene regulation and genetic polymorphisms. Chemico-Biological Interactions, 129, 77–97.CrossRefPubMed

30.

Reddy, V. N., Kasahara, E., Hiraoka, M., Lin, L. R., & Ho, Y. S. (2004). Effects of variation in superoxide dismutases (SOD) on oxidative stress and apoptosis in lens epithelium. Experimental Eye Research, 79, 859–868.CrossRefPubMed

31.

Wang, Y., Xu, Y., Wang, H., Xue, P., Li, X., Li, B., et al. (2009). Arsenic induces mitochondria-dependent apoptosis by reactive oxygen species generation rather than glutathione depletion in Chang human hepatocytes. Archives of Toxicology, 83, 899–908.CrossRefPubMed

Titel: Arsenic Induces Apoptosis of Human Umbilical Vein Endothelial Cells Through Mitochondrial Pathways
verfasst von: Yanfen Shi
Yudan Wei
Shanshan Qu
Yang Wang
Yulin Li
Ronggui Li
Publikationsdatum: 01.09.2010
Verlag: Humana Press Inc
Erschienen in: Cardiovascular Toxicology / Ausgabe 3/2010
Print ISSN: 1530-7905
Elektronische ISSN: 1559-0259
DOI: https://doi.org/10.1007/s12012-010-9073-z

Springer Medizin

Abstract

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