The Solvent and Treatment Regimen of Sodium Selenite Cause Its Effects to Vary on the Radiation Response of Human Bronchial Cells from Tumour and Normal Tissues

Overview

Journal Med Oncol

Publisher Springer

Specialty Oncology

Date 2020 Nov 18

PMID 33205219

Citations 2

Authors

Katrin Manda

Stephan Kriesen

Guido Hildebrandt

Affiliations

Soon will be listed here.

Abstract

Sodium selenite is often given to moderate the side effects of cancer therapy to enhance the cellular defence of non-cancerous cells. To determine whether sodium selenite during radiotherapy protects not only normal cells but also cancer cells, which would imply a reduction of the desired effect of irradiation on tumour during radiotherapy, the effect of the combined treatment of irradiation and sodium selenite was investigated. Human bronchial cells from carcinoma (A549) and normal tissue (BEAS-2B) were treated with sodium selenite and effects on growth and in combination with radiation on metabolic activity and cell cycle distribution were studied. The influence on radiosensitivity was determined via colony forming assays using different solvents of sodium selenite and treatment schedules. It was shown that sodium selenite inhibits growth and influences cell cycle distribution of both normal and tumour cells. Metabolic activity of normal cells decreased more rapidly compared to that of cancer cells. The influence of sodium selenite on radiation response depended on the different treatment schedules and was strongly affected by the solvent of the agent. It could be shown that the effect of sodium selenite on radiation response is strongly dependent on the respective experimental in vitro conditions and ranges from lead to an initially suspected but ultimately no real radioprotection to radiosensitizing up to no effect in one and the same cell line. This might be a reason for controversially described cell responses to radiation under the influence of sodium selenite in studies so far.

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References

Bruntz R, Belshoff A, Zhang Y, Macedo J, Higashi R, Lane A . Inhibition of Anaplerotic Glutaminolysis Underlies Selenite Toxicity in Human Lung Cancer. Proteomics. 2019; 19(21-22):e1800486. PMC: 7153719. DOI: 10.1002/pmic.201800486. View

Abul-Hassan K, Lehnert B, Guant L, Walmsley R . Abnormal DNA repair in selenium-treated human cells. Mutat Res. 2004; 565(1):45-51. DOI: 10.1016/j.mrgentox.2004.09.004. View

Trachootham D, Alexandre J, Huang P . Targeting cancer cells by ROS-mediated mechanisms: a radical therapeutic approach?. Nat Rev Drug Discov. 2009; 8(7):579-91. DOI: 10.1038/nrd2803. View

Berthier S, Arnaud J, Champelovier P, Col E, Garrel C, Cottet C . Anticancer properties of sodium selenite in human glioblastoma cell cluster spheroids. J Trace Elem Med Biol. 2017; 44:161-176. DOI: 10.1016/j.jtemb.2017.04.012. View

Plesca D, Mazumder S, Almasan A . DNA damage response and apoptosis. Methods Enzymol. 2008; 446:107-22. PMC: 2911482. DOI: 10.1016/S0076-6879(08)01606-6. View

Zhao R, Xiang N, Domann F, Zhong W . Effects of selenite and genistein on G2/M cell cycle arrest and apoptosis in human prostate cancer cells. Nutr Cancer. 2009; 61(3):397-407. PMC: 2724066. DOI: 10.1080/01635580802582751. View

Chen J, Boylan L, Wu C, Spallholz J . Oxidation of glutathione and superoxide generation by inorganic and organic selenium compounds. Biofactors. 2008; 31(1):55-66. DOI: 10.1002/biof.5520310106. View

Kim E, Sohn S, Kwon H, Kim S, Kim M, Lee S . Sodium selenite induces superoxide-mediated mitochondrial damage and subsequent autophagic cell death in malignant glioma cells. Cancer Res. 2007; 67(13):6314-24. DOI: 10.1158/0008-5472.CAN-06-4217. View

Brozmanova J, Manikova D, Vlckova V, Chovanec M . Selenium: a double-edged sword for defense and offence in cancer. Arch Toxicol. 2010; 84(12):919-38. DOI: 10.1007/s00204-010-0595-8. View

10.

Wallenberg M, Olm E, Hebert C, Bjornstedt M, Fernandes A . Selenium compounds are substrates for glutaredoxins: a novel pathway for selenium metabolism and a potential mechanism for selenium-mediated cytotoxicity. Biochem J. 2010; 429(1):85-93. DOI: 10.1042/BJ20100368. View

11.

Hoefig C, Renko K, Kohrle J, Birringer M, Schomburg L . Comparison of different selenocompounds with respect to nutritional value vs. toxicity using liver cells in culture. J Nutr Biochem. 2010; 22(10):945-55. DOI: 10.1016/j.jnutbio.2010.08.006. View

12.

Lipinski B . Redox-Active Selenium in Health and Disease: A Conceptual Review. Mini Rev Med Chem. 2016; 19(9):720-726. DOI: 10.2174/1389557517666161104125022. View

13.

Park S, Kim J, Chi G, Kim G, Chang Y, Moon S . Induction of apoptosis and autophagy by sodium selenite in A549 human lung carcinoma cells through generation of reactive oxygen species. Toxicol Lett. 2012; 212(3):252-61. DOI: 10.1016/j.toxlet.2012.06.007. View

14.

Xiang N, Zhao R, Zhong W . Sodium selenite induces apoptosis by generation of superoxide via the mitochondrial-dependent pathway in human prostate cancer cells. Cancer Chemother Pharmacol. 2008; 63(2):351-62. PMC: 2592502. DOI: 10.1007/s00280-008-0745-3. View

15.

Husbeck B, Peehl D, Knox S . Redox modulation of human prostate carcinoma cells by selenite increases radiation-induced cell killing. Free Radic Biol Med. 2004; 38(1):50-7. DOI: 10.1016/j.freeradbiomed.2004.09.022. View

16.

Jiang C, Wang Z, Ganther H, Lu J . Distinct effects of methylseleninic acid versus selenite on apoptosis, cell cycle, and protein kinase pathways in DU145 human prostate cancer cells. Mol Cancer Ther. 2002; 1(12):1059-66. View

17.

Verma P, Kunwar A, Priyadarsini K . Effect of Low-Dose Selenium Supplementation on the Genotoxicity, Tissue Injury and Survival of Mice Exposed to Acute Whole-Body Irradiation. Biol Trace Elem Res. 2017; 179(1):130-139. DOI: 10.1007/s12011-017-0955-9. View

18.

Frisk P, Saetre A, Couce B, Stenerlow B, Carlsson J, Lindh U . Effects of Pb2+, Ni2+, Hg2+ and Se4+ on cultured cells. Analysis of uptake, toxicity and influence on radiosensitivity. Biometals. 1997; 10(4):263-70. DOI: 10.1023/a:1018316214877. View

19.

Wallenberg M, Misra S, Wasik A, Marzano C, Bjornstedt M, Gandin V . Selenium induces a multi-targeted cell death process in addition to ROS formation. J Cell Mol Med. 2014; 18(4):671-84. PMC: 4000118. DOI: 10.1111/jcmm.12214. View

20.

Luo H, Yang Y, Huang F, Li F, Jiang Q, Shi K . Selenite induces apoptosis in colorectal cancer cells via AKT-mediated inhibition of β-catenin survival axis. Cancer Lett. 2011; 315(1):78-85. DOI: 10.1016/j.canlet.2011.10.014. View