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1,3-Dichloro-2-Propanol (1,3-DCP) Induced Cell Damage
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 Title & Authors
1,3-Dichloro-2-Propanol (1,3-DCP) Induced Cell Damage
Jeong, Ji-Hak; Sin, Ik-Jae; Sin, Yeong-Min; Park, Heung-Jai; An, Won-Gun;
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 Abstract
Endocrine disrupting compounds (EDC's) are chemicals that either mimic endogenous hormones interfering with pharmacokinetics or act by other mechanisms. Some endocrine disrupters were reported to be chemical substances that cause apoptosis in cells. A number of reports have indicated that 1,3-DCP, one of the EDC's may act as an endocrine disrupter and also has possible carcinogenic effects. 1,3-DCP, present in commercial protein hydrolysates used for human nutrition, are genotoxic and 1,3-dichloro-2-propanol induced tumors in rats. In the present study, it was investigated whether 1,3-DCP induces ROS generation and apotosis in A549 adenocarcinoma cells. Here we show that 1,3-DCP inhibits the growth of lung cancer cell lines and generates reactive oxygen species (ROS), a major cause of DNA damage and genetic instability, It was investigated that 1,3-DCP increases G1 phase cells after 12 hours, thereafter abruptly draws A549 cells to G0 state after 24 hours by flow cytometric analysis. 1,3-DCP induces p53 and activation time- and dose-dependently by 24 hours, while the level was decreased after 48 hours. These results suggest that 1,3-DCP, an EDC's generates ROS and regulates genes involved with cell cycle and apoptosis.
 Keywords
1,3-Dichloro-2-propanol (1,3-DCP);Endocrine disrupting compounds (EDC's);Apoptosis;ROS;P53;P21;
 Language
Korean
 Cited by
 References
1.
Budavari, S., 1989, The Merck index, Merck, Rahway, 3058pp

2.
L'Huillier, N., M. K. Pratten and R. H. Clothier, 2002, The relative embryotoxicity of 1,3-dichloro-2-propanol on primary chick embryonic cells. Toxicol In Vitro., 16(4), 433442 crossref(new window)

3.
Talcott, R. E. and J. King, 1984, Mutagenic impurities in 1,3-dichloropropene preparations. J. Natl. Cancer Inst., 72(5), 1113-1116

4.
Piasecki, A:., A. Ruge and H. Marquardt, 1990, Malignant transformation of mouse M2fibroblasts by glycerol chlorohydrines contained in protein hydrolysates and commercial food, Arzneirnittelforschung, 40(9), 10541055

5.
Shiozaki, T., Y. Mizobata, H. Sugimoto, T. Yoshioka and T. Sugimoto, 1994, Fulminant hepatitis following exposure to dichlorohydrin-report of two cases, Hum. Exp, ToxicoI., 13(4), 267-270 crossref(new window)

6.
Hahn, H., E. Eder and C. Deininger, 1991, Genotoxicity of 1,3-dichloro-2-propanol in the SOS chromotest and in the Ames test. Elucidation of the genotoxic mechanism, Chern. BioI. Interact., 80(1), 73-88 crossref(new window)

7.
Omura, M., M. Hirata, M. Zhao, A. Tanaka and N. Inoue, 1995, Comparative testicular toxicities of two isomers of dichloropropanol, 2,3-dichloro-l-propanol, and 1,3-dichloro-2propanol, and their metabolites alpha-chlorohydrin and epichlorohydrin, and the potent testicular toxicant 1,2-dibromo-3-chloropropane. Bull. Environ. Contam. Toxicol., 55(1), 1-7 crossref(new window)

8.
Katoh, T., J Haratake, S. Nakano, M. Kikuchi, M. Yoshikawa and K. Arashidani, 1998, Dosedependent effects of dichloropropanol on liver histology and lipid peroxidation in rats. Ind. Health, 36(4), 318-323 crossref(new window)

9.
Ellis, R. E., J. Y. Yuan and H. R. Horvitz, 1991, Mechanisms and functions of cell death. Annu. Rev. Cell BioI., 7, 663-698 crossref(new window)

10.
Shimizu, T., C.X., Cao, RG. Shao and Y. Pommier, 1998, Larnin B phosphorylation by protein kinase calpha and proteolysis during apoptosis in human leukemia HL60 cells. J BioI. Chern., 273(5), 8669-8674 crossref(new window)

11.
Green, D. and G. Kroemer, 1998, The central executioners of apoptosis: caspases or mitochondria? Trends Cell BioI., 8(7), 267-271 crossref(new window)

12.
Liu, X. M., J. Z. Shao, L. X. Xiang and X. Y. Chen, 2006, Cytotoxic effects and apoptosis induction of atrazine in a grass carp (Ctenopharyngodon idellus) cell line. Environ. Toxicol., 21(1), 80-89 crossref(new window)

13.
Chen, T. J, J Y. Jeng, C. W. Lin, C. Y. Wu and Y. C. Chen, 2006, Quercetin inhibition of ROS-dependent and -independent apoptosis in rat glioma C6 cells, Toxicology, 223(1-2), 113-126 crossref(new window)

14.
Martirosyan, A., S. Leonard, X. Shi, B. Griffith, P. Gannett and J Strobl, 2006, Actions of a histone deacetylase inhibitor NSC3852 (5-nitroso-8-quinolinoI) link reactive oxygen species to cell differentiation and apoptosis in MCF-7 human mammary tumor cells, J Pharmacal. Exp. Ther., 317(2), 546-552 crossref(new window)

15.
Pathak, N. and S. Khandelwal, 2006, Oxidative stress and apoptotic changes in murine splenocytes exposed to cadmium. Toxicology, 220(1), 26-36 crossref(new window)

16.
Bargonetti, J and J. J. Manfredi, Multiple roles of the tumor suppressor p.53, Curro Opin, Oncol., 14(1), 86-91

17.
Choisy-Rossi, C., P. Reisdorf and E. YonishRouach, 1998, Mechanisms of p.53- induced apoptosis: in search of genes which are regulated during p.53-mediated cell death. Toxicol. Lett., 102-103, 491-496

18.
Hansen, R. and M. Oren, 1997, p.53: from inductive signal to cellular effect. Curro Opin. Genet. Dev., 7(1), 46-51 crossref(new window)

19.
Blagosklonny, M. V., 2002, P53: an ubiquitous target of anticancer drugs. Int. J. Cancer, 98(2), 161-166 crossref(new window)

20.
Romano, M. F., R. Avellino, A. Petrella, R. Bisogni, S. Romano and S. Venuta, 2004, Rapamycin inhibits doxorubicin-induced NFkappaB/Rel nuclear activity and enhances the apoptosis of melanoma cells, Eur. J. Cancer, 40(18), 2829-2836 crossref(new window)

21.
Soengas, M. S., R. M. Alarcon, H. Yoshida, A. J. Giaccia, R. Hakem, T. W. Mak and S. W. Lowe, 1999, Apaf-1 and caspase-9 in p.53- dependent apoptosis and tumor inhibition. Science, 284(5411), 156-159 crossref(new window)

22.
Gao, C. and N. Tsuchida, 1999, Activation of caspases in p.53-induced transactivation-independent apoptosis. Jpn. J. Cancer Res., 90(2), 180-187 crossref(new window)

23.
Fisher, D. E., 1994, Apoptosis in cancer therapy: crossing the threshold. Cell, 78(4), 539542 crossref(new window)

24.
Wang, S. and W. S. El-Deiry, 2004, The p.53 pathway: targets for the development of novel cancer therapeutics. Cancer Treat. Res., 119, 175-187 crossref(new window)

25.
Roninson, I. B., 2002, Oncogenic functions of tumour suppressor p.2(Wafl/Cipl/ Sdil): association with cell senescence and tumour-promoting activities of stromal fibroblasts. Cancer Lett., 179(1), 1-14 crossref(new window)

26.
Dumont, P., M. Burton, Q. M. Chen, E. S. Gonos, C. Frippiat, J.B. Mazarati, F. Eliaers, J. Remade and O. Toussaint, 2000, Induction of replicative senescence biomarkers by sublethal oxidative stresses in normal human fibroblast. Free Radic. Biol. Med., 28(3), 361-373 crossref(new window)

27.
Morisaki, H., A. Ando, Y. Nagata, O. PereiraSmith, J.R. Smith, K Ikeda and M. Nakanishi, 1999, Complex mechanisms underlying impaired activation of Cdk4 and Cdk2 in replicative senescence: roles of p16, p21, and cydin D1. Exp. Cell Res., 253(2), 503-510 crossref(new window)

28.
Hattangadi, D. K, G. A. DeMasters, T. D. Walker, K R. Jones, X. Di, IF. Newsham and D. A. Gewirtz, 2004, Influence of p.53 and caspase 3 activity on cell death and senescence in response to methotrexate in the breast tumor cell. Biochem. Pharmacol., 68(9), 1699-1708 crossref(new window)

29.
Choisy-Rossi, C., P. Reisdorf and E. YonishRouach, 1998, Mechanisms of p.53- induced apoptosis: in search of genes which are regulated during p.53-meeliated cell death. Toxico.l Lett., 102-103, 491-496

30.
el-Deiry, W. S., T. Tokino, V. E. Velculescu, D. B. Levy, R. Parsons, J. M. Trent, D. Lin, W. E. Mercer, K.W. Kinzler and B. Vogelstein, 1993, WAFl, a potential mediator of p.53 tumor suppression. Cell, 75(4), 817-825 crossref(new window)