Investigation of Possible Genotoxic and Cytotoxic Effects of Differential Boron Compounds in CCL 62 (Hela Contaminant) Human Amniotic Ephitelial Cell Line
Epidemiyolojik ve in vitro çalışmalarında bor bileşiklerinin anti karsinojenik olabilecekleri gösterilmiştir. Sitogenetik yönden stabil olan hücre hatlarında kromozom aberasyonları, kardeş kromatit değişimi gibi testlerle yapılan çalışmalarda borun herhangi bir genotoksik etkisi ortaya konulmamıştır. Bu çalışmada ise farklı bor bileşikleri olan BA (borik asit), BP (boraks pentahidrat) ve DPD (disodyum pentaborat dekahidrat)’ ın 250, 500 ve 1000µM dozlarında uygulanmasıyla, sitogenetik olarak stabil olmayan CCL 62 (He La kontaminant) hücre hattındaki arında var olan sitogenetik bozulma üzerine olan etkilerinin araştırılması amaçlanmıştır. Bu amaçla hücre hatlarına bor bileşikleri uygulamasını takiben sitotoksisite için hücre canlılık testi (MTT) ve genotoksisite için kromozom aberasyonu (KA) ve mikroçekirdek (MÇ) testleri uygulanmış ve bor bileşiklerinin her bir dozunda meydana gelen KA’larının ve MÇ’lerin frekansları hesaplanmıştır. Tür, doz ve süreye bağlı olarak bor bileşiklerinin CCL-62 (insan amniyotik epitelyal) hücre hatlarının proliferasyonunu etkilediği görülmüştür. KA ve MÇ analizi verilerine göre ise; herhangi bir bor bileşiği uygulanmayan kontrol grubu hücrelerle, bor bileşikleri uygulanan hücrelerin KA ve MÇ sayıları karşılaştırıldığında kontrol grubu ve bor bileşiklerinin uygulandığı gruplar arasında anlamlı fark saptanamamıştır (p>0,05). Sonuç olarak bileşik türü, doz ve süreye bağlı olarak BA, BP ve DPD’ nin CCL 62 hücre hatlarının proliferasyonunu etkilediği, diğer taraftan bu hücre hatlarında var olan sitogenetik bozulma üzerine arttırıcı ya da azaltıcı bir etkisi olmadığı gösterilmiştir.
Investigation of Possible Genotoxic and Cytotoxic Effects of Differential Boron Compounds in CCL 62 (Hela Contaminant) Human Amniotic Ephitelial Cell Line
Epidemiological and in vitro studies have showed that boron may have anti-carcinogenic properties. Chromosome aberrations assay and sister chromatid exchange assays have showed that boron has no genotoxic effects on cytogenetically stable cell lines. Aim of this investigation is determine to effects of different boron compounds which are boric acid (BA), borax pentahydrate (BP) and disodium pentaborate decahydrate (DPD) ) on exist cytogenetic disruption with variable doses (250, 500 and 1000µM ) on cytogenitically unstabel CCL 62 (HeLa Contaminant) cell line. In order to test this hypothesis, following the boron treatment on the cell lines for cytotoxcity was performed using MTT that cell viability assay. For genotoxicity was used chromosome aberrations assay (CAs) and micronucleus assay (MN), CAs and MN frequency calculated in each boron dose. Boron compaunds effected proliferation of CCL 62 (human amniotic ephitelial) cell lines in a time, species and dose dependent manner. According to data obtained from CAs and MN assays, no significant difference was found between control groups which were not treated any of boron compaund with boron treated groups (p>0,05). In conclusion, we established that BA, BP, and DPD effected proliferation of CCL 62 cell lines in a time, compaund and dose dependent manner, however no evidence was observed suggesting these compounds cause an increase or decrease in the level of existing cytogenetic defects in these cell lines.
___
- IPCS Environmental Health Criteria for Boron, vol. 204. World Health Organization, Geneva, 1998.
- U.S.EPA. Toxicology review of boron and compounds in support of information on integrated risk information (IRIS). National Center for Environmental Assessment, Washington DC, 200 Erişim: [http://www.epa.gov/iris ]. ECETOC Technical Report, Reproductive and general toxicology of some inorganic borates and risks assessment for human beings. European Centre for Ecotoxicology and Toxicology of Chemicals, No. 63, Brussels, Belgium, 1995. Dieter MP. Toxicity and carcinogenicity studies of boric acid in male and female B6C3Fl Mice. Environ Health Perspect. 1994;102(Suppl. 7):93-7.
- Uçkun Z. Bor maruziyetinin insanlar üzerindeki genotoksik etkilerinin araştırılması. Ankara Üniversitesi, Sağlık Bilimleri Enstitüsü, Yüksek Lisans Tezi, 2006.
- Türkez H. Bazı bor bileşiklerinin in vitro şartlarda periferal insan kanı üzerine genetik ve biyokimyasal etkileri. Atatürk Üniversitesi Fen Bilimleri Enstitüsü, Doktora Tezi, 2007.
- Barranco WT, Hudak PF, Eckhert CD. Evaluation of ecological and in vitro effects of boron on prostate cancer risk (United States). Cancer Causes Control. 2007;18:71–7.
- Park M, Li Q, Shcheynikov N, Muallem S, Zeng W. Borate transport and cell growth and proliferation. Cell Cycle. 2005;4:24-6.
- Gallardo-Williams MT, Maronpot RR, Wine RN, Brunssen SH, Chapin RE. Inhibition of the enzymatic activity of prostate-specific antigen by boric acid and 3-nitrophenyl boronicacid. The Prostate. 2003;54:44-9.
- Barranco WT, Eckhert CD. Boric acid inhibits human prostate cancer cell proliferation. Cancer Letters. 2004;216;21–9.
- Mahabir S, Spitz MR, Barrera SL, Dong YQ, Eastham C, Forman MR. Dietary boron and hormone replacement therapy as risk factors for lung cancer in women. Am J Epidemiol. 2008;167:1070–80.
- Korkmaz M, Uzgören E, Bakırdere S, Aydın F, Ataman OY. Effects of dietary boron on cervical cytopathology and on micronucleus frequency in exfoliated buccal cells. Environ Toxicol. 2007;22:17–25.
- Fenech M. The in vitro micronucleus technique. Mutat Res. 2000;455:81–95.
- Freshney RI. Culture of Animal Cells: A Manual of Basic Technique. 5th ed. John Wiley & Sons, Inc, New Jersey, 2005;262-3.
- Hunt CD, Boron. In: Macrae, R, Robinson RK, Sadler MJ, eds, Encyclopedia of Food Science, Food Technology and Nutrition. London: Academic Press. 1993;440–7.
- Geyikoğlu F, Türkez H. Boron compounds reduce vanadium tetraoxide genotoxicity in human lymphocytes. Environ Toxicol Pharmacol. 2008;26:342
- Park M, Li Q, Shcheynikov N, Zeng W, Muallem S. NaBC1 is a ubiquitous electrogenic Na+-Coupled borate transporter essential for cellular boron homeostasis and cell growth and proliferation. Mol Cell. 2004;16:331-41.
- Henderson K, Stella SL, Kobylewski S, Eckhert CD. Receptor activated Ca2+ release is inhibited by boric acid in prostate cancer cells. Plos One. 2009;4(6):e6009.
- Müezzinoğlu T, Korkmaz M, Neşe N, Bakırdere S, Arslan Y, Ataman OY, Lekili M. Prevalence of prostate cancer in high boron-exposed population: a community-based study. Biological Trace Element Research. 2011;144(13):49-57.