Akrilamidin İn-vivo Genotoksisitesi Üzerine Fenolik Bileşiklerden Pelargonidin ve Gallik Asidin Etkileri

Year 2020, Volume: 7 Issue: 1, 9 - 27, 28.06.2020

Pinar Aksu Kılıçle , Abdullah Doğan

Abstract

Akrilamid genotoksik etkili olup, muhtemel karsinojenler arasında sınıflandırılmıştır. Endüstride kullanım alanı olan akrilamid, ayrıca yüksek ısıda pişirilen karbonhidratça zengin gıdalarda bulunmaktadır. Bu çalışmanın amacı, fare kemik iliği hücrelerinde akrilamidin genotoksisitesine karşı pelargonidin ve gallik asitin etkilerini ortaya çıkarmaktır. Akrilamidin genotoksik etkilerini araştırmak amacıyla kromozomal aberasyon, mikronükleus ve mitotik indeks testleri kullanıldı. Araştırmada, akrilamidin genotoksisitesine karşı pelargonidin ve gallik asitin antigenotoksik etkileri aynı yöntemlerle çalışıldı. Araştırma sonucunda Akrilamidin in vivo klastojenik etkisinin olduğu saptandı. Akrilamidin bu spesifik etkisinin doza bağlı olduğu tespit edildi. Araştırmada, Gallik asitin genotoksik ve sitotoksik etkili olmadığı belirlendi. Kromozomal aberasyon, mikronükeus ve mitotik indeks testlerinde Gallik asitin, Akrilamidin neden olduğu genotoksisite frekansında önemli derecede düşüşe neden olduğu gözlendi. Pelargonidin’in genotoksik ve sitotoksik etkileri bulunmadı. Bu araştırmada kullanılan kromozomal aberasyon, mikronükleus, ve mitotoik indeks testleri sonucuna göre, akrilamidin genotoksik ve sitotoksik, gallik asit ve pelergonidin’in ise antigenotoksik etkili olduğu, ayrıca gallik asitin pelargonidin’den daha güçlü antigenotoksik etki gösterdiği saptandı.

Supporting Institution

Kafkas Üniversitesi Bilimsel Araştırma Projeleri Koordinasyon Birimi

Project Number

2010-VF-47

Thanks

*Bu çalışma Kafkas Üniversitesi Bilimsel Araştırma Projeleri Koordinasyon Birimi tarafından Doktora Tez Projesi olarak desteklenmiştir. (Proje Numarası: 2010-VF-47).

Effects of Pelargonidine and Gallic Acid as Phenolic Compounds on In-vivo Genotoxicity of Acrylamide

Abstract

Acrylamide is genotoxic and is classified among possible carcinogens. Acrylamide, which has an area of use in the industry, is also found in carbohydrate-rich foods cooked at high temperatures. The aim of this study is to reveal the effects of pelargonidine and gallic acid against the genotoxic effect of acrylamide in mouse bone marrow cells. Chromosomal aberration, micronucleus and mitotic index tests were used to investigate the genotoxic effects of acrylamide. In addition, the antigenotoxic effect of pelargonidine and gallic acid against the genotoxicity of acrylamide was investigated by same methods. As a result of the research, it was determined that acrylamide had a clastogenic effect in vivo. These acrylamide-specific effects were dose-dependent. In this study, it was determined that gallic acid was not genotoxic and cytotoxic. In chromosomal aberration, micronucleus and mitotic index tests, gallic acid caused a significant decrease in the frequency of genotoxicity caused by acrylamide. The genotoxic and cytotoxic effects of pelargonidine were not found. According to the results of chromosomal aberration, micronucleus, and mitotoic index tests used in this study, acrylamide was found to have a genotoxic and cytotoxic effect, gallic acid and pelergonidine had an antigenotoxic effect, and gallic acid had a stronger antigenotoxic effect than pelargonidine.

Keywords

Acrylamide, Gallic acid, Pelargonidine, Chromosomal aberration, Micronucleus

Project Number

2010-VF-47

References

• Referans1: Abramsson-Zetterberg L. (2003). The dose-response relationship at very low doses of acrylamide is linear in the flow cytometer-based mouse micronucleus assay. Journal of Mutation Research, 535: 215-222.
• Referans2: Adler I. D., Schmid T. E., Baumgartner A. (2002). Induction of aneuploidy in male mouse germ cells detected by the sperm-FISH assay: a review of the presented data base. Mutation Research/Genetic Toxicology and Environmental Mutagenesis, 504, 173-182.
• Referans3: Alzahrani H.A.S. (2011)i Protective effect of l-carnitine against acrylamide-induced DNA damage in somatic and germ cells of mice. Journal of Biological Sciences, 18 (1): 29-36.
• Referans4: Anderson D. (1988). Human biomonitoring. Journal Mutation Research, 204: 353-541.
• Referans5: Besaratinia A., Pfeifer GP. (2005). DNA adduction and mutagenic properties of acrylamide. Journal Mutation Research, 580: 31-40.
• Referans6: Bianchini F.,Vainio H. (2001). Allium vegetables and organosulfur compounds: do they help prevent cancer. Environmental Health Perspectives, 109 (9): 893-902.
• Referans7: Burdurlu H.S., Karadeniz F. (2006). Gıdalarda akrilamid oluşumu ve önemi. Türkiye 9. Gıda Kongresi. 24-26 Mayıs, Bolu.
• Referans8: Cao J., Beisker W., Nüsse M., Adler I.D. (1993). Flow cytometric detection of micronuclei induced by chemicals in poly-and normochromatic erythrocytes of mouse peripheral blood. Mutagenesis, 8 (6): 533-541.
• Referans9: Carrano A.V., Natarajan A.T. (1988). Consideration for population monitoring using cytogenetic techniques. Journal Mutation Research, 204: 379-406.
• Referans10: Claeys W.L., Vleeschouwer K.D., Hendrickx M.E.(2005). Quantifing the formation of carcinogens during food processing acrylamide. Journal of Food Science and Technology, 16, 181-193.
• Referans11: Çelik E., Çelik G.Y. (2007). Bitki uçucu yağlarının antimikrobiyal özellikleri. Orlab On-Line Mikrobiyoloji Dergisi, 5 (2): 1-6.
• Referans12: Delazar A., Çelik S., Göktürk R.S., Ünal O., Nahar L., Sarker S.D. (2005). Two acylated flavonoid glycosides from stachys bombycina, and their free radical scavenging activity. Journal of Pharmazie, 60 (11): 878-880.
• Referans13: Dobrzyńska M., Lenarczyk M., Gajewski A.K. (1990). Induction of dominant lethal mutations by combines X-ray-acrylamide treatment in male mice. Mutation Research/Genetic Toxicology and Environmental Mutagenesis, 232 ( 2): 209-215.
• Referans14: Fenech M., Crott W.J. (2002). Micronuclei, nucleoplasmic bridges and nuclear buds induced in folic acid deficient human lymphocytes-evidence for breakage-fusion-bridge cycles in the cytokinesis-block micronucleus assay. Journal Mutation Research, 504: 131-136.
• Referans15: Hagmar L., Brogger A., Hansteen I.L., Heim S., Högstedt B., Knudaen L., Lambert B., Linnainmaa K., Mitelman F., Nordenson I., Reuterwall C., Salomaa S., Skerfving S., Sorsa M. (1994). Cancer risk in human predicted by increased levels of chromosomal aberrations in lymphocytes: Nordic study group on the health risk of chromosome damage. Journal of Cancer Research, 54: 2919-2922.
• Referans16: Háznagy-Radnaı E., Czıgle S., Zupkó I., Falkay G., and Máthe I. (2006). Comparison of antioxidant activity in enzyme-independent system of six stachys species. Fitoterapia, 77 (8): 521-524.
• Referans17: Heddle J.A., Cimino M.C., Hayashi M., Romagna F., Shelby M.D., Tucker J.D., Vanparys P., Mac Gregor J.T. (1991). Micronuclei as an index of cytogenetic damage: Past, present, and future. Journal of Environmental and Molecular Mutagenesis, 18: 277-291.
• Referans18: Hollman P.C.H., Hertog M.G.L., Katan M.B. (1996). Analysis and health effects of flavonoids. Journal Food Chemistry, 57: 43-46.
• Referans19: IARC (1997). (International Agency for Research on Cancer) : IARC Monographs on the evaluation of carcinogenic risks to humans, Volume 60: Some Industrial Chemicals, Geneva, Switzerland. 389-433.
• Referans20: Khanum F., Anilakumar KR., Viswanathan KR. (2004). Anticarcinogenic properties of garlic: a review. Critical Reviews in Food Science and Nutrition, 44 (6): 479-488.
• Referans21: Kukıć J., Petrović S., Niketic M. (2006). Antioxidant activity of four endemic stachys taxa. Biological and Pharmaceutical Bulletin, 29 (4): 725-729.
• Referans22: LoPachin RM., Canady RA. (2004). Acrylamide toxicities and food safety: Session IV Summary and Research Needs. NeuroToxicology, 25: 507-509.
• Referans23: Matkowski A., Piotrowska M. (2006). Antioxidant and free radical scavenging activities of some medicinal plants from the Lamiaceae. Fitoterapia, 77, 346-353.
• Referans24: Mei N., Hu J., Churchwell M.I., Guo L., Moore M.M., Doerge D.R., Chen T. (2008). Genotoxiceffects of acrylamide and glycidamide in mouse lymphoma cells. Food and Chemical Toxicology, 46 (2): 628-636.
• Referans25: Mottram D.S., Wedzicha B.L., Dodson A.T. (2002). Acrylamide is formed in the maillard reaction. Nature, 419, 448-449.
• Referans26: Okur Ö.D., Seydim Z.G. (2004). Gıdalarda ısıl işlem sonucunda oluşan kanserojen ve mutajen maddeler. Süleyman Demirel Üniversitesi Fen Bilimleri Enstitüsü Dergisi, 8-3, 80-85.
• Referans27: Padma V.V., Sowmya P., Arun Felix T., Baskaran R., Poornima P. (2011). Protective effect of gallic acid against lindane induced toxicity in experimental rats. Food and Chemical Toxicology, 49 (4): 991-998.
• Referans28: Paulsson B., Grawe J., Törnqvist, M. (2002). Hemoglobin adducts and micronucleus frequencies in mouse and rat after acrylamide or N-methylolacrylamide treatment. Mutation Research-Genetic Toxicology And Environmental Mutagenesis, 516 (1-2): 101-111.
• Referans29: Preston R.J., Dean B.J., Galloway S., Holden H., McFee A. F., Shelby M. (1987). Mammalian in vivo cytogenetic assays Anaylsis of chromosome aberrations in bone marrow cells. Journal Mutation Research. 189:157-165.
• Referans30: Roy M., Sen S., Chakraborti A.S. (2008). Action of pelargonidin on hyperglycemia and oxidative damage in diabetic rats: Implication for glycation-induced hemoglobin modification. Journal of Life Sciences, 82, (21-22): 1102-1110.
• Referans31: Schmid W. (1975). The micronucleus test. Journal Mutation Research, 31:9-15.
• Referans32: Sowjanya B.L., Devi K.R., Madhavi D. (2009). Modulatory effects of garlic extract against the cyclophosphamide induced genotoxicity in human lymphocytes in vitro. Journal of Environmental Biology, 30 (5): 663-666.
• Referans33: Stadler R.H., Blank I., Varga N., Robert F., Hau J., Guy,P.A., Robert M.C., Riediker S. (2002). Acrylamide from maillard reaction products. Nature, 419, 449-450.
• Referans34: Titenko-Holland N., Ahlborn T., Lowe X., Shang N., Smith M.T., Wyrobek A.J. (1998). Micronuclei and developmental abnormalities in 4-day Mouse embryos after paternal treatment with acrylamide. Environmental and Molecular Mutagenesis, 31, 206-217.
• Referans35: Tucker J.D., Auletta A., Cimino M.C., Dearfıeld K.L., Jacobsonkram D., Tice R.R., Carrano A.V. (1993). Sister-Chromatid Exchange: Second Report of the Gene-Tox Program. Journal Mutation Research. 297: 101-180.
• Referans36: Von Mühlendahl K.E., Otto M. (2003). Acrylamide: more than just another food toxicant. Journal of Pediatrics, 162: 447-448.
• Referans37: Yang H.J., Lee S.H., Jin Y., Choi J.H., Han C,H., Lee M.H. (2005). Genotoxicity and toxicological effects of acrylamide on reproductive system in male rats. Journal of Veterinary Science, 6 (2): 103-109.
• Referans38: Yener Y., Dikmenli M. (2009). Increased micronucleus frequency in rat bone marrow after acrylamide treatment. Food and Chemical Toxicology, 47 (8): 2120-2123.