Risk Assessment of Food Coloring Agents on DNA Damage Using RAPD Markers

Risk Assessment of Food Coloring Agents on DNA Damage Using RAPD Markers

In this study, faba bean (Vicia faba) seedlings were used as bioindicator to determine genotoxic effect of synthetic dyes currentlyused as food color additives in many countries.Novel short-term assays are required to substantiate the batteryof assessment methods for evaluating the genotoxicity of candidate substances. Therefore, an attempt has been made to evaluate randomlyamplified polymorphic DNA (RAPD) analysis for its potentialto establish genotoxic effect of colored food. For the preliminary assessment, this study compared the effects occurring at molecular levels in Vicia faba exposed to colored food at concentrations inthe range of 0.2% to 18.2% . The qualitative modifications arising in random amplified polymorphic DNA (RAPD)profiles as a measure of DNA effects were compared with control. Results suggested thattreatments of the above test food samples reflectingchanges in RAPD profiles. Changes in RAPD patterns included variation in band intensity; loss of normal bands and appearance of new bands compared with control. These results indicated that DNA polymorphisms detected by RAPD analysis could be used as an investigation tool for environmental toxicology and as a useful biomarker assay for the detection of genotoxic effects of food dyes. In conclusion, the measurementof parameters at molecular levels is valuablefor investigating the specific effects of agents interactingwith DNA. Ultimately, this methodology may allow the ecotoxicologicalexamination of the link between molecular alterations and measurableadverse effects at higher levels of biological organization

___

  • [1] V. K. Macioszek and A.K. Kononowicz 2004. The evaluation of the genotoxicity of two commonly used food colors; Quinoline Yellow (E104) and Brilliant Black BN (E151). Cellular an d molecular Biology letters 9: 107-122.
  • [2] R. Kroes and G. Kozianowski 2002. Threshold of Toxicological Concern in Food Safety Assessment. Toxicology Letters 127(1-3):43-6,
  • [3] A. Das and A. Mukherjee 2004. Genotoxicity Testing of the Food Colours Amaranth and Tartrazine. Int J Hum Genet, 4(4): 277-280).
  • [4] S. Tsuda, M. Murakami, N. Matsusaka, K. Kano, K .Taniguchi and Y.F.Sasaki 2001. DNA Damage Induced by Red Food Dyes Orally Administered to Pregnant and Male Mice Toxicological Sciences 61, 92-99.
  • [5] E. Zeiger 1993. Mutagenicity of chemicals added to foods. Mutat. Res. 290 ,53-61.
  • [6] G.A. LeBlanc and L. Bain (1997). Chronic toxicity of environmental contaminants: sentinels and biomarkers. Environ. Health Perspect., 105, 65–80.
  • [7] OECD (1998). Mammalian erythrocyte micronucleus test. no. 474. In Addenum to OCDE Guidelines for Testing Chemicals 1998. OCDE, France.
  • [8] Y.F. Sasaki, S. Kawaguchi, A. Kamaya, M. Ohshita, K. Kabasawa and K. Iwama, 2002. The comet assay with 8 mouse organs: results with 39 currently used food additives .Mutat Res, 519: 103-109.
  • [9] F. A. Atienzar, V. V. Cheung, A. N. Jha and M. H. Depledge 2001. Fitness Parameters and DNA Effects are Sensitive Indicators of Copper-Induced Toxicity in Daphnia magna . Toxicological Sciences 59, 241- 250 .
  • [10] S.S. Sandhu, F.J. Serres, H.N. Goplan, et al., 1994. Environmental Monitoring for genotoxicity with plant systems. Results and recommendations. Mutat. Res. 310 : 257-263.
  • [11] J.J. Doyle and J.L. Doyle (1990). Isolation of plant DNA from fresh tissue. Focus, 12:13-15.
  • [12] J.Williams, A.R. Kubelik, J.K. Livak, J.A. Rafalski and S.V. Tingey, 1990. DNA polymorphism amplified by arbitrary primers are useful as genetic markers. Nucleic Acids Res., 18: 6535.
  • [13] J. Sambrook , E.F. Fritsch and T. Maniatis (1989). Molecular cloning: a laboratory manual. Cold Spring Harbor, New York.
  • [14] C. Becerril, M. Ferrero and A. Castaño 2002. Detection by RAPD of genetic alterations in vitro: Amplification and Conservation conditions of DNA extracts. Toxicology Mechanisms and Methods , 12 ( 2), 155-167.
  • [15] E. Tuormaa, 1994. The adverse effects of food Additives on health (Booklet). Journal of Orthomolecular Medicine, 9 (4):225- 243.
  • [16] O. Danylchenko and B. Sorochinsky 2005. Use of RAPD assay for the detection of mutation changes in plant DNA induced by UV-B and γ-rays. BMC Plant Biol; 5(1): S9.
  • [17] B. S. Selvi , V. Ponnuswami and T. Sumathi 2007. Identification of DNA Polymorphism induced by Gamma Ray Irradiation in Amla (Emblica Officinalis Gaertn.) Grafts of V M and V M Generation. Journal of Applied Sciences Research, 3(12): 1933-1935.
  • [18] W. Liu, Y.S. Yang, P.J. Li, Q.X. Zhou, L.J. Xie and Y.P. Han. 2008. Risk assessment of cadmiumcontaminated soil on plant DNA damage using RAPD and physiological indices. Hazard Mate r. 18
  • [19] R. D. Combes and R. B. Haveland-Smith 1982. A review of the genotoxicity of food, drug and cosmetic colours and other azo, triphenylmethane and xanthene dyes. Mutat Res, 98: 101-248.
  • [20] A.K. Giri 1991. Food dyes in India: mutagenic and clastogenic potentials- A review. Proc Indian Natn Sci Acad, B57: 183-198.
  • [21] F. A. Atienzar, M. Conradi, A. J. Evenden, A. N. Jha, and M. H. Depledge 1999. Qualitative assessment of genotoxicity using random amplified polymorphic DNA: Comparison of genomic template stability with key fitness parameters in Daphnia magna exposed to benzo[a]pyrene. Environ. T oxicol. Chem. 18, 2275– 2282.
  • [22] C. Becerril , M. Ferrero, F. Sanz, and A. Castano 1999. Detection of mitomycin C-induced genetic damage in fish cells by use of RAPD. Mutagenesis 14, 449–456.
  • [23] F. A. Atienzar, B. Cordi, M. E. Donkin, A. J. Evenden, A. N. Jha and M. H. Depledge, 2000a. Comparison of ultraviolet-induced genotoxicity detected by random amplified polymorphic DNA with chlorophyll fluorescence and growth in a marine macroalgae, Palmaria palmata . Aquat. Toxicol. 50, 1–12.
  • [24] H. De Wolfe, R. Blust and T. Backeljau 2004. The use of RAPD in ecotoxicology. Mutat Res. 566(3):249-62.
  • [25] F. A. Atienzar, 2000. Development of the random amplified polymorphic DNA (RAPD) technique to measure the effects of genotoxins in aquatic organisms. Ph.D. T hesis (DXN034438), University of Plymouth, UK.
  • [26] J. R Nelson, C. W. Lawrence and D. C. Hinkle, 1996. Thymine-thymine dimer bypass by yeast DNA polymerase. Science 272, 1646–1649
  • [27] N.S. Srikanth, A. Mudipalli, A.E. Maccubbin and H.L. Gurtoo, (1994). Mutations in a shuttle vector exposed to activated mitomycin C. Mol. Carcinog. , 10, 23–29.
  • [28] A.E. Maccubbin, A. Mudipalli, S.S.Nadadur, N. Ersing, and H.L Gurtoo 1997. Mutations induced in a shuttle vector plasmid exposed to monofunctionally activated mitomycin C. Environ. Mol. Mutagen. , 29, 143–151.
  • [29] L.K. Riesenberg 1996. Homology among RAPD fragments in interspecific comparisons. Mol. Ecol., 5, 99–105.
  • [30] J.Ramser, C.Lopez-Peralta, R.Wetzel, K. Weising, and G. Kahl 1996. Genomic variation and relationships in aerial yam (Dioscores bulbifera L.) detected by ramdon amplified polymorphic DNA. Genome, 39,1725.
  • [31] S. Noel and S. K. Rath 2006. Randomly amplified polymorphic DNA as a tool for genotoxicity: an assessment. Toxicology and Industrial Health,. 22, (6), 267-275.
  • [32] Y. C. Lee, V.C. Yang and T. S. Wang 2007. Use of RAPD to detect sodium arsenite-induced DNA damage in human lymphoblastoid cells. Toxicology 239 108–115.
Journal of Applied Biological Sciences-Cover
  • ISSN: 1307-1130
  • Başlangıç: 2007
  • Yayıncı: Nobel Bilim ve Araştırma Merkezi