Genotoxic damage induced by extracts of peach, Prunus persica grown in Cácota Norte de Santander
Abstract
Peach Production in Colombia is concentrated in the departments of Boyacá, Cundinamarca, Norte de Santander, Santander, Antioquia, Caldas and Nariño, the main producer is Boyacá with 677 ha, especially in the municipality of Sotaquirá and in other municipalities such as Jenesano, Nuevo Colón, Combita and Tuta; the third production department is Norte de Santander with 480 Ha. Currently the production is concentrated mainly in the municipalities of Chitagá, Pamplonita and Cacota. Pesticides are considered one of the main factors of environmental pollution; As it is known they are widely used to improve the production of food in agriculture and for the control of pests and disease vectors, many have been classified as carcinogenic, because they induce damage to the genetic material. In this work the genotoxicity produced by extracts of peach (Prunus pérsica (L.) Batsch) cultivated in Cacota, Norte de Santander was determined. The comet assay was used for the evaluation of gemoxic activity. The results obtained indicate that the peach extracts induce lesions in the DNA of human lymphocytes, which vary according to the dose of the extract. Considering that the peach is an export product and high consumption in our region, the intake of this could become a risk factor for the population.Keywords
Peach, genotoxicity, comet assay, pesticides, Cácota, Norte de Santander, Colombia.
References
[1] Carranza C., Miranda D. Zonificación actual de los sistemas de producción de frutales caducifolios en Colombia. Situación actual, sistemas de cultivo y plan de desarrollo. Soc. Col. Cienc. Hort. 2013; 67-86.
[2] Xiang Guanggang, Li Diqiu, Yuan Jian- zhong, Guan Jingmin, Zhai Huifeng, Shi Mingan, Tao Liming. Carbamate insecticide methomyl confers cytotoxicity through DNA damage induction. Food and Chemical toxicology. 2013; 53: 352-358.
[3] Bolognesi C., Peluso M., Degan P., Rabboni R., Munnia A., Abbondandolo A. Genotoxic effects of the carbamate insecticide, methyo- myl. II. In vivo studies with pure compound and the technical formulation, “Lannate 25” Environmental and Molécular Mutagenesis. 1994; 235–242.
[4] Falck GC, Hirvonen A., Scarpato R., Saari- koski ST, Migliore L, Norppa H. Micronucleic in blood lymphocytes and genetic poly- morphism for GSTM1, GSTT1 and NAT2 in pesticide-exposed greenhouse workers Mutation Research. 1991; 441: 225–237.
[5] Sun XY, Jin YT, Wu B, Wang WQ, Pang XL, Wang J. Study on genotoxicity of aldicarb and methomyl. Huan Jing Ke Xue .2010; 31: 2973–2980.
[6] Pabuena Duban E., Ortiz Isabel C., López Juan, Orozco Luz J., Quijano Parra Alfonso, Pardo Enrique, Meléndez Iván. Actividad genotóxica inducida por extracto de fresa fumigada con pesticidas en Pamplona, Norte de Santander, Colombia. Universidad, Ciencia y Tecnología. 2015; 19: 76.
[7] Simoniello, M.F.; Kleinsorge, E.C.; Scag- netti, J.A.; Grigolato, R.A.; Poletta, G.L. y Carballo, M.A., 2008. DNA damage in workers occupationally exposed to pesticide mixtures. J. Appl. Toxicol. 28, 8: 957-965.
[8] Haibing Li, Yuling Li, Jing Cheng. Mo- lécularly Imprinted Silica Nanospheres Embedded CdSe Quantum Dots for Highly Selective and Sensitive Optosensing of Pyrethroids. Central China Normal Univer- sity, China. 2010; 22: 2451–2457.
[9] Oudou HC, Alonso RM, Bruun Hansen HC. Voltammetric behaviour of the synthetic pyrethroid lambda-cyhalothrin and its de- termination in soil and well water. Analytica chemical Acta 2004; 523: 69–74.
[10] Idris S, Ambali S., Ayo J. Cytotoxicity of chlorpyrifos and cypermethrin: the ameliorative effects of antioxidants. Afr J Biotechnol. 2012; 11 (99): 16461-16467.
[11] Collins AR, Dobson VL., Dusinska M., Kennedy G, Stetina R. The comet assay: what can it really tell us.Mutat. 1997; 375 : 183–193.
[12] Meléndez I., Pedro E., Quijano A. Actividad genotóxica de aguas antes y después de clorar en la planta de potabilización Empo- pamplona. Bistua:Revista de la Facultad de Ciencias Básicas.2015.13(2):12-23.
[13] Meléndez Gélvez I., Martínez Montañez ML, Quijano Parra A. Actividad mutagénica y genotóxica en el material particulado fracción respirable MP2,5 en Pamplona, Norte de Santander, Colombia. Iatreia. 2012; 25 (4): 347-356.
[14] Vargas V., Migliavacca S., Melo A., Horn R. Genotoxicity assessment in aquatic environments under the influence of heavy metals and organic contaminants. Mut.2001; 490: 141-158.
[15] Bull S., Fletcher K., Boobis AR, Battershill JM, Evidence for genotoxicity of pesticides in pesticide applicators: a review. Mutagen- esis, 2006; 21 (2): 93-103.
[16] Bertoncini CR, Meneghini R. DNA strand breaks produced by oxidative stress in mam- malian cells exhibit 3′-phosphoglycolate ter- mini Nucleic Acids. 1995; 23: 2995–3002.
[17] Shrivastava R, Upreti RK, Seth PK, Chatur- vedi UC. Effects of chromium on the immune system FEMS Immunol. Med. Microbiol. 2002; 34 (1): 1–7.
[18] Nesnow S., Roop BC, Lambert G., Kadiiska M., Mason RP, Cullen W.R, Mass MJ. DNA damage induced by methylated trivalent arsenicals is mediated by reactive oxygen species. Chemical Research Toxicology. 2002; 15: 1627–1634.
[19] Basu A, Ghosh P, Das JK, Banerjee A, Ray K, Giri AK. Micronuclei as biomarkers of carcinogen exposure in populations exposed to arsenic through drinking water in West Bengal, India: a comparative study in three cell types. Cancer Epidemiology Biomarkers and Prevention. 2004; 13: 820–827.
[20] Mahata J., Basu A., Ghoshal S., Sarkar JN, Roy AK, Poddar G., Nandy AK, Banerjee A., Ray K., Natarajan AT, Nilsson R, Giri AK. Chromosomal aberrations and sister chromatid exchanges in individuals exposed to arsenic through drinking water in West Bengal, India. Mutation Research. 2003; 534: 133–143.
[21] Ling YH, Jiang JD, Holland JF, Perez Soler R. Arsenic trioxide polymerization of mi- crotubules and mitotic arrest before apop- tosis in human tumor cell lines Molécular Pharmacology. 2002; 62: 529–538.
[22] Nesnow S., Roop BC, Lambert G., Kadiiska M., Mason RP, Cullen WR, Mass MJ. DNA damage induced by methylated trivalent arsenicals is mediated by reactive oxygen species. Chemical Research Toxicology. 2002; 15: 1627–1634.
[23] Antherieu S., Ledirac N., Luzy AP., Lenor- mand P., Caron JC, Rahmani R. Endosulfan decreases cell growth and apoptosis in hu- man HaCaT keratinocytes: Partial ROS-de- pendent ERK1/2 mechanism. J Cell Physiol. 2007; 213: 177-86.
[24] Chaudhuri K, Selvaraj S, Pal AK. Studies on the genotoxicity of endosulfan in bacterial systems.1999. Mutat Res 439 (1): 63-7.
[25] IARC. 1987. Hexachlorocyclohexanes. In Overall Evaluations of Carcinogenicity. IARC Monographs on the Evaluation of Carcinogenic Risk of Chemicals to Humans, suppl. 7. Lyon, France: International Agency for Research on Cancer.pp. 220-222.
[26] Schulte-Hermann R, Parzefall W. 1981. Failure to discriminate initiation from promotion of liver tumors in a long-term study with the phenobarbital-type inducer alpha-hexachlorocyclohexane and the role of sustained stimulation of hepatic growth and monooxygenases. Cancer Res 41(10): 4140-4146
[27] Ecobicon, D.J. Toxic effects of pesticides. In: Klaassen et al. (eds). Casarett and Doull’s Toxicology: The basic science of poisons, 4th ed. New York: Maxwell McMillan Per- gamon; 1991:573-580
[28] 132. Volpe, E., Sambucci, M., Battistini, L., Borsellino, G., 2016. Fas-Fas ligand: checkpoint of T cell functions in multiple sclerosis. Front. Immunol. 7, 382.
[29] Wei, J., Zhang, L., Ren, L., Zhang, J., Yu, Y.,Wang, J., Duan, J., Peng, C., Sun, Z., Zhou,X., 2017. Endosulfan inhibits prolifer- ation through the Notch signaling Path way in human umbilical vein endothelial cells. Environ. Pollut. 221, 26–36.
[30] Chen, Z.Y., Liu, C., Lu, Y.H., Yang, L.L., Li, M., He, M.D., et al., 2016. Cadmium exposure enhances bisphenol A-induced genotoxicity through 8-oxoguanine-DNA glycosylase-1 OGG1 inhibition in NIH3T3 fibroblast cells. Cell. Physiol. Biochem. 39, 961–974.
[31] Sebastian, R., Raghavan, S.C., 2016. Induc- tion of DNA damage and erroneous repair can explain genomic instability caused by Endosulfan.
[32] Palou, R., Palou, G., Quintana, D.G., 2016. A role for the spindle assembly checkpoint in the DNA damage response. Curr. Genet
[33] Wei, J., Zhang, L., Wang, J., Guo, F., Li, Y., Zhou, X., Sun, Z., 2015. Endosulfan inducing blood hypercoagulability and endothelial cells apoptosis via the death re- ceptor pathway in Wistar rats. Toxicol. Res. 4, 1282–1288