Effect of pollution represented by Polycyclic Aromatic Hydrocarbons on the levels of p53 and some antioxidant enzymes in Baghdad traffic police
Keywords:PAHs, p53 tumor protein, Catalase, G-Px, DNA
Objectives: To ascertain the protective effect of p53 tumor protein by monitoring its levels in comparison with the levels of antioxidant enzymes, against any type of cancer that can be caused by chronic exposure of traffic policemen to air pollutants.
Methods: This study comprises 140 participants, who have been divided into two groups (Traffic police and Office police). PAHs were analyzed for each participant by GC/FID while p53 protein and antioxidant enzymes were measured by the ELISA technique.
Results: The concentrations of polycyclic aromatic hydrocarbons and p53 tumor protein were high in the blood of traffic police compared to office police, while higher levels of antioxidant enzymes (Catalase and G-Px) were observed in the blood of office police.
Conclusion: Exposure to PAHs can cause oxidative stress, which can damage DNA and lead to cancer. However, because natural endogenous biomolecules like p53 protein can neutralize PAHs' carcinogenic effects, their elevation has a beneficial anti-cancer effect by reducing oxidative stress and preventing tumorigenesis.
Miller, M. R., (2020) . Oxidative stress and the cardiovascular effects of air pollution . Free radical biology and medicine , 151 : 69–87.
Brook, R. D., Rajagopalan, S., Pope, C. A., 3rd, Brook, J. R., Bhatnagar, A., Diez-Roux, A. V., and et. al. (2010). Particulate matter air pollution and cardiovascular disease: An update to the scientific statement from the American Heart Association. Circulation, 121 (21) : 2331–2378.
Liu, C., Zhang, Y., and Weschler, C. J. (2014). The impact of mass transfer limitations on size distributions of particle associated SVOCs in outdoor and indoor environments. The Science of the total environment, 497-498 : 401–411.
Andersen, Z. J., Pedersen, M., Weinmayr, G., Stafoggia, M., Galassi, C., Jørgensen, J. T., and et. al. (2018). Long-term exposure to ambient air pollution and incidence of brain tumor: the European Study of Cohorts for Air Pollution Effects (ESCAPE). Neuro-oncology, 20(3) : 420–432.
Su, S. Y., Liaw, Y. P., Jhuang, J. R., Hsu, S. Y., Chiang, C. J., Yang, Y. W. and Lee, W. C. (2019). Associations between ambient air pollution and cancer incidence in Taiwan: an ecological study of geographical variations. BMC public health, 19(1) : 1496.
León, S. P. Z. and López , F. D. (2020).Polycyclic Aromatic Hydrocarbons and their Association with Breast Cancer. Bangladesh Journal of Medical Science, 19 (2) : 194–199 .
Zhang, L., Jin, Y., Huang, M., and Penning, T. M. (2012). The Role of Human Aldo-KetoReductases in the Metabolic Activation and Detoxication of Polycyclic Aromatic Hydrocarbons: Interconversion of PAH Catechols and PAH O-Quinones . Frontiers in pharmacology, 3 : 193.
Clergé, A., Le Goff, J., Lopez, C., Ledauphin, J. and Delépée, R. (2019). Oxy-PAHs : occurrence in the environment and potential genotoxic/mutagenic risk assessment for human health. Critical reviews in toxicology, 49(4) : 302–328.
Huszno, J., and Grzybowska, E. (2018). TP53 mutations and SNPs as prognostic and predictive factors in patients with breast cancer. Oncology letters, 16(1) : 34–40.
Perri, F., Pisconti, S., and VittoriaScarpati, G. Della. (2016).p53 mutations and cancer: A tight linkage. Annals of Translational Medicine, 4(24) : 2–5.
Al-Tu’ma, F.J. ; Al-Zubaidi, R.D. ; Al-Khaleeli, A.M.B. and Abo-Almaali, H.M. (Summer 2016). Polymorphism of tumor suppressor gene (p53) Codon 72 in Iraqi patients with acute myocardial infarction. J Contemp Med Sci, 2 (7) : 74–76.
Chen J. (2016). The Cell-Cycle Arrest and Apoptotic Functions of p53 in Tumor Initiation and Progression. Cold Spring Harbor perspectives in medicine, 6(3), a026104.
Grochola, L. F., Zeron-Medina, J., Mériaux, S., and Bond, G. L. (2010).Single-nucleotide polymorphisms in the p53 signaling pathway. Cold Spring Harbor perspectives in biology, 2(5) : a001032.
Kucab, J. E., Phillips, D. H., and Arlt, V. M. (2010).Linking environmental carcinogen exposure to TP53 mutations in human tumours using the human TP53 knock-in (Hupki) mouse model. The FEBS journal, 277(12) : 2567–2583.
Asco, M., Shami, S. and Crook, T. (2002).The p53 pathway in breast cancer. Breast Cancer Res 4 : 70.
Da Silva Junior, F. C., Felipe, M., Castro, D., Araújo, S., Sisenando, H., and Batistuzzo de Medeiros, S. R. (2021). A look beyond the priority: A systematic review of the genotoxic, mutagenic, and carcinogenic endpoints of non-priority PAHs. Environmental pollution (Barking, Essex:1987), 278 :116838.
Rubin H. (2001). Synergistic mechanisms in carcinogenesis by polycyclic aromatic hydrocarbons and by tobacco smoke: a bio-historical perspective with updates. Carcinogenesis, 22(12) :1903–1930.
Chen, S., Nguyen, N., Tamura, K., Karin, M., and Tukey, R. H. (2003). The role of the Ah receptor and p38 in benzo[a]pyrene–7,8 - dihydrodiol and benzo[a]pyrene-7,8-dihydrodiol-9,10-epoxide-induced apoptosis. The Journal of biological chemistry, 278(21) :19526–19533.
Raghad H Al-Ani and Estabraq AR. Al-Wasiti. (2021). The Adverse Effect of Air Pollution with Polycyclic Aromatic hydrocarbon (PAH) on 8-OXO-DG and gene expression (HOGG1) in Midland Refineries Company-Daura Refinery Workers. Indian Journal of Forensic Medicine and Toxicology, 15(3) : 2651–2656.
Chaichan, M.T., Kazem, H.A. and Abed, T.A. (2016).Traffic and outdoor air pollution levels near highways in Baghdad, Iraq. Environ Dev Sustain 20 : 589–603.
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