PROTEIN AND DNA DAMAGE IN RELATION TO ENVIRONMENTAL POLLUTANT LEVELS AND GENETIC POLYMORPHISMS IN KIDNEY, STOMACH AND BREAST CANCER PATIENTS.

Autor: Orhan, Hilmi, Süzen, Sinan, Kocagöz, Rasih, Onat, İlgen, Demirbügen, Merve, Turna, Burak, Atilla, Koray, Yeniay, Levent, Tiftikçioğlu, Yiğit, Sarsık, Banu, Zekioğlu, Osman, Özdemir, Murat, Göktepe, Berk, Serin, Gürdeniz, Gür, Ersin
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Zdroj: Turkish Journal of Biochemistry / Turk Biyokimya Dergisi; 2019 Supplement, Vol. 44, p12-13, 2p
Abstrakt: Environmental pollutants such as organochlorine pesticides (OCPs), polychlorinated biphenyls (PCBs) and polybrominated diphenyl ethers (PBDEs), so called persistent organic pollutants (POPs) have been known to interfere various ion channels in organism, which is the main mechanism of action especially for OCPs. Furthermore, all PCBs and several congeners of OCPs and PBDEs were recently listed as "carcinogen" by the IARC depending on evaluation of epidemiological studies. On the other hand, there have been very little data on the relation between various cancers and tissue burden of these toxicants. In majority of the human studies on a possible association between POPs and cancers, exposure data have been based on statement-based interviews, which potentially impair the accuracy and reliability of quantitative assessment. In order to accurately assess whether environmental exposure to POPs increase risk of kidney, stomach and breast cancers, tumour tissues as well as blood and urines were collected from surgically operated patients. Cellular DNA and protein oxidative damage markers (8-OHdG and dityrosine, respectively), have also been analysed in the patient and healthy control groups, and assessed whether there are changes in these parameters. The data suggest that majority of POPs in cancerous tissues were associated with cancers in patients, while they are less conclusive in blood of the same patients. DNA and protein damage markers were found to be higher in urines of kidney cancer patients compared to healthy volunteers, although inter-individual variability obscured statistical significances. Current findings confirmed that glutathione S-transferase theta1 (GSTT1) nullpolymorphism is a risk factor Bforro ukgidhnte tyo cyaonuc ebry, |a nEdP cIyptsowchicrohme P450 1A1 (CYP1A1) is a risk factor for stomach cancer. Data suggest that environmental exposure to POPs may induce tumour initiation and/or progression in humans however, blood concentrations of the same pollutants do not adequately reflect tissue concentrations except dichlorodiphenyldichloroethylene (DDE), the major metabolite of the notorious organochlorine pesticide dichlorodiphenyltrichloroethylene (DDT). Possible role of interaction of POPs with ion channels in cancer initiation and/or progression remain to be explored. [ABSTRACT FROM AUTHOR]
Databáze: Complementary Index