The role of tissue persistent organic pollutants and genetic polymorphisms in patients with benign and malignant kidney tumors.

Environ Toxicol Pharmacol

Department of Pharmaceutical Toxicology, Faculty of Pharmacy, Ege University, Bornova, İzmir 35040,  Türki̇ye; İzmir Biomedicine and Genome Center (İBG-İzmir), Balcova, İzmir 35340, Türkiye. Electronic address:

Published: September 2024

AI Article Synopsis

  • - This study investigated the link between exposure to persistent organic pollutants (POPs) and the development of kidney tumors, analyzing samples from patients who had kidney surgery and a control group for comparison.
  • - Researchers measured POP concentrations in blood and various kidney-associated tissues, and assessed urinary markers indicating oxidative stress and potential DNA damage.
  • - Findings suggested a connection between high levels of certain POPs and an increased risk of kidney cancer, with specific genetic factors, like the GSTT1 null polymorphism, potentially influencing this risk.

Article Abstract

This study aimed to explore whether there is an association between environmental exposure to POPs and kidney tumor induction, and whether blood POP concentrations reflect kidney tissue concentrations. POP derivatives were determined in blood, tumor tissue, tumor surrounding tissue, and perirenal fat tissue samples taken from patients who underwent surgery for renal tumors. A voluntary control group was recruited for blood and urine samples as well. Urinary excretions of o,o'-dityrosine, chlorotyrosine, nitrotyrosine, and 8-OHdG were measured in the same patients. The possible role of genetic polymorphisms in CYP1A1, GST isozymes P, M, and T, and hOGG1 genes on the predisposition to renal cancer was investigated. Some POPs have been found to be associated with kidney cancer, as evidenced by their significantly high ORs. 8-OHdG levels were significantly higher compared to the control group. The GSTT1 null polymorphism can be a risk factor for malignant but not for benign kidney tumors.

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http://dx.doi.org/10.1016/j.etap.2024.104495DOI Listing

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