The Inhibitory Effect of Vitamin E on Cigarette Smoke-Induced Oxidative Damage to the Rat Urothelium: Can It Prevent Transitional Cell Carcinoma?

Abstract

Introduction: We aimed to detect reactive oxygen species (ROS) and assess subsequent carcinogenesis in terms of cellular proliferation in the bladder and kidney epithelial tissues of rats exposed to cigarette smoke (CS), and to investigate the changes following vitamin E treatment. Materials and Methods: Twenty-four male Sprague-Dawley rats were divided into 3 groups: group 1 was kept intact; group 2 was subjected to CS exposure for 8 weeks, and group 3 received intraperitoneal vitamin E injections (200 mg/kg/week) for 8 weeks in addition to CS exposure. Histological examination and Ki67 antigen expression measurements were made from bladder and renal pelvic tissue sections. Luminol-amplified chemiluminescence was used to measure ROS levels. All results were compared using a one-way ANOVA test. Results: In CS-exposed rats, light microscopy of renal and bladder tissues revealed nonspecific epithelial changes; however, Ki67 expression was significantly increased in bladder tissues compared to other groups (17.5 ± 4.7, 35 ± 2.9 and 18.7 ± 5.1% in groups 1, 2 and 3, respectively, p < 0.05). Chemiluminescence levels in bladder and renal tissues were also significantly higher in the CS-exposed animals (78.1 ± 11.4, 148 ± 13.3, 97.8 ± 6.1 rlu/mg for the bladder, and 99.8 ± 12.2, 176.1 ± 27.9, 67.1 ± 9 rlu/mg, for renal pelvic tissues, respectively, p < 0.05). Conclusions: Vitamin E can alleviate CS-induced oxidative damage in rat bladder and kidney epithelium suggesting a potential role for vitamin E in the prevention of CS-mediated carcinogenesis.