The inhibitory effect of vitamin E on cigarette smoke-induced oxidative damage to the rat urothelium: Can it prevent transitional cell carcinoma?

Onol F. F., Demir A., Temiz Y., YÜKSEL M., Eren F., Turkeri L.

UROLOGIA INTERNATIONALIS, cilt.78, sa.2, ss.150-154, 2007 (SCI-Expanded) identifier identifier identifier identifier

  • Yayın Türü: Makale / Tam Makale
  • Cilt numarası: 78 Sayı: 2
  • Basım Tarihi: 2007
  • Doi Numarası: 10.1159/000098074
  • Dergi Adı: UROLOGIA INTERNATIONALIS
  • Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus
  • Sayfa Sayıları: ss.150-154
  • Anahtar Kelimeler: transitional cell carcinoma, cigarette smoke, oxidative damage, prevention, vitamin E, BLADDER-CANCER, DNA-ADDUCTS, LIPID-PEROXIDATION, BETA-CAROTENE, PLASMA, DIETARY, TISSUE, COHORT, BLOOD, LUNG
  • Acıbadem Mehmet Ali Aydınlar Üniversitesi Adresli: Hayır

Özet

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. Copyright (c) 2007 S. Karger AG, Basel.