A Quick Review of Redox State in Cancer: Focus to Bladder.

A cell is dying when there is no repair after damage. Indeed, the etiology of cancers associates with damaged or unrepaired cells. Cancer results from imbalance between cell's oxidant and antioxidant defenses. This study aimed to review formation of cancer associated to oxidative stress. Tumorgenesis is caused by deregulation of the redox homeostasis by reactive oxygen species that stimulate the formation of tumor by starting an abnormal introduction of signaling nets. Proliferation accompanied by uncontrolled growth could lead to development of mass cancer cells. Kinases/phosphatases, transcription factors, reactive oxygen-nitrogen species and signal transduction are the most important cascades. The biology of tumor is affected by: 1) redox control through growth factor receptor signal, 2) superoxidase production due to small amount of oxygen, 3) infiltrating cytotoxic immune cells, 4) anticancer treatments, 5) repetitive ischemia-reperfusion cycles due to irregular blood supply and 6) inflammation. Keywords: Oxidant; Anti-oxidant; Cancer; Bladder.

Bladder cancer: total antioxidant capacity and pharmacotherapy with vitamin-E.

PURPOSE: Free radicals play an important role in the different complex course of carcinogenesis. Higher concentrations of reactive oxygen species are highly associated with the presence of tumors. The urinary bladder organ is also a target for many carcinogens. The major objective of this investigation was to measure the role of redox state or total antioxidant capacity (T-AOC) and antioxidant functions of vitamin E in patients with low-grade papillary cancer of the bladder (BC). METHODS: The blood sample was used for measurement of the T-AOC by the Trolox-TAC assay kit. Thirty-five patients with BC and thirty-five healthy subjects that matched for age were entered in this study. The obtained data were analyzed using the Statistical Package (SPSS Inc, Chicago, IL, USA). The significance level was set at p ≤ 0.05. RESULTS: In healthy controls, the mean ± SD for T-AOC was 91.8 ± 16.6 (U/ml), that was significantly higher when compared to the mean value of 24.5 ± 28.9 (U/ml) in patients with BC (p = 0.00). The difference in concentration of T-AOC before and after prescription of vitamin E was encountered with a p value of 0.16. CONCLUSIONS: By reference to the significant difference between T-AOC in patients and healthy controls, our results strongly suggest a low level of T-AOC in patients with BC. The obtained changes in T-AOC before and after management with vitamin E recommended additional consideration associates with different stages and grade of tumor in patients with BC.