in: The Urinary Bladder: Structure, Functions and Clinical Aspects, NICOLINE J. MIKKELSEN, Editor, NOVA Publications , New-York, pp.107-133, 2020
In the developed countries bladder cancer is the ninth most
frequently seen cancer and it affects men more frequently than women.
The risk factors of bladder cancer are tobacco smoke, environmental
pollutants, workplace conditions, and life style. The differences in the
metabolism of these chemicals have recently been suggested as modifiers
of individual susceptibility to environmentally induced bladder cancer.
Recent studies indicated antioxidant system imbalance caused oxidative
stress in the formation and development of this disease. These
carcinogens activate the cytochrome p450 systems and cause DNA
damage which starts tumor initiation. Some phase II enzymes play
effective role for the protection from cancer progression such as GST,GPx, soluble Sulphotrasferases (SULT), and epoxide hydrolases.
Glutathione S transferases detoxify chemical carcinogens. GST T1 and
GST1 null genotype polymorphism have an increased role in the
susceptibility of bladder cancer progression both in Caucasian and Asian
populations. GPx polymorphism was also found to be associated with
developing bladder cancer. Sulfotransferases (SULT) are enzymes
affecting catalyzation of carcinogenic compunds. It has been found that
Sult1A1 polymorphism took place at reduced risk of bladder cancer.
Bladder cancer is also found to be related to exposure of aromatic
amines after detoxification by NAT2 (N acetyl transferase) slow
acetylation form of the enzyme. This section reviews new basic
developments on the role of the polymorphisms in Glutathione gene
family enzyme transferases (GST), (GR), GPx, Soluble sulfotransferases
(SULT), carcinogen metabolizing enzymes N-acetyltransferase (NAT),
with significance on the susceptibility to urinary bladder cancer.