Introduction and Objectives
Activation of lipid peroxidation and oxidizing damages inducing by reduce of antioxidant system, plays an importance or principal role in pathogeneses. These are condition of various cancers, inflammatory process, arterioscleroses and other diseases. Therefore, we studied the alternation of lipid peroxidation, catalase activity and amount of H2O2 in mitochondrial and microsomal fractions of human prostate tissues at different pathology.
Material and Methods
Human post-operational fiber-muscular prostate tissues with following pathological forms: benign prostatic hyperplasia (BPH), prostate intraepithelial neoplasia (PIN) and prostate atypical adenomatous hyperplasia (AAH) were used as experimental material. The lipid peroxidation was assessed by the malonildialdehyde (MDA). Catalase activity and amount of the H2O2 were determined by the colorimetric method according to Aebi.
The statistically treatment of experiments has been revealed that the amount of MDA was significantly increased in PIN tissue compared with BPH. From the other side, amount of MDA was significantly increased in subcellular fractions of AAH tissue compared with PIN. This effect is comparative much towards BPH. Catalase activity and amount of H2O2 were assessed in all tested prostate tissues also. The obtained results show that it takes place the respectable reduction of catalase activity as mitochondria as microsome in PIN and prostate AAH tissues as compare with BPH. Herewith level of H2O2 is increased in both – mitochondrial and microsomal fractions with complication of BPH (in PIN and AAH tissues). There is not significant change of the catalase activity and the amount of H2O2 among PIN and prostate AAH tissues.
Therefore the lipid peroxidation is increased, the catalase activity is fallen down and the amount of H2O2 is increased in the mitochondria and microsome with complication of prostate disease. It is clear, that intensification of peroxidation processes provokes oxidizing damages, that condition of neoplasic growth of prostate cells.
© 2009 European Association of Urology. Published by Elsevier Inc. All rights reserved.