Ectonucleotide pyrophosphatase/phosphodiesterase (E-NPP) and adenosine deaminase (ADA) activities in prostate cancer patients: influence of Gleason score, treatment and bone metastasis.

The relation between adenine nucleotides and cancer has already been described in literature. Considering that the enzymes ectonucleotide pyrophosphatase/phosphodiesterase (E-NPP) and adenosine deaminase (ADA) act together to control nucleotide levels, we aimed to investigate the role of these enzymes in prostate cancer (PCa). E-NPP and ADA activities were determined in serum and platelets of PCa patients and controls. We also verified the influence of the Gleason score, bone metastasis and treatment in the enzyme activities. Platelets and serum E-NPP activity increased, whereas ADA activity in serum decreased in PCa patients. In addition, Gleason score, metastasis and treatment influenced E-NPP and ADA activities. We may propose that E-NPP and ADA are involved in the development of PCa. Moreover, E-NPP and ADA activities are modified in PCa patients with distinct Gleason score, with bone metastasis, as well as in patients under treatment.

Cholinesterase activities and biochemical determinations in patients with prostate cancer: influence of Gleason score, treatment and bone metastasis.

Prostate cancer (PCa) is the sixth most common type of cancer worldwide. Cholinesterase is well known as having non-cholinergic functions such as cellular proliferation and differentiation, suggesting a possible influence of cholinesterase in tumorogenesis. Thus, the aim of this study was to investigate the whole blood acetylcholinesterase (AChE) and plasma butyrylcholinesterase (BChE) activities and some biochemical parameters in PCa patients. This study was performed in 66 PCa patients and 40 control subjects. AChE and BChE activities were determined in PCa patients and the influence of the Gleason score; bone metastasis and treatment in the enzyme activities were also verified. Furthermore, we also analyzed possible biochemical alterations in these patients. AChE and BChE activities decreased in PCa patients in relation to the control group and various biochemical changes were observed in these patients. Moreover, Gleason score, metastasis and treatment influenced cholinesterase activities and biochemical determinations. Our results suggest that cholinesterases activities and biochemical parameters are altered in PCa. These facts support the idea that the drop in the cholinesterase activity and the consequent increased amount of acetylcholine could lead to a cholinergic overstimulation and increase the cell proliferation in PCa.

Oxidative stress and antioxidant status in prostate cancer patients: relation to Gleason score, treatment and bone metastasis.

Over the last decade, epidemiological, experimental and clinical studies have implicated oxidative stress in the development and progression of prostate cancer. In the present study, we evaluated the oxidative status and antioxidant defense in patients with prostate cancer (PCa) taking into consideration: treatment, Gleason score and bone metastasis. For this, we measured concentrations of plasmatic thiobarbituric acid reactive substances (TBARS), serum protein carbonylation, whole blood catalase (CAT) and superoxide dismutase (SOD) activities, as well as the plasma and erythrocyte thiol levels and serum vitamin C and E concentration. This study was performed on 55 patients with PCa and 55 healthy men. TBARS levels and serum protein carbonylation were higher in PCa patients than in controls and altered levels of antioxidants were found in these patients. CAT activity was decreased and SOD activity was higher in PCa patients when compared with controls. Non-protein thiol levels were increased, however, serum vitamin C and vitamin E content were reduced in PCa patients when compared with controls. In addition, different parameters analyzed in PCa patients based on metastasis, treatment and Gleason score showed changes in oxidative stress biomarkers and antioxidant defenses. These findings may indicate an imbalance in the oxidant/antioxidant status, supporting the idea that oxidative stress plays a role in PCa, moreover, the oxidative profile appear to be modified by bone metastasis, treatment and Gleason score.