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[Justification of a use of additional antioxidant therapy in experimental models of chronic bacterial prostatitis].

AIM
To study the changes of the main parameters of the oxidative status in prostate after standard antimicrobial monotherapy and to justify a use of additional antioxidant therapy in various experimental models of chronic bacterial prostatitis (CBP).


MATERIAL AND METHODS
A total of 60 outbred adult male healthy rats weighing 180-200 grams were used in the experiment. In a control group, 20 intact rats were included. Two experimental groups of 20 animals each were formed and in each group two subgroups (n=10) were distinguished. Two series of experiments were performed in the episodic and relapse models of CBP (based on the Nickel J.C. (1990) and Goto T. (1991)), respectively, with an evaluation of the efficiency of antimicrobial monotherapy (levofloxacin 12.5 mg/kg/day per os for 20 days) in each of the subgroups. In prostate homogenates the levels of CFUs, active forms of oxygen (ROS), diene conjugates and malonic dialdehyde, as well as an activity of superoxide dismutase (SOD) and succinate dehydrogenase (SDH)) were evaluated.


RESULTS
The microbiological efficiency of standard antimicrobial monotherapy in the episodic model of CBP was higher than in the recurrent model (90.0% vs 80.0, respectively, p<0.05). The degree of free radical aggression and a severity of lipid peroxidation in recurrent CBP were significantly higher, and the activity of SOD and SDH was significantly lower than in the episodic model of CBP (p<0.05). In both models, residual oxidative stress persisted in the prostate tissue after antimicrobial therapy, indicating an incompleteness (in the case of episodic model of CBP) or decompensation (in case of recurrent CBP) of the antioxidant defense system.


CONCLUSION
A persisting of residual oxidative stress after a course of etiotropic antimicrobial monotherapy in the prostate has justified a necessity of the additional administration of antioxidants (antihypoxants) for a combined pharmacotherapy of CBP.