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Published on: January 16, 2013
Increased oxidative stress and oxidative damage associated with chronic bacterial prostatitis
Jun-Fu Zhou1, Wei-Qiang Xiao, Yi-Chun Zheng
1Laboratory for Free Radical Medicine, Second Affiliated Hospital, College of Medicine, Zhejiang University, 88 Jiefang Road, Hangzhou 310009, China. jfzhou@zju.edu.cn
Chronic bacterial prostatitis elevates oxidative stress and damage, indicated by increased nitric oxide and malondialdehyde, and decreased antioxidants. This oxidative stress correlates with disease duration.
Area of Science:
- Urology
- Biochemistry
- Oxidative Stress Research
Background:
- Chronic bacterial prostatitis (CBP) is a persistent condition.
- Oxidative stress plays a role in various inflammatory diseases.
- The specific impact of CBP on oxidative stress markers is not fully elucidated.
Purpose of the Study:
- To investigate oxidative stress and damage in chronic bacterial prostatitis patients (CBPP).
- To explore the underlying mechanisms of oxidative stress in CBPP.
- To determine the relationship between disease duration and oxidative stress markers.
Main Methods:
- A case-control study involving 70 CBPP and 70 healthy adult volunteers (HAV).
- Measurement of plasma nitric oxide (NO), vitamin C (VC), vitamin E (VE), and beta-carotene (beta-CAR).
- Assay of erythrocyte malondialdehyde (MDA) and activities of superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPX) via spectrophotometry.
Main Results:
- CBPP patients exhibited significantly higher plasma NO and erythrocyte MDA levels compared to HAV.
- CBPP patients showed significantly lower plasma VC, VE, beta-CAR, and erythrocyte SOD, CAT, and GPX activities.
- Disease duration in CBPP correlated with increased NO and MDA, and decreased antioxidant markers.
Conclusions:
- Chronic bacterial prostatitis is associated with increased oxidative stress and damage.
- The observed oxidative stress is closely linked to the duration of the disease.
- These findings highlight the role of oxidative mechanisms in the pathophysiology of CBP.
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