Abstract
To evaluate the potential relationship between benign prostatic hyperplasia (BPH) and the arachidonic acid (AA) metabolome, a UHPLC—MS/MS method has been developed and validated for simultaneous determination of AA and its cyclooxygenase(COX) and lipoxygenase(LOX) pathway metabolites (15-HETE, 12-HETE, TXA2, 5-HETE, AA, PGI2, PGF2α, 8-HETE, PGD2, PGE2 and LTB4) in rat tissues. The analytes were extracted from tissue samples with a protein precipitation procedure and then separated on a Shim-pack XR-ODSC18 column with 0.05% formic acid in water (pH adjusted with dilute ammonia) and methanol:acetonitrile (20:80, v/v). Detection was performed on a UHPLC—MS/MS system with electrospray negative ionization (ESI) and a multiple reaction-monitoring mode. The lower limits of quantification (LLOQ) were 0.25–50 ng/mL for all of the analytes in the prostate, seminal, bladder, liver and kidney tissues. The absolute recoveries of the analytes from all of the tissues were more than 50%. By means of the method developed, the AA metabolites in tissue samples from Sham and BPH group rats were determined. The eleven biomarkers in the BPH group prostate, seminal, bladder, liver and kidney tissues were significantly higher than those of the sham group, indicating that BPH fortified the inducible expression of COX and LOX, as well as increased the production of AA and eicosanoids. The method described here offers a useful tool for the evaluation of complex regulatory eicosanoids responses in vivo.
Highlights
Benign prostatic hyperplasia (BPH) is the most common benign tumor in men, showing an age-related incidence
Because it dramatically enhanced the response of eicosanoids with an adequate lower limits of quantification (LLOQ), and it slightly suppressed the intensity of the eicosanoids
The results indicate that prostates harvested from BPH animals have a marked increase in the expression of both LOX and COX, and it lead to a greater induction of prostatic cell growth
Summary
Benign prostatic hyperplasia (BPH) is the most common benign tumor in men, showing an age-related incidence. BPH represents a pattern of unregulated but non-malignant growth characterized by an increase in prostate epithelial and stromal cells [1]. The exact pathogenesis of BPH is still unclear, but several clinical and experimental observations indicate that inflammation in the prostate gland is closely associated with the development of BPH [2, 3, 4]. Benign Prostatic Hyperplasia and Arachidonic Metabolism present prostatic inflammation in histologic diagnosis [5]. Inflammation mediated through the upregulation of lipid and protein mediators released by inflammatory cells contributes to the tissue injury driving local angiogenesis. The most important inflammatory pathway is the metabolism of arachidonic acid (AA) and it has been associated with the development of BPH. Due to the importance of these mediators, it is necessary to systematically evaluate their changes in a biological matrix
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