Department of Microbiology, Tartu University, Ravila 19, Tartu 50411, Estonia.
Med Hypotheses. 2011 Nov;77(5):837-40. doi: 10.1016/j.mehy.2011.07.050. Epub 2011 Aug 19.
Prostatitis is a disease that seriously affects the quality of patients' life. In the majority of cases, chronic prostatitis (chronic pelvic pain syndrome--CPPS) has an unclear pathogenesis. Anti-inflammatory and anti-infectious treatments have remained controversial. According to the latest research, prostatitis has been associated with oxidative stress (OxS) and/or OxS-related genetic polymorphisms. We have observed that prostatitis patients have systemic OxS in case of inflammation and pain. We propose a new explanation for the role of OxS in the pathogenesis of prostatitis and describe the putative OxS-related pathways in detail. The neural vicious circle starts by activation of primary sensory afferents. Glutamate mediates the signal to the neurons in the dorsal horn of the spinal cord, and facilitates calcium influx into their mitochondria. The latter causes an increased production of superoxide radicals. If the superoxide production is not effectively controlled by mitochondrial superoxide dismutase (Mn-SOD), then superoxide leads to OxS and lipid peroxidation. Consequent release of electrophilic lipid peroxidation products (LPP) from dorsal horn of the spinal cord causes pain by activating the primary sensory afferents, again. Additional LPP-mediated causes of pain include glutathione depletion and neuron sensitisation by isoprostanes. Excretion of LPP into urine may exert positive feedback as well. Currently, different information exists about chronic prostatitis (inflammation, pain, oxidative stress, neural sensitisation, lower urinary tract symptoms). The clear links between these data are actually absent. We propose that vicious circle based on LPP, especially isoprostanes, is the linking mechanism.
前列腺炎是一种严重影响患者生活质量的疾病。在大多数情况下,慢性前列腺炎(慢性骨盆疼痛综合征-CPPS)的发病机制尚不清楚。抗炎和抗感染治疗一直存在争议。根据最新的研究,前列腺炎与氧化应激(OxS)和/或 OxS 相关的遗传多态性有关。我们观察到前列腺炎患者在炎症和疼痛时存在全身 OxS。我们提出了 OxS 在前列腺炎发病机制中的作用的新解释,并详细描述了推测的 OxS 相关途径。神经恶性循环始于初级感觉传入纤维的激活。谷氨酸介导信号传递到脊髓背角的神经元,并促进钙进入其线粒体。后者导致超氧自由基的产生增加。如果线粒体超氧化物歧化酶(Mn-SOD)不能有效控制超氧化物的产生,那么超氧化物就会导致 OxS 和脂质过氧化。随后,来自脊髓背角的亲电子脂质过氧化产物(LPP)的释放通过激活初级感觉传入纤维再次引起疼痛。LPP 介导的其他疼痛原因包括谷胱甘肽耗竭和神经元敏化作用由异前列烷引起。LPP 排入尿液的排泄也可能产生正反馈。目前,关于慢性前列腺炎(炎症、疼痛、氧化应激、神经敏化、下尿路症状)存在不同的信息。这些数据之间的明确联系实际上并不存在。我们提出,基于 LPP,特别是异前列烷的恶性循环是连接机制。