Does low testosterone cause prostate problems

Abstract Background The role of myeloperoxidase MPO is essential in the killing of phagocytosed bacteria. Certain steroid hormones increase MPO plasma concentration.

Our aim was to test the effect of MPO, its inhibitor indomethacin, and certain steroid hormones on bactericidal activity. Methods Human polymorphonuclear leukocytes PMN were incubated with opsonised Escherichia coli and either MPO, indomethacin, estradiol, or hydrocortisone.

Background

Intracellular killing capacity was evaluated with UV microscopy after treatment with fluorescent dye. Next, an in vivo experiment was performed with nine groups of rats: in the first phase of the study indomethacin treatment and Pasteurella multocida infection Iiindomethacin treatment without infection I0untreated control with infection Mi and untreated control without infection M0 ; in the second phase of the study rats with infection and testosterone treatment NTcastration, infection and testosterone treatment CTcastration, infection and estradiol treatment CEnon-castrated infected control N0and castrated infected control C0.

After treatment bacteria were reisolated from the liver and heart blood on agar plates, and laboratory parameters were analyzed.

Results Indomethacin does low testosterone cause prostate problems not have a remarkable effect on the bacterial killing of PMNs, while the other compounds increased bacterial killing to various degrees. In the animal model indomethacin and infection caused a poor clinical state, a great number of reisolated bacteria, elevated white blood cell WBC count, decreased C-reactive protein CRP and serum albumin levels.

Testosterone treatment resulted in less bacterial colony numbers in group NT, but not in group CT compared to respective controls N0, C0. Estradiol treatment CE decreased colony numbers compared to control C0.

Indomethacin treatment and castration weaken immune responses and clinical state of infected rats, while testosterone and estradiol have a beneficial effect.

Background Free radicals are very reactive compounds with one or more unpaired electrons on their outer orbitals. They are of great importance in the bacterial killing role of macrophages.

The most important reactive oxygen radical is the superoxide anion with limited reactivity, but it can be converted into other more reactive radicals. HOCl deploys bactericidal activity on the bacteria ingested in the phagosome. Additionally, chloramines generated by HOCl reacting with phagosomal proteins also contribute to bacterial killing, but the full consequences of this are not yet clear [ 12 ].

Int J Mol Sci. Published online Jan 8. Copyright © by the authors. This article has been cited by other articles in PMC.

The tissues are protected against free radicals by antioxidant enzymes such as SOD, catalase, glutathione reductase, α1-antitripsinpeptides with thiol groups glutathione, thioredoxin family and nutritional antioxidants vitamin C and E, carotenoids, trace elements [ 23 ]. Certain steroid hormones also play a role in antioxidant defence through various mechanisms. In our previous work we demonstrated that cortisol, ß-oestradiol E2progesterone, and testosterone decreased the superoxide release from human PMNs, while aldosterone and cortexolone, the precursor of cortisol did not have such property [ 4 ].

In the literature the most extensively studied steroid hormone is E2. It enhances the cellular anti-oxidative defence molecules, reduces the production of reactive oxygen species ROSactivates endothelial, inducible and neuronal nitric oxide synthase, and neutralizes the excess ROS in various cell types [ 5 ].

The mechanism of antioxidant action of hydrocortisone is scantly studied in the literature.

1. Introduction

It is mainly referred to as the main biomarker of stress, which leads to oxidative changes [ 6 ]. Other glucocorticoids have both glucocorticoid receptor mediated genomic and a rapid non-genomic antioxidant effect [ 89 ].

The antioxidant effect of testosterone is ambiguous in the literature. In one study it showed a receptor-mediated antioxidant effect in vitro on cerebellar granule cells [ 10 ], but according to others it caused a decrease in the activity of antioxidant enzymes and led to lipid peroxidation in the prostate and testis of rodents [ 1112 ].

MPO has also been reported to have antioxidant capacity despite its known free radical producing activity. In fact, it has been found, that MPO release and activity in PMNs can be enhanced by certain steroids, like E2, testosterone, and prednisolone. Thus, the antioxidant effect of these steroid hormones might be carried out at least in part by the elevation of MPO activity and release [ 14 — 16 ].

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On the other hand, the MPO inhibitor indomethacin, a non-steroidal anti-inflammatory drug, a nonselective cyclooxygenase inhibitor increases free radical production in PMNs [ 1417 ].

This could mean a beneficial effect in the bactericidal activity of PMNs. In our present studies we aimed to evaluate the effect of indomethacin on ex vivo and in vivo bactericidal function. We also tested MPO, E2, and hydrocortisone on antibacterial capability of human PMNs, and the effect of indomethacin, testosterone, and E2 on Ráadásul a prosztatitis gyógyítás in vivo rat model.

Our ultimate aim was to evaluate if indomethacin can be useful as an adjuvant therapy in septic patients.

Since the two experimental models are different, benign prostatic hyperplasia infertility sex steroids have various effects on many participants of the immune system besides PMNs, the comparison of the results of the two experiments needs caution. Methods Ex vivo effect of indomethacin, MPO, estradiol, and hydrocortisone on the bactericidal activity of human isolated PMNs Isolation of PMNs Venous blood was drawn from 6 male and 5 does low testosterone cause prostate problems donors, aged 23—40 years.

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All volunteers were non-smokers, took no medications, did not suffer from any known disease and consented to participation. The blood was taken into EDTA tubes between 8—9 a. PMNs were separated within 2 hours of blood drawing with the following method.

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The blood was applied to Histopaque Sigma, —1 in layers for the sedimentation of red blood cells and put aside for an hour. Granulocytes thus separated were buffer-washed twice and centrifuged with × g. The bacterial strain was cultivated on blood agar plates overnight at 37°C.

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