Purpose: We aimed to evaluate the effects of dehydroepiandrosterone (DHEA) on antioxidant enzyme activities, lipid peroxidation, and histopathologic changes in both testes after unilateral testicular torsion and detorsion.
Methods: Twenty-four adult male Sprague-Dawley rats were randomly divided into 4 groups (n = 6 for each group): sham operation, torsion/detorsion (T/D), T/D + vehicle, and T/D + DHEA. Three hours before detorsion, 50 mg/kg DHEA was given intraperitoneally to the T/D + DHEA group. Testicular ischemia was achieved by twisting the left testis 720 degrees clockwise for 3 hours, and reperfusion was allowed for 24 hours after detorsion. In all groups, bilateral orchiectomies to determine the testicular tissue catalase (CAT) and superoxide dismutase activities and malondialdehyde (MDA) levels and histopathologic examination were performed.
Results: Compared with those from the sham group, CAT activities in the ipsilateral testis obtained from the T/D group were significantly lower and MDA levels were significantly higher (P < .05 for all). Administration of DHEA prevented increases in MDA levels and decreases in CAT and superoxide dismutase activities when compared to the T/D group. Specimens from the T/D and the T/D + vehicle groups had a significantly greater histologic injury than the specimens from the sham and the T/D + DHEA groups had (P < .01 for both).
Conclusions: The results suggest that DHEA may be a protective agent for preventing biochemical and histopathologic changes related to oxidative stress in testicular injury caused by testis torsion.
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http://dx.doi.org/10.1016/j.jpedsurg.2007.05.033 | DOI Listing |
Fertil Steril
September 2024
Department of Public Health, University of Naples Federico II, Naples, Italy.
Hypertension
January 2016
From the Medizinische Klinik und Poliklinik IV (T.A.W., A.S.D., M.B., A.R., Y.R., F.B., M.R.) and Klinische Radiologie (M.T.), Klinikum der Ludwig-Maximilians-Universität München, Munich, Germany; Division of Internal Medicine and Hypertension, Department of Medical Sciences, University of Turin, Turin, Italy (T.A.W.); Institute of Clinical Chemistry and Laboratory Medicine (M.P., G.E.) and Department of Internal Medicine III (J.W.M.L., G.E.), Technische Universtät Dresden, Dresden, Germany; and Department of Internal Medicine, Radboud University Medical Center, Nijmegen, The Netherlands (T.D., J.W.M.L., J.D.).
Primary aldosteronism comprises 2 main subtypes: unilateral aldosterone-producing adenoma (APA) and bilateral adrenal hyperplasia. Somatic KCNJ5 mutations are found in APA at a prevalence of around 40% that drive and sustain aldosterone excess. Somatic APA mutations have been described in other genes (CACNA1D, ATP1A1, and ATP2B3) albeit at a lower frequency.
View Article and Find Full Text PDFAndrologia
February 2008
Department of Urology, School of Medicine, Ataturk University, Erzurum, Turkey.
In the present study, we aimed to evaluate the effects of dehydroepiandrosterone (DHEA) on apoptosis of testicular germ cells after repair of testicular torsion in rats. Twenty-four adult male Sprague-Dawley rats were randomly divided into four groups, with six rats in each group: sham operation, torsion/detorsion (T/D), T/D + vehicle, and T/D + DHEA. Three hours before detorsion, 50 mg kg(-1) DHEA was given intraperitoneally to T/D + DHEA group.
View Article and Find Full Text PDFJ Pediatr Surg
October 2007
Department of Biochemistry, School of Medicine, Ataturk University, TR-25240 Erzurum, Turkey.
Purpose: We aimed to evaluate the effects of dehydroepiandrosterone (DHEA) on antioxidant enzyme activities, lipid peroxidation, and histopathologic changes in both testes after unilateral testicular torsion and detorsion.
Methods: Twenty-four adult male Sprague-Dawley rats were randomly divided into 4 groups (n = 6 for each group): sham operation, torsion/detorsion (T/D), T/D + vehicle, and T/D + DHEA. Three hours before detorsion, 50 mg/kg DHEA was given intraperitoneally to the T/D + DHEA group.
Atherosclerosis
February 1998
Department of Preventive Cardiology, St. Francis Hospital, Roslyn, NY 11576-1348, USA.
Oxidation of low-density lipoprotein (LDL) is postulated to be essential for the development of atherosclerosis. LY-139478 is a new non-steroidal potent estrogen analog, but its effects on in vitro LDL oxidation have not been completely elucidated. We investigated the ability of LY-139478 to inhibit in vitro copper sulfate-mediated LDL oxidation using several methods, including conjugated diene (CD) accumulation, relative electrophoretic mobility on agarose gel, thiobarbituric acid-reactive substances (TBARS) assay, and superoxide anions scavenging activity.
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