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19 records – page 1 of 2.

[A case of arrhenoblastoma of the ovary]

https://arctichealth.org/en/permalink/ahliterature28896
Source
Pediatr Akus Ginekol. 1965 Jan-Feb;1:48
Publication Type
Article
Author
I P Gomeniuk
E V Gitel'man
Source
Pediatr Akus Ginekol. 1965 Jan-Feb;1:48
Language
Ukrainian
Publication Type
Article
Keywords
Adult
Female
Humans
Ovarian Neoplasms
Sertoli-Leydig Cell Tumor
PubMed ID
4294696 View in PubMed
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Aging and the brown Norway rat leydig cell antioxidant defense system.

https://arctichealth.org/en/permalink/ahliterature83080
Source
J Androl. 2006 Mar-Apr;27(2):240-7
Publication Type
Article
Author
Luo Lindi
Chen Haolin
Trush Michael A
Show Matthew D
Anway Matthew D
Zirkin Barry R
Author Affiliation
Division of Reproductive Biology, Department of Biochemistry and Molecular Biology, Johns Hopkins University Bloomberg School of Public Health, Baltimore, Maryland 21205, USA. lluo@jhsph.edu
Source
J Androl. 2006 Mar-Apr;27(2):240-7
Language
English
Publication Type
Article
Keywords
Aging - physiology
Animals
Antioxidants - metabolism
Glutathione Peroxidase - genetics - metabolism
Leydig Cells - enzymology
Male
RNA, Messenger - genetics
Rats
Rats, Inbred BN
Superoxide Dismutase - genetics - metabolism
Testis - growth & development
Transcription, Genetic
Abstract
Previous studies have shown that testosterone production by the Leydig cells of aged Brown Norway rats is reduced from the relatively high levels produced by Leydig cells of young rats and that this reduction is not secondary to decreased serum luteinizing hormone concentration. The free radical theory of aging proposes that imbalance between pro-oxidants and the antioxidant defense system ultimately results in oxidative damage to cellular processes. With this in mind, we hypothesized herein that age-related reductions in steroidogenesis by Brown Norway rat Leydig cells may be associated with the impairment of the antioxidant defense system of these cells. To begin to test this hypothesis, we compared the activities and steady-state mRNA and protein levels of the antioxidant enzymes copper zinc (CuZn) superoxide dismutase (CuZnSOD, SOD1), manganese (Mn) superoxide dismutase (MnSOD, SOD2), and glutathione peroxidase (GPx) and the levels of reduced and oxidized glutathione in Leydig cells isolated from the testes of young (4-month-old) and aged (20-month-old) Brown Norway rats. For some studies, Leydig cells were isolated separately from aged testes that either had regressed because of age-related losses of germ cells or that were nonregressed. SOD (total) and GPx activities were found to decrease significantly with age whether or not the testes were regressed. CuZnSOD and MnSOD mRNA levels decreased with aging, though the magnitude of the decreases were considerably lower than the respective decreases in enzyme activities. GPx mRNA levels also decreased, which is consistent with the decreases seen in enzyme activity. MnSOD protein expression declined with age, and to a lesser extent, CuZnSOD did as well. Reduced and oxidized glutathione also exhibited age-related reductions in cells from both normal and regressed aged testes. The age-related decreases in Leydig cell antioxidant enzyme activities, gene expression, and protein levels and in glutathione were consistent with the hypothesis that the loss of steroidogenic function that accompanies Leydig cell aging may result in part from a decrease in the fidelity of the cellular antioxidant defense system.
PubMed ID
16304208 View in PubMed
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Amniotic fluid phthalate levels and male fetal gonad function.

https://arctichealth.org/en/permalink/ahliterature264835
Source
Epidemiology. 2015 Jan;26(1):91-9
Publication Type
Article
Date
Jan-2015
Author
Morten Søndergaard Jensen
Ravinder Anand-Ivell
Bent Nørgaard-Pedersen
Bo A G Jönsson
Jens Peter Bonde
David M Hougaard
Arieh Cohen
Christian H Lindh
Richard Ivell
Gunnar Toft
Source
Epidemiology. 2015 Jan;26(1):91-9
Date
Jan-2015
Language
English
Publication Type
Article
Keywords
Adult
Amniotic Fluid - chemistry
Case-Control Studies
Cryptorchidism - epidemiology
Denmark - epidemiology
Diethylhexyl Phthalate - analysis
Environmental Exposure - statistics & numerical data
Female
Gonadal Steroid Hormones - analysis
Humans
Hydrocortisone - analysis
Hypospadias - epidemiology
Immunoassay
Infant, Newborn
Insulin - analysis
Leydig Cells
Linear Models
Logistic Models
Male
Mass Spectrometry
Phthalic Acids - analysis
Pregnancy
Proteins - analysis
Abstract
Prenatal exposure to phthalates may pose a threat to human male reproduction. However, additional knowledge about the in vivo effect in humans is needed, and reported associations with genital abnormalities are inconclusive. We aimed to study prenatal di(2-ethylhexyl) phthalate (DEHP) and diisononyl phthalate (DiNP) exposure in relation to cryptorchidism, hypospadias, and human fetal Leydig cell function.
We studied 270 cryptorchidism cases, 75 hypospadias cases, and 300 controls. Second-trimester amniotic fluid samples were available from a Danish pregnancy-screening biobank (n = 25,105) covering 1980-1996. We assayed metabolites of DEHP and DiNP (n = 645) and steroid hormones (n = 545) by mass spectrometry. We assayed insulin-like factor 3 by immunoassay (n = 475) and analyzed data using linear or logistic regression.
Mono(2-ethyl-5-carboxypentyl) phthalate (5cx-MEPP, DEHP metabolite) was not consistently associated with cryptorchidism or hypospadias. However, we observed an 18% higher (95% confidence interval [CI] = 5%-33%) testosterone level, and a 41% lower (-56% to -21%) insulin-like factor 3 level in the highest 5cx-MEPP tertile compared with the lowest. Mono(4-methyl-7-carboxyheptyl) phthalate (7cx-MMeHP, DiNP metabolite) showed elevated odds ratio point estimates for having cryptorchidism (odds ratio = 1.28 [95% CI = 0.80 to 2.01]) and hypospadias (1.69 [0.78 to 3.67]), but was not consistently associated with the steroid hormones or insulin-like factor 3.
Data on the DEHP metabolite indicate possible interference with human male fetal gonadal function. Considering the DiNP metabolite, we cannot exclude (nor statistically confirm) an association with hypospadias and, less strongly, with cryptorchidism.
PubMed ID
25384265 View in PubMed
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[Case of the month: Leydig cell testicular tumor].

https://arctichealth.org/en/permalink/ahliterature100436
Source
Laeknabladid. 2010 Sep;96(9):545, 547
Publication Type
Article
Date
Sep-2010

Does HCG treatment induce inflammation-like changes in undescended testes in boys?

https://arctichealth.org/en/permalink/ahliterature36390
Source
J Pediatr Surg. 1993 Feb;28(2):254-8
Publication Type
Article
Date
Feb-1993
Author
M. Hjertkvist
G. Läckgren
L. Plöen
A. Bergh
Author Affiliation
Department of Surgery, University of Umeå, Sweden.
Source
J Pediatr Surg. 1993 Feb;28(2):254-8
Date
Feb-1993
Language
English
Publication Type
Article
Keywords
Biopsy
Child
Child, Preschool
Chorionic Gonadotropin - administration & dosage - adverse effects - therapeutic use
Cryptorchidism - drug therapy - pathology - surgery
Erythrocytes - drug effects
Follow-Up Studies
Hospitals, University
Humans
Inflammation
Leydig Cells - drug effects
Male
Microcirculation - drug effects
Neutrophils - drug effects
Research Support, Non-U.S. Gov't
Sweden
Time Factors
Treatment Failure
Abstract
Twenty-two cryptorchid boys previously unsuccessfully treated with human chorionic gonadotropin (hCG) were operated. Testicular biopsies were taken and a routine orchidopexy was performed in each case. As controls eight cryptorchid boys without prior hormonal treatment were operated in the same way. A mild inflammation-like reaction was found in the cryptorchid testes in the period immediately following the last hCG injection. However, in testes studied 6 to 12 months after the last hCG injection there were no apparent signs of hCG-induced tubular damage.
PubMed ID
8094747 View in PubMed
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Effect of glutathione depletion on Leydig cell steroidogenesis in young and old brown Norway rats.

https://arctichealth.org/en/permalink/ahliterature86392
Source
Endocrinology. 2008 May;149(5):2612-9
Publication Type
Article
Date
May-2008
Author
Chen Haolin
Pechenino Angela S
Liu June
Beattie Matthew C
Brown Terry R
Zirkin Barry R
Author Affiliation
Division of Reproductive Biology, Department of Biochemistry and Molecular Biology, Johns Hopkins Bloomberg School of Public Health, Baltimore, Maryland 21205, USA. hchen@jhsph.edu
Source
Endocrinology. 2008 May;149(5):2612-9
Date
May-2008
Language
English
Publication Type
Article
Keywords
Aging - drug effects - metabolism
Animals
Antimetabolites - pharmacology
Buthionine Sulfoximine - pharmacology
Cell Survival - drug effects
Cells, Cultured
Glutathione - antagonists & inhibitors - physiology
Leydig Cells - drug effects - metabolism
Male
Rats
Rats, Inbred BN
Steroids - metabolism
Testosterone - metabolism
Abstract
Changes in the oxidant/antioxidant environment of aging Leydig cells have been shown to be correlated with the reduced ability of these cells to produce testosterone. With this in mind, we hypothesized that the experimental depletion of glutathione (GSH), an abundant Leydig cell intracellular antioxidant, might result in reduced testosterone production. Incubation of Leydig cells isolated from the testes of adult Brown Norway rats with buthionine sulfoximine (BSO) reduced GSH content by more than 70% and testosterone production by about 40%. The antioxidants vitamin E, N-tert-butyl-alpha-phenylnitrone and Trolox countered BSO's effect on steroidogenesis but not on GSH depletion. Together, BSO and glutathione ethyl ester maintained intracellular GSH and also testosterone production, whereas 1,2-dithiole-3-thione, which increases intracellular GSH, increased testosterone production. In vivo studies also were conducted. Young (4 month old) and old (24 month old) rats were injected with BSO twice a day for 7 d, after which Leydig cells were isolated and analyzed in vitro. BSO treatment reduced Leydig cell GSH content by 70% and the ability of the Leydig cells to produce testosterone by more than 50%. As with aging, decreases were seen in LH-stimulated cAMP production, steroidogenic acute regulatory protein, cholesterol side-chain cleavage, 3beta-hydroxysteroid dehydrogenase, and 17alpha-hydroxylase/17,20-lyase. The results of these studies, taken together, are consistent with the hypothesis that alteration in the oxidant/antioxidant environment may play a significant, causative role in the age-related reduced ability of Leydig cells to produce testosterone.
PubMed ID
18202138 View in PubMed
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Functional study of a recombinant form of human LHbeta-subunit variant carrying the Gly(102)Ser mutation found in Asian populations.

https://arctichealth.org/en/permalink/ahliterature18862
Source
Mol Hum Reprod. 2002 Oct;8(10):887-92
Publication Type
Article
Date
Oct-2002
Author
Tarja Lamminen
Min Jiang
Pulak R Manna
Pirjo Pakarinen
Henrik Simonsen
Rene J Herrera
Ilpo Huhtaniemi
Author Affiliation
Department of Physiology, Institute of Biomedicine, University of Turku, Kiinamyllynkatu 10, FIN-20520 Turku, Finland.
Source
Mol Hum Reprod. 2002 Oct;8(10):887-92
Date
Oct-2002
Language
English
Publication Type
Article
Keywords
Animals
Asia
Asian Continental Ancestry Group - genetics
Cells, Cultured
Cyclic AMP - metabolism
Denmark
Finland
Glycine
Humans
India
Leydig Cell Tumor - genetics - metabolism
Luteinizing Hormone, beta Subunit - genetics - metabolism - pharmacology
Mice
Point Mutation
Progesterone - biosynthesis
Receptors, LH - metabolism
Recombinant Proteins - genetics - metabolism
Research Support, Non-U.S. Gov't
Research Support, U.S. Gov't, P.H.S.
Rwanda
Serine
Signal Transduction
Variation (Genetics)
Abstract
Genetic variants of human LH caused by amino acid replacements in the beta-subunit have been demonstrated to affect reproductive function. Occurrence of a G(1502)A substitution in the LHbeta gene leading to Gly(102)Ser replacement of the LHbeta protein has been found to be associated with infertility in the Singapore Chinese population. In the present study, a search for this LHbeta allele from 383 DNA samples from different continents, using a PCR-based strategy, demonstrated its total absence in these populations. Functional properties of the variant (V) (Gly(102)Ser substitution) LHbeta subunit were assessed using a recombinant (r) form of V-LH produced in HEK293 cells, in comparison with wild-type (WT) LH or hCG. The synthesized V-LH was purified by a single step of immunoaffinity chromatography, and it had a molecular weight of 30 kDa as determined by SDS-PAGE. The affinities of the WT-hCG and rV-LH in mouse Leydig tumour (mLT-1) cell LH receptor binding were similar, with K(d) values of 0.140 +/- 0.03 and 0.156 +/- 0.01 nmol/l respectively. Likewise, the effects of WT- and V-rLH preparations on mLT-1 cell cAMP and progesterone production were concentration-dependent and with similar biopotencies. In addition, HEK293 cells expressing the human LH receptor documented similar dose-dependent increases in inositol phosphate production by the two rLH forms. In conclusion, these findings demonstrate that Gly(102)Ser mutation of the LHbeta gene does not affect receptor binding and bioactivity of the hormone, when tested in vitro.
PubMed ID
12356936 View in PubMed
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Leydig cell dysfunction, systemic inflammation and metabolic syndrome in long-term testicular cancer survivors.

https://arctichealth.org/en/permalink/ahliterature286268
Source
Eur J Cancer. 2017 Oct;84:9-17
Publication Type
Article
Date
Oct-2017
Author
M. Bandak
N. Jørgensen
A. Juul
J. Lauritsen
P S Oturai
J. Mortensen
P. Hojman
J W Helge
G. Daugaard
Source
Eur J Cancer. 2017 Oct;84:9-17
Date
Oct-2017
Language
English
Publication Type
Article
Keywords
Adult
Biomarkers - blood
Case-Control Studies
Denmark - epidemiology
Hormone Replacement Therapy
Humans
Inflammation - blood - diagnosis - epidemiology - prevention & control
Leydig Cells - metabolism - pathology
Luteinizing Hormone - blood
Male
Metabolic Syndrome X - blood - diagnosis - epidemiology - prevention & control
Middle Aged
Prevalence
Protective factors
Risk factors
Survivors
Testicular Neoplasms - therapy
Testosterone - blood - deficiency - therapeutic use
Time Factors
Treatment Outcome
Abstract
Twenty to thirty percent of testicular cancer (TC) survivors have elevated serum levels of luteinising hormone (LH) with or without corresponding low testosterone levels (Leydig cell dysfunction) during clinical follow-up for TC. However, it remains to be clarified if this subgroup of TC survivors has an increased long-term risk of systemic inflammation and metabolic syndrome (MetS) when compared with TC survivors with normal Leydig cell function during follow-up.
TC survivors with Leydig cell dysfunction and a control group of TC survivors with normal Leydig cell function during follow-up were eligible for participation in the study. Markers of systemic inflammation and prevalence of MetS were compared between TC survivors with Leydig cell dysfunction and the control group.
Of 158 included TC survivors, 28 (18%) had uncompensated Leydig cell dysfunction, 59 (37%) had compensated Leydig cell dysfunction and 71 (45%) had normal Leydig cell function during follow-up. MetS and markers of systemic inflammation were evaluated at a median follow-up of 9.7 years (interquartile range 4.1-17.1) after TC treatment. The prevalence of MetS was significantly lower among patients with compensated Leydig cell dysfunction during follow-up (12% versus 27%, p = 0.04), whereas there was no difference between TC survivors with uncompensated Leydig cell dysfunction and controls (33% versus 27%, p = 0.5). Apart from high-sensitivity C-reactive protein which was higher in TC survivors with uncompensated Leydig cell dysfunction during follow-up, there was no evidence of increased systemic inflammation in patients with Leydig cell dysfunction during clinical follow-up. Total testosterone at follow-up was significantly associated with MetS, whereas there was no association between LH and MetS.
We did not find evidence that TC survivors with Leydig cell dysfunction during clinical follow-up had increased long-term risk of MetS. Total testosterone at follow-up was significantly associated with MetS. The study is registered at www.clinicaltrials.govNCT02240966.
PubMed ID
28772110 View in PubMed
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19 records – page 1 of 2.