Disease relevance of testosterone

• In six of six men with prostate cancer, PC-SPES decreased serum testosterone concentrations (P<0.05), and in eight of eight patients it decreased serum concentrations of prostate-specific antigen [1].
• We investigated increased production of testosterone and androstenedione in 44 women with unexplained adult-onset hirsutism, 41 of whom had normal-sized ovaries [2].
• Preventing the conversion of testosterone to its tissue-active form, dihydrotestosterone, by inhibiting the enzyme 5 alpha-reductase could decrease the action of androgens in their target tissues; in the prostate the result might be a decrease in prostatic hyperplasia and therefore in symptoms of urinary obstruction [3].
• Nine of 13 pubertal boys (ages 11 to 16) had moderate to severe gynecomastia and germinal aplasia, a 10-fold increase in mean (+/- S.D.) serum follicle-stimulating hormone (34.8 +/- 20.5 mlU per milliliter), a threefold increase in mean luteinizing hormone (17.8 +/- 9.8 mlU per milliliter) and reduced serum testosterone levels [4].
• These results indicate that alcohol markedly affects testosterone metabolism independently of cirrhosis or nutritional factors [5].

Psychiatry related information on testosterone

• They have plasma testosterone levels in the high normal range, show an excellent response to testosterone and are unique models for evaluating the effect of testosterone, as compared with a female upbringing, in determining gender identity [6].
• Classical conditioning: induction of luteinizing hormone and testosterone secretion in anticipation of sexual activity [7].
• Testosterone given during a critical period in prenatal or immediate postnatal life causes permanent organizational effects on brain structure and function in laboratory animals [8].
• Follow-up evaluations of penile blood pressure, bulbocavernosus reflex response latency, and plasma concentrations of testosterone and prolactin allowed localization of probable organic deficits [9].
• Possible subtypes of affective disorder suggested by differences in cerebral laterality and testosterone. A preliminary report [10].

High impact information on testosterone

• Clearly some like relaxin and inhibin function as important hormones, and ABP, for example, probably functions importantly in transporting testosterone down the tubule [11].
• Despite an appreciable placebo response, the higher testosterone dose resulted in further increases in scores for frequency of sexual activity and pleasure-orgasm in the Brief index of Sexual Functioning for Women (P=0.03 for both comparisons with placebo) [12].
• We evaluated the effects of transdermal testosterone in women who had impaired sexual function after surgically induced menopause [12].
• Lack of Ahch causes progressive degeneration of the testicular germinal epithelium independent of abnormalities in gonadotropin and testosterone production and results in male sterility [13].
• Defects in the conversion of androstenedione to testosterone in the fetal testes by the enzyme 17 beta-hydroxysteroid dehydrogenase (17 beta-HSD) give rise to genetic males with female external genitalia [14].

Chemical compound and disease context of testosterone

• If a late-onset form exists, hypogonadism and gynecomastia caused by decreased testosterone production and increased estrogen production, respectively, would be expected as the major clinical manifestations in men [15].
• All the women with adrenal tumors had elevated basal serum concentrations of testosterone or dehydroepiandrosterone sulfate, as compared with 36 of the 73 women with non-neoplastic hirsutism (sensitivity, 100 percent; 95 percent confidence interval, 77 to 100; specificity, 50 percent; 95 percent confidence interval, 38 to 62) [16].
• beta-Retinoic acid inhibits and reverses testosterone-induced hyperplasia in mouse prostate organ cultures [17].
• Albeit the clinical picture of aging in men is reminiscent of that of hypogonadism in young men and decreased testosterone production appears to play a role in part of these clinical changes in at least some elderly men, the clinical relevancy of the age-related decline in sex steroid levels in men has not been unequivocally established [18].
• During sensory intake, Type A hyperresponsivity was found for testosterone and, among those subjects with a positive family history of hypertension, for cortisol [19].

Biological context of testosterone

• Testosterone treatment in adolescent boys with constitutional delay in growth and development [20].
• The major effect of testosterone appears to be the regulation of the abundance of specific RNA sequences [21].
• From the epithelial and mesenchymal components, reciprocal recombinations were prepared and cultivated on millipore filter in the presence of testosterone [22].
• Synergistic interaction of testosterone and oestradiol inhibits spermatogenesis in rats [23].
• It has been suggested that female birds put more resources into eggs fathered by attractive males by laying larger eggs or by adding more testosterone, but this inference could be undermined if eggs of different sex are provisioned differently, as these studies did not control for sex differences [24].

Anatomical context of testosterone

• The patients had normal or elevated concentrations of plasma androgens, normal production rates of testosterone and dihydrotestosterone, elevated serum levels of luteinizing hormone and normal 5alpha-reductase activity in skin fibroblasts [25].
• In the male mouse, regression of the mammary gland anlagen is induced by testosterone during embryonic life [22].
• The results show that testosterone induces detachment and degeneration of the buds via the mesenchyme [22].
• The primary function of the testosterone secreted by Leydig cells is the maintenance of spermatogenesis and hence fertility [26].
• This action of testosterone is mediated by the Sertoli cells which nourish and support the developing spermatozoa [26].

Associations of testosterone with other chemical compounds

• In combination with androgen-insensitive Tfm- mesenchyme, the wild-type buds survived the action of testosterone [22].
• Dihydrotestosterone and testosterone levels rose and exceeded normal values after therapy [27].
• Luteinizing hormone stimulates testicular Leydig cells to produce testosterone by binding to a receptor that activates the G protein Gs and adenylyl cyclase [28].
• Macromolecules, steroid binding and testosterone secretion by rabbit testes [29].
• Moreover, leuprorelin treatment reversed the behavioral and histopathological phenotypes that were once caused by transient increases in serum testosterone [30].

Gene context of testosterone

• Corticotropin-releasing hormone (CRH), the principal neuropeptide regulator of pituitary ACTH secretion, is also produced at peripheral inflammatory sites, where it acts as a proinflammatory cytokine, and by the Leydig cell of the testis, where it exerts autocrine inhibition of testosterone biosynthesis [31].
• In neonatal mice, AMH was not inhibited by intratesticular testosterone, due to the lack of expression of the androgen receptor in Sertoli cells [32].
• RESULTS: The risk of HCC increased with increasing concentrations of testosterone (odds ratio [OR](highest versus lowest tertile) = 2.97; 95% confidence interval [CI] = 1.54 to 5.70; P(trend) <.001) and with increasing number of the V allele of the SRD5A2 V89L polymorphism (OR(VV versus LL genotype) = 2.47; 95% CI = 1.21 to 5.03; P(trend) =.011) [33].
• Testosterone upregulated both VEGF and its endothelial receptor, VEGF-R2/Quek1/KDR, in HVC [34].
• We evaluated whether testosterone inhibited TNFalpha-induced VCAM-1 expression via its conversion to estradiol by the enzyme aromatase in human umbilical vein endothelial cells (HUVEC) [35].

Analytical, diagnostic and therapeutic context of testosterone

• We assessed the clinical activity of PC-SPES in eight patients with hormone-sensitive prostate cancer by measuring serum prostate-specific antigen and testosterone concentrations during and after treatment [1].
• Transdermal testosterone treatment in women with impaired sexual function after oophorectomy [12].
• Plasma testosterone levels were similar in the two groups and increased equally in response to an intramuscular injection of 2000 units of human chorionic gonadotropin [36].
• To examine the hypothesis that the plasma of boys with familial male precocious puberty contains a novel stimulator of testicular testosterone production, we developed a bioassay using adult male cynomolgus monkeys [37].
• Throughout the follow-up period, all patients had normal testicular function as determined by Tanner staging at physical examination and by serum gonadotropin and testosterone levels [38].

References