Displaying all 18 publications

  1. Mohd Mokhtar H, Giribabu N, Kassim N, Muniandy S, Salleh N
    J Steroid Biochem Mol Biol, 2014 Oct;144 Pt B:361-72.
    PMID: 25125390 DOI: 10.1016/j.jsbmb.2014.08.007
    Estrogen is known to stimulate uterine fluid and Cl(-) secretion via CFTR. This study investigated testosterone effect on these changes in a rat model.
    Matched MeSH terms: Testosterone/pharmacology*
  2. Kuah KB
    Med J Malaysia, 1975 Mar;30(3):223-6.
    PMID: 1160683
    Matched MeSH terms: Testosterone/pharmacology
  3. Ramli NSK, Giribabu N, Karim K, Salleh N
    J. Mol. Histol., 2019 Feb;50(1):21-34.
    PMID: 30430402 DOI: 10.1007/s10735-018-9804-1
    Precise regulation of vas deferens fluid volume which is important for sperm survival might be influenced by testosterone. In order to investigate changes in vas deferens fluid volume and aquoporins (AQP) isoforms expression under testosterone influence, orchidectomized Sprague-Dawley rats were given 125 and 250 µg/kg/day testosterone with or without flutamide, an androgen receptor blocker or finasteride, a 5alpha-reductase inhibitor for seven consecutive days. Following treatment completion, vas deferens was perfused and changes in the fluid secretion rate and osmolality were determined in the presence of acetazolamide. Rats were then sacrificed and vas deferens was harvested for histology, tissue expression and distribution analyses of AQP-1, AQP-2, AQP-5, AQP-7 and AQP-9 proteins by Western blotting and immunohistochemistry, respectively. Our findings indicate that testosterone causes vas deferens fluid secretion rate to increase, which was antagonized by acetazolamide. Fluid osmolality increased following testosterone treatment and further increased when acetazolamide was given. Co-administration of flutamide or finasteride with testosterone causing both fluid secretion rate and osmolality to decrease. Histology revealed increased size of vas deferens lumen with increased thickness of vas deferens stroma. Expression of AQP-1, AQP-2 and AQP-9 were detected in vas deferens but not AQP-5 and AQP-7, and the levels of these proteins were increased by testosterone treatment mainly at the apical membrane of vas deferens epithelium. In conclusion, increased in vas deferens fluid secretion rate under testosterone influence mediated via the up-regulation of AQP-1, 2 and 9 might be important for vas deferens fluid homeostasis in order to ensure normal male fertility.
    Matched MeSH terms: Testosterone/pharmacology*
  4. Ang HH, Cheang HS
    Arch Pharm Res, 2001 Oct;24(5):437-40.
    PMID: 11693547 DOI: 10.1007/BF02975191
    It has been reported that Eurycoma longifolia Jack commonly known as Tongkat Ali has gained notoreity as a symbol of man's ego and strength by the Malaysian men because it increases male virility and sexual prowess during sexual activities. As such, the effects of 200, 400 and 800 mg/kg of butanol, methanol, water and chloroform fractions of E. longifolia Jack were studied on the laevator ani muscle in both uncastrated and testosterone-stimulated castrated intact male rats after dosing them for 12 consecutive weeks. Results showed that 800 mg/kg of butanol, methanol, water and chloroform fractions of E. longifolia Jack significantly increased (p<0.05) the leavator ani muscle to 58.56+/-1.22, 58.23+/-0.31, 60.21 +/-0.86 and 62.35 +/-0.98 mg/100 g body weight, respectively, when compared with the control (untreated) in the uncastrated intact male rats and 49.23+/-0.82, 52.23+/-0.36, 50.21+/-0.66 and 52.35+/-0.58 mg/100 g body weight, respectively, when compared to control (untreated) in the testosterone-stimulated castrated intact male rats. Hence, the pro-androgenic effect as shown by this study further supported the traditional use of this plant as an aphrodisiac.
    Matched MeSH terms: Testosterone/pharmacology*
  5. Mokhtar HM, Giribabu N, Muniandy S, Salleh N
    Int J Clin Exp Pathol, 2014;7(5):1967-76.
    PMID: 24966906
    Pinopode, a progesterone-dependent endometrial projection which appears during uterine receptivity period, participates in blastocyst implantation. Blastocyst loosely attaches to pinopode via L-selectin ligand (MECA-79). We hypothesized that pinopode and MECA-79 expressions were affected by testosterone. Therefore, the effect of testosterone on pinopode and MECA-79 expressions during uterine receptivity period were investigated.
    Matched MeSH terms: Testosterone/pharmacology*
  6. Salleh N, Mokhtar HM, Kassim NM, Giribabu N
    J. Membr. Biol., 2015 Dec;248(6):1097-105.
    PMID: 26198330 DOI: 10.1007/s00232-015-9823-8
    Testosterone has been reported to cause a decrease in uterine fluid volume in which this could involve the aquaporins (AQPs). This study aimed to investigate effect of testosterone on uterine AQP-1, 5, and 7 expressions in order to explain the reported reduction in uterine fluid volume under testosterone influence. Ovariectomized adult female rats received peanut oil, testosterone (1 mg/kg/day), estrogen (0.2 µg/kg/day), or combined estrogen plus testosterone for three consecutive days. Other groups received 3 days estrogen followed by 2 days either peanut oil or testosterone with or without flutamide or finasteride. A day after last injection, uteri were harvested, and the levels of AQP-1, 5, and 7 messenger RNA (mRNA) in uterine tissue homogenates were analyzed by real-time PCR (qPCR). Distributions of AQP-1, 5, and 7 proteins in uterus were observed by immunofluorescence. Levels of AQP-1 mRNA were elevated in rats receiving either estrogen or testosterone-only treatment; however, levels of AQP-5 and 7 mRNAs were elevated in rats receiving testosterone-only treatment. In rats pre-treated with estrogen, testosterone treatment resulted in higher AQP-1, 5, and 7 mRNA levels compared to vehicle treatment. Testosterone effects were antagonized by flutamide but not finasteride. Immunofluorescence study showed that AQP-1 was highly distributed in uterine lumenal epithelium following estrogen or testosterone-only treatment. However, AQP-5 and 7 distributions were high in uterine lumenal epithelium following testosterone-only treatment. Testosterone-induced up-regulation of AQP-1, 5, and 7 expressions in uterus could explain the observed reduction in uterine fluid volume as reported under this condition.
    Matched MeSH terms: Testosterone/pharmacology*
  7. Nwe KH, Hamid A, Morat PB, Khalid BA
    Steroids, 2000 Jan;65(1):40-5.
    PMID: 10624835
    11Beta-hydroxysteroid dehydrogenase (11beta-HSD) Type I enzyme is found in testis and liver. In Leydig cell cultures, 11beta-HSD activity is reported to be primarily oxidative while another report concluded that is primarily reductive. Hepatic 11beta-HSD preferentially catalyzes reduction and the reaction direction is unaffected by the external factors. Recent analysis of testicular 11beta-HSD revealed two kinetically distinct components. In the present study, various steroid hormones or glycyrrhizic acid (GCA), given for 1 week, or thyroxine given for 5 weeks to normal intact rats had different effects on the 11beta-HSD oxidative activity in testis and liver. Deoxycorticosterone, dexamethasone, progesterone, thyroxine, and clomiphene citrate increased testicular 11beta-HSD oxidative activity, but decreased hepatic enzyme activity except for deoxycorticosterone (unchanged). Corticosterone and testosterone decreased 11beta-HSD oxidative activity in testis but not that of liver (which was unchanged). Estradiol, GCA and adrenalectomy lowered oxidative activity of 11beta-HSD in testis and liver, but the degrees of reduction were different. The in vivo effects of glucocorticoids too were different, even in the same organ. Dexamethasone, a pure glucocorticoid, has greater affinity for glucocorticoid receptors (GR) than corticosterone. The direct effects of dexamethasone via GR in increasing testicular 11beta-HSD oxidative activity may override its indirect effects. Possibly, the reverse occurs with corticosterone treatment, as it has both glucocorticoid and mineralocorticoid effects. Because both organs have Type I isoenzyme, the difference in 11beta-HSD oxidative activities of these two organs could be attributable to the presence of an additional isozyme in testis or differences in tissue-specific regulatory mechanisms.
    Matched MeSH terms: Testosterone/pharmacology
  8. Kamis AB, Ahmad RA, Badrul-Munir MZ
    Parasitol Res, 1992;78(5):388-91.
    PMID: 1495916
    Gonadectomized male albino rats aged 7 weeks were given 1.5 mg/kg testosterone propionate daily and inoculated with 50 third-stage larvae of Angiostrongylus malaysiensis. The treatment significantly increased the number of larvae and adult worms recovered from the brain and pulmonary arteries, respectively, and the rats exhibited smaller thymus glands. The total numbers of leukocytes, monocytes, neutrophils, and especially eosinophils increased significantly post-infection, but the counts were higher in the untreated infected controls. Presumably, immunosuppressive effects of testosterone may at least partly be responsible for the higher loads of A. malaysiensis worms found in male rats as compared with females in the field.
    Matched MeSH terms: Testosterone/pharmacology*
  9. Nwe KH, Morat PB, Khalid BA
    Gen. Pharmacol., 1997 May;28(5):661-4.
    PMID: 9184798
    1. Sex steroids have been shown to regulate the biosynthesis of 11 beta-hydroxysteroid dehydrogenase (11 beta-HSD). 2. In vitro studies showed that oestradiol (E2) or testosterone (T) can interfere with the bioassay of enzyme activity, but not progesterone (P4). 3. For in vivo studies, the activity of 11 beta-HSD in the testis of normal and adrenalectomized (ADX) adult male Wistar rats was determined following a daily IM injection of sex steroids for 7 days. 4. The 11 beta-HSD activity was significantly reduced (P < 0.01) either by E2 or T in normal and ADX rats. The enzyme activity in normal rats given both T and E2 was even lower (P < 0.001) than when E2 was given alone. 5. P4 given to normal and ADX rats increased the enzyme activity higher than normal (P < 0.001). 6. The presence of corticosteroids influenced the effects of E2, but not of T and P4, on 11 beta-HSD activity. 7. E2 and T downregulate 11 beta-HSD activity, whereas P4 increased it. E2 did not act through lowering T level.
    Matched MeSH terms: Testosterone/pharmacology
  10. Mohamad NV, Wong SK, Wan Hasan WN, Jolly JJ, Nur-Farhana MF, Ima-Nirwana S, et al.
    Aging Male, 2019 Jun;22(2):129-140.
    PMID: 29925283 DOI: 10.1080/13685538.2018.1482487
    Testosterone is the predominant gonadal androgen in men. Low testosterone levels are found to be associated with an increased in metabolic risk and systematic inflammation. Since adipose tissue is a source of inflammatory cytokines, testosterone may regulate inflammation by acting on adipose tissue. This review aimed to explore the role of testosterone in inflammation and its mechanism of action. Both animal studies and human studies showed that (1) testosterone deficiency was associated with an increase in pro-inflammatory cytokines; (2) testosterone substitution reduced pro-inflammatory cytokines. The suppression of inflammation by testosterone were observed in patients with coronary artery disease, prostate cancer and diabetes mellitus through the increase in anti-inflammatory cytokines (IL-10) and the decrease in pro-inflammatory cytokines (IL-1β, IL-6, and TNF-α). Despite these, some studies also reported a non-significant relationship. In conclusion, testosterone may possess anti-inflammatory properties but its magnitude is debatable. More evidence is needed to validate the use of testosterone as a marker and in the management of chronic inflammatory diseases.
    Matched MeSH terms: Testosterone/pharmacology
  11. Mokhtar MH, Giribabu N, Salleh N
    In Vivo, 2019 12 29;34(1):225-231.
    PMID: 31882482 DOI: 10.21873/invivo.11764
    BACKGROUND/AIM: It was hypothesized that endometrial tight junction morphology and expression of tight junction proteins i.e., claudin-4 and occludin in the uterus, are affected by testosterone. Therefore, the effects of testosterone on these parameters in the uterus during receptivity period were investigated.

    MATERIALS AND METHODS: Ovariectomized adult female rats were given testosterone (1 mg/kg/day) alone or in combination with flutamide or finasteride between days 6 to 8 of sex-steroid replacement treatment, which was considered the period of uterine receptivity. Ultramorphology of tight junctions was visualized by transmission electron microscopy while distribution and expression of claudin-4 and occludin were examined by immunofluorescence and real-time polymerase chain reaction respectively.

    RESULTS: Administration of testosterone caused loss of tight junction complexity and down-regulated expression of claudin-4 and occludin in the uterus.

    CONCLUSION: Decreased endometrial tight junction complexity and expression of claudin-4 and occludin in the uterus during receptivity period by testosterone may interfere with embryo attachment and subsequent implantation.

    Matched MeSH terms: Testosterone/pharmacology*
  12. Ang HH, Cheang HS, Yusof AP
    Exp Anim, 2000 Jan;49(1):35-8.
    PMID: 10803359 DOI: 10.1538/expanim.49.35
    We studied the effects of Eurycoma longifolia Jack, commonly known as Tongkat Ali in Malaysia, on the initiation of sexual performance and the weights of sexual accessories in inexperienced castrated male rats. The doses of 200, 400 and 800 mg/kg body weight, which were extracted from E. longifolia Jack, were orally administered to the rats twice daily for 10 days prior to the tests and continued throughout the test period. Testosterone was used as a positive control after injecting 15 mg/kg daily subcutaneously for 32 days. Results showed that E. longifolia Jack produced a dose-dependent increase in sexual performance of the treated animals, but the E. longifolia Jack groups showed lower sexual performance in mounting, intromission and ejaculation than the testosterone group. Further results also showed that E. longifolia Jack promoted the growth of both ventral prostate and seminal vesicles as compared with the control, but the growth of sexual accessories at 800 mg/kg of butanol, methanol, water and chloroform fractions of E. longifolia Jack was less than that of testosterone treated group. The present study therefore gives further evidence of the folkuse of E. longifolia as an aphrodisiac.
    Matched MeSH terms: Testosterone/pharmacology
  13. Chin KY, Ima-Nirwana S
    Clin Interv Aging, 2014;9:1247-59.
    PMID: 25120355 DOI: 10.2147/CIA.S67016
    BACKGROUND: Previous animal models have demonstrated that tocotrienol is a potential treatment for postmenopausal osteoporosis. This study evaluated the antiosteoporotic effects of annatto-derived tocotrienol (AnTT) using a testosterone-deficient osteoporotic rat model.
    METHODS: Forty rats were divided randomly into baseline, sham, orchidectomized, AnTT, and testosterone groups. The baseline group was euthanized without undergoing any surgical treatment or intervention. The remaining groups underwent orchidectomy, with the exception of the sham group. AnTT 60 mg/kg/day was given orally to the AnTT group, while the testosterone group received testosterone enanthate 7 mg/kg per week intramuscularly for 8 weeks. Structural changes in trabecular bone at the proximal tibia were examined using microcomputed tomography. Structural and dynamic changes at the distal femur were examined using histomorphometric methods. Serum osteocalcin and C-terminal of type 1 collagen crosslinks were measured. Bone-related gene expression in the distal femur was examined.
    RESULTS: There were significant degenerative changes in structural indices in the orchidectomized group (P<0.05), but no significant changes in dynamic indices, bone remodeling markers, or gene expression (P>0.05) when compared with the sham group. The AnTT group showed significant improvement in structural indices at the femur (P<0.05) and significantly increased expression of bone formation genes (P<0.05). Testosterone was more effective than AnTT in preventing degeneration of bone structural indices in the femur and tibia (P<0.05).
    CONCLUSION: AnTT supplementation improves bone health in testosterone-deficient rats by enhancing bone formation. Its potential should be evaluated further by varying the dosage and treatment duration.
    KEYWORDS: bone remodeling; osteoporosis; testosterone; tocotrienol
    Matched MeSH terms: Testosterone/pharmacology
  14. George A, Henkel R
    Andrologia, 2014 Sep;46(7):708-21.
    PMID: 24386995 DOI: 10.1111/and.12214
    The testosterone deficiency syndrome (TDS) is characterised by numerous symptoms, including low libido, increased fat mass, fatigue, erectile dysfunction or osteoporosis, and up to 80% of men will experience some kind of ageing males' symptoms. This is caused by the age-depending decline in serum testosterone levels with concentrations being about 40-50% lower in men older than 60 years compared with young men. This significant decline in testosterone levels is further closely linked with medical conditions such as obesity, metabolic syndrome, diabetes or hypertension. The conventional way of treating TDS is the testosterone replacement therapy (TRT), for which preparations are on the market. Apart from the beneficial effects of TRT, significant adverse side effects have been described, and prostate cancer (PCa) as absolute contraindication is debated. Eurycoma longifolia (Tongkat Ali; TA) is natural alternative to TRT and has been shown to restore serum testosterone levels, thus significantly improving sexual health. This includes significant positive effects on bone health and physical condition of patients. In addition, a significant antihyperglycaemic effect and cytotoxicity against PCas cells has been shown. Thus far, at therapeutic concentrations, no significant side effects of the treatment were obvious. Therefore, TA might be a safe alternative to TRT.
    Matched MeSH terms: Testosterone/pharmacology
  15. Ab Rahman NS, Abd Majid FA, Abd Wahid ME, Zainudin AN, Zainol SN, Ismail HF, et al.
    Drug Metab Lett, 2018;12(1):62-67.
    PMID: 29542427 DOI: 10.2174/1872312812666180314112457
    BACKGROUND: SynacinnTM contains five standardized herbal extracts of Orthosiphon Stamineus (OS), Syzygium polyanthum (SZ), Curcuma xantorrizza (CX), Cinnamomum zeylanicum (CZ) and Andrographis paniculata (AP) and is standardized against phytochemical markers of rosmarinic acid, gallic acid, curcumin, catechin and andrographolide respectively. This herbal medicine has been used as health supplement for diabetes. SynacinnTM is recommended to be consumed as supplement to the diabetic drugs. However, herb-drug interaction of SynacinnTM polyherbal with present drugs is unknown.

    METHODS: This study was designed to investigate the effect of SynacinnTM and its individual biomarkers on drug metabolizing enzymes (CYP1A2, CYP2B6, CYP2C8, CYP2C9, CYP2C19, CYP2D6, CYP3A4 (Midazolam), CYP3A4 (Testosteron)), to assess its herb-drug interaction potential through cytochrome P450 inhibition assay. This study was conducted using liquid chromatography- tandem mass spectroscopy (LC-MS/MS) using probe substrates using human liver microsomes against CYP1A2, CYP2B6, CYP2C8, CYP2C9, CYP2C19, CYP2D6, CYP3A4 (Midazolam) and CYP3A4 (Testosteron).

    RESULTS: Result showed that SynacinnTM at maximum concentration (5000 µg/ml) 100% inhibit CYP1A2, CYP2B6, CYP2C8, CYP2C9, CYP2C19, CYP2D6, CYP3A4 (Midazolam) and CYP3A4 (Testosteron). IC50 values determined were 0.23, 0.60, 0.47, 0.78, 1.23, 0.99, 1.01, and 0.91 mg/ml for CYP 1A2, 2B6, 2C8, 2C9, 2C19, 2D6, 3A4 (midazolam) and 3A4 (testosterone), respectively. Meanwhile, all individual biomarkers showed no, less or moderate inhibitory effect towards all the tested CYP450 except for curcumin that showed inhibition of CYP2C8 (91%), CYP2C9 (81%) and CYP2C19 (72%) at 10µM.

    CONCLUSION: Curcumin was found to be an active constituent that might contribute to the inhibition of SynacinnTM against CYP2C8, CYP2C9 and CYP2C19. It can be suggested that SynacinnTM can be consumed separately from a drug known to be metabolized by all tested CYP450 enzymes.

    Matched MeSH terms: Testosterone/pharmacology
  16. Khadijah Ramli NS, Giribabu N, Muniandy S, Salleh N
    Theriogenology, 2018 Mar 01;108:354-361.
    PMID: 29294437 DOI: 10.1016/j.theriogenology.2017.12.035
    Precise regulation of vas deferens fluid pH is essential for sperm. However, the mechanisms underlying effect of testosterone on vas deferens fluid pH have never been identified, which could involve changes in expression and functional activity of vacoular (V)-ATPase.

    METHODS: Orchidectomized, adult male Sprague-Dawley rats were treated subcutaneously with 125 μg/kg/day and 250 μg/kg/day testosterone with or without flutamide (androgen receptor blocker) and finasteride (5α-reductase inhibitor) for seven (7) days. Following treatment completion, in vivo perfusion of vas deferens lumen was performed and changes in fluid secretion rate, pH and HCO3- content were measured with and without bafilomycin, a V-ATPase inhibitor. Rats were then sacrificed and vas deferens were harvested and subjected for V-ATPase A1 and B1/2 protein expression and distribution analysis by western blotting and immunohistochemistry, respectively.

    RESULTS: In sham-operated and testosterone-treated orchidectomized rats, higher fluid secretion rate, which was not antagonized by bafilomycin but lower HCO3- content and pH which were antagonized by bafilomycin were observed when compared to orchidectomized-only and orchidectomized, testosterone-treated rats receiving flutamide or finasteride, respectively. Bafilomycin had no effect on fluid secretion rate, HCO3- content and pH in orchidectomized and testosterone-treated orchidectomized rats receiving flutamide and finasteride. V-ATPase A1 and B1/2 proteins were expressed at high levels in vas deferens and were highly distributed at the apical membrane of luminal epithelium and in muscle layer of this organ, mainly in sham and testosterone-treated orchidectomized rats.

    CONCLUSIONS: V-ATPase is involved in acidification of vas deferens fluid under testosterone influence.

    Matched MeSH terms: Testosterone/pharmacology*
  17. Dehghan F, Muniandy S, Yusof A, Salleh N
    Int J Mol Sci, 2014;15(3):4619-34.
    PMID: 24642882 DOI: 10.3390/ijms15034619
    Ovarian steroids such as estrogen and progesterone have been reported to influence knee laxity. The effect of testosterone, however, remains unknown. This study investigated the effect of testosterone on the knee range of motion (ROM) and the molecular mechanisms that might involve changes in the expression of relaxin receptor isoforms, Rxfp1 and Rxfp2 in the patella tendon and lateral collateral ligament of the female rat knee. Ovariectomized adult female Wistar rats received three days treatment with peanut oil (control), testosterone (125 and 250 μg/kg) and testosterone (125 and 250 μg/kg) plus flutamide, an androgen receptor blocker or finasteride, a 5α-reductase inhibitor. Duplicate groups received similar treatment however in the presence of relaxin (25 ng/kg). A day after the last drug injection, knee passive ROM was measured by using a digital miniature goniometer. Both tendon and ligament were harvested and then analysed for protein and mRNA expression for Rxfp1 and Rxfp2 respectively. Knee passive ROM, Rxfp1 and Rxfp2 expression were significantly reduced following treatment with testosterone. Flutamide or finasteride administration antagonized the testosterone effect. Concomitant administration of testosterone and relaxin did not result in a significant change in knee ROM as compared to testosterone only treatment; however this was significantly increased following flutamide or finasteride addition. Testosterone effect on knee passive ROM is likely mediated via dihydro-testosterone (DHT), and involves downregulation of Rxfp1 and Rxfp2 expression, which may provide the mechanism underlying testosterone-induced decrease in female knee laxity.
    Matched MeSH terms: Dihydrotestosterone/pharmacology*; Testosterone/pharmacology*
  18. Tan WS, Low WY, Ng CJ, Tan WK, Tong SF, Ho C, et al.
    BJU Int, 2013 Jun;111(7):1130-40.
    PMID: 23651425 DOI: 10.1111/bju.12037
    OBJECTIVE: To evaluate the efficacy and safety of long-acting i.m. testosterone undecanoate (TU) in Malaysian men with testosterone deficiency (TD).

    PATIENTS AND METHODS: A total of 120 men, aged 40-70 years, with TD (serum total testosterone [TT] ≤ 12 nmol/L) were randomised to receive either i.m. TU (1000 mg) or placebo. In all, 58 and 56 men in the placebo and treatment arm, respectively, completed the study. Participants were seen six times in the 48-week period and the following data were collected: physical examination results, haemoglobin, haematocrit, TT, lipid profile, fasting blood glucose, sex hormone-binding globulin, liver function test, prostate- specific antigen (PSA) and adverse events.

    RESULTS: The mean (sd) age of the participants was 53.4 (7.6) years. A significant increase in serum TT (P < 0.001), PSA (P = 0.010), haematocrit (P < 0.001), haemoglobin (P < 0.001) and total bilirubin (P = 0.001) were seen in the treatment arm over the 48-week period. Two men in the placebo arm and one man in the treatment arm developed myocardial infarction. Common adverse events observed in the treatment arm included itching/swelling/pain at the site of injection, flushing and acne. Overall, TU injections were well tolerated.

    CONCLUSIONS: TU significantly increases serum testosterone in men with TD. PSA, haemoglobin and haematocrit were significantly elevated but were within clinically safe limits. There was no significant adverse reaction that led to the cessation of treatment.

    Matched MeSH terms: Testosterone/pharmacology
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