• Title, Summary, Keyword: dehydroepiandrosterone

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Dehydroepiandrosterone and cortisol concentrations in the cerebrospinal fluid of dogs

  • Mongillo, Paolo;Bernardini, Marco;Prana, Elisa;Balducci, Federica;Gabai, Gianfranco;Marinelli, Lieta
    • Korean Journal of Veterinary Research
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    • v.57 no.1
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    • pp.47-50
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    • 2017
  • Concentrations of cortisol, dehydroepiandrosterone and dehydroepiandrosterone-sulfate were measured by performing radioimmunoassay of the cerebrospinal fluid of 68 dogs diagnosed with idiopathic epilepsy or inflammatory, degenerative, or non-neurological disease. No steroid concentration differences were found among diagnoses. Dehydroepiandrosterone and dehydroepiandrosterone-sulfate concentrations were higher in males than in females and dehydroepiandrosterone-sulfate decreased with increasing age. No sex or age effects were observed on cortisol or hormone ratios. Although limited to a relatively small sample, our results show sex- and age-dependent variations in these neurosteroid concentrations in cerebrospinal fluid. The role of such variations in the pathophysiology of the dog brain warrants further investigation.

Responsiveness of the Thoracic Aorta in Rats Treated with Dehydroepiandrosterone (DHEA) (Dehydroepiandrosterone(DHEA)의 투여에 의한 rat 흉대동맥의 반응성 변화)

  • 박관하
    • Biomolecules & Therapeutics
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    • v.9 no.2
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    • pp.119-124
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    • 2001
  • In order to determine the role of dehydroepiandrosterone (DHEA), the important sex-steroid hormone precursor, in vascular reactivity in rats, animals were treated for two weeks with DHEA or sex hormones, and the vascorelaxant and contractile responses of isolated aorta were examined. DHEA diminished the acetylcholine (ACh)-induced relaxation in female rats, while the drug was without effect in males. Testoterone lowered the vasorelaxant activity to ACh in either sex. 17$\beta$-Estradiol enhanced ACh-induced vasorelaxation in male rats, but this female sex hormone did not influence in females. In male rats, the androgen receptor antagonist flutamide also enhanced vasorelaxant action of ACh. When the male rat aorta was incubated in vitro with a nitric oxide (NO) synthase inhibitor L-NAME, phenylephrine-induced contraction was greatly potentiated in DHEA-pretreated rats compared to control ones. The present results suggest that DHEA stimulates mainly androgen in female, but both androgen and estrogen in male rats. The participation of NO In the modulation of vascular reactivity with pretreated DHEA was also considered.

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Effects of Vitamin E and Dehydroepiandrosterone on the Formation of Preneoplastic Lesions in Rat Hepatocellular Carcinogenesis (비타민 E와 Dehydroepiandrosterone이 화학적 발암원으로 유도한 쥐간의 전암성 병변에 미치는 영향)

  • Kim, Sook-Hee;Choi, Hay-Mie
    • Journal of Nutrition and Health
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    • v.38 no.5
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    • pp.364-372
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    • 2005
  • This study is designed to examine the effects of dietary supplementation with vitamin E and dehydroepiandrosterone (DHEA) on the formation of preneoplastic lesions in diethylnitrosamine (DEN) induced rat hepatocarcinogenesis. All Weaning male Sprague-Dawley rats were initiated by a single dose of DEN (200mg/kg body weight), subjected to two­thirds partial hepatectomy 3 weeks later and were sacrificed 8 weeks after DEN initiation. Two weeks after initiation, rats were fed Purina purified rodent diet 5053 (Ralston Purina Rat chow, USA) with $1.5\%$ (15,000 IU/kg diet) vitamin E, $0.5\%$ DHEA and both of those supplemented diet for 6 weeks. Placental glutathione S-transferase (GST-P) positive foci, the activities of catalase, total-glutathione peroxidase (GPx) , glutathione reductase (GR), glutathione S-transferase (GST) and thiobarbituric acid reactive substances (TBARS) contents were decreased significantly by vitaimin E supplement. On the other hand GST-P positive foci number, Cu/Zn-superoxide dismutase (SOD) and glucose 6-phosphatase (G6Pase) activities weren't changed by vitamin E supplement. It might suggest that protective effect of vitamin E against hepatocarcinogens is not involved in the formation of the GST-P positive foci but related to the expansion of that. It seemed that vitamin E supplement helped endogenous defense system in carcinogenesis by decreasing TBARS contents, $H_2O_2$, organic peroxides. Therefore, vitamin E seemed to protect cell from free radical damage in carcinogenesis. By DHEA supplement liver weight and liver/body ratio were increased, the area and number of GST-P positive foci, the activities of catalase, GR, total GPx, GST and the TBARS contents were decreased significantly. On the other hand Cu/Zn-SOD and G6Pase activities weren't changed by DHEA supplement. In hepatocarcinogenesis the activities of antioxidant enzymes weren't increased by DHEA supplement. DHEA did not increase the oxidative stress, while DHEA seems to have anticarcinogenic effect in rats hepatocarcinogenesis.

The Effect of Dehydroepiandrosterone on Isoproterenol-induced Cardiomyopathy in Rats

  • Jeong, Ji-Hoon;Kim, Chan-Woong;Yim, Sung-Hyuk;Shin, Yong-Kyoo;Park, Kyung-Wha;Park, Eon-Sub
    • The Korean Journal of Physiology and Pharmacology
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    • v.10 no.2
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    • pp.79-83
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    • 2006
  • We evaluated therapeutic and preventive properties of dehydroepiandrosterone (DHEA), a weak androgenic steroid, against isoproterenol-induced cardiomyopathy. The cardiomyopathy was induced by daily i.p. administration of isoproterenol to rats for five days. One group of rats were given with daily s.c. for 5 days during isoproterenol and the other group with daily s.c. DHEA for total 10 days, including 5 days before and during isoproterenol. The animals were killed after each treatment, and cardiac muscle failure was evaluated using histopathologic examination and biochemical indices. DHEA was found to reduce the damaged area and inhibit the elevation in the serum levels of glutamic oxaloacetic transaminase (SGOT), lactate dehydrogenase (LDH), skeletal muscle creatine kinase (CK) and heart creatine kinase (CK-MB) induced by isoproterenol. We also assayed widely used oxidative stress parameters, including thiobarbituric acid reactive substances (TBARS), superoxide dismutase (SOD), catalase and glutathion peroxidase (GPx). DHEA decreased the escalated level of TBARS and enhanced the anti oxidant defense reaction with an increase in Mn-SOD and Cu/Zn-SOD. On the other hand, the treatment with DHEA did not affect catalase and GPx activity. The present study indicates that DHEA has a therapeutic and preventive effect against isoproterenol-induced cardiomyopathy and its effects may depend largely on the increase in SOD activity.

Pro-Oxidantive Effect of Dehydroepiandrosterone on Indomethacin-Induced Acute Gastritis in Rats

  • Kim, Beom-Gyu;Yim, Sung-Hyuk;Jeong, Seong-Jin;Choi, Yoo-Shin;Nam, Yun-Sung;Jeong, Ji-Hoon;Yun, Sin-Weon;Do, Jae-Hyuk;Lim, Hyun-Muck;Park, Eon-Sub
    • Biomolecules & Therapeutics
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    • v.17 no.1
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    • pp.57-61
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    • 2009
  • This study examined whether or not a pretreatment with dehydroepiandrosterone (DHEA) has an effect on indomethacin-induced gastric mucosal damage. The DHEA group, male Sprague-Dawley rats, was administrated with DHEA orally at a dose of 4 mg/day for one week before inducing gastritis with indomethacin (50 mg/kg, p.o.). Histological assay, lipid peroxidation assay, superoxide dismutase (SOD), glutathione peroxidase (GPx) and Catalase activities were determined. Interestingly, it was found that the DHEA pretreatment attenuated the gastric lesion area induced by indomethacin. Rather, the pretreatment with high dose of DHEA led to submucosal edema, leukocyte infiltration in submucosa and mucosal necrosis. The levels of MDA in the DHEA pretreatment were also higher than those in the rats given with vehicle pretreatment. This suggests that the DHEA pretreatment deteriorates severe inflammation in indomethacin-induced gastritis. DHEA supplementation significantly increased SOD activity in the gastric mucosa. However, the catalase and GPx activities were not altered by DHEA. The co-administration of DHEA with an indomethacin might not offer a protective effect against the acute gastritis induced by indomethacin.

Modulation of Chemical Carcinogen-Induced Unscheduled DNA Synthesis by Dehydroepiandrosterone (DHEA) in the Primary Rat Hepatocytes

  • Kim, Seung-Hee;Han, Hyung-Mee;Kang, Seog-Youn;Jung, Ki-Kyung;Kim, Tae-Gyun;Oh, Hye-Young;Lee, Young-Kyung;Rheu, Hang-Mook
    • Archives of Pharmacal Research
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    • v.22 no.5
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    • pp.474-478
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    • 1999
  • Modulation of unscheduled DNA synthesis by dehydroepiandrosterone (DHEA) after exposure to various chemical carcinogens was investigated in the primary rat hepatocytes. Unscheduled DNA synthesis was induced by treatment of such direct acting carcinogens as methly methanesulfonate (MMS) and ethyl methanesulfonate (EMS) or procarcinogens including benzo(a)pyrene (BaP) and 7, 12-dimethylbenz(a)anthracene (DMBA). Unscheduled DNA synthesis was determined by measuring [methyl-3H]thymidine radioactivity incorporated into nuclear DNA of hepatocytes treated with carcinogens in the presence or absence of DHEA. Hydroxyurea $(5{\times}10^{-3} M)$was added to growth medium to selectively suppress normal replication. DHEA at concentrations ranging from $(1{\times}10^{-6} M)$ to$(5{\times}10^{-4} M)$ did not significantly inhibit unscheduled DNA synthesis induced by either MMS $(1{\times}10^{-4} M)$ or EMS $(1{\times}10^{-2} M)$. In contrast, DHEA-significantly inhibited unscheduled DNA synthesis induced by BaP $(6.5{\times}10^{-5} M)$ and DMBA.$(2{\times}10^{-5} M)$. DHEA-induced hepatotoxicity in rats was examined using lactate dehydrogenase (LDH) release as an indicator of cytotoxicity. DHEA exhibit no significant increase in LDH release compared with the control at 18 h. These data suggest that nontoxic concentration of DHEA does not affect the DNA excision repair process, but it probably influence the enzymatic system responsible for the metabolic activation of procarcinogens and thereby decreases the amount of the effective DNA adducts formed by the ultimate reactive carcinogenic species.

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Dehydroepiandrosterone Sulfate Level Varies Nonlinearly with Symptom Severity in Major Depressive Disorder

  • Uh, Dasom;Jeong, Hyun-Ghang;Choi, Kwang-Yeon;Oh, So-Young;Lee, Suji;Kim, Seung-Hyun;Joe, Sook-Haeng
    • Clinical Psychopharmacology and Neuroscience
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    • v.15 no.2
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    • pp.163-169
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    • 2017
  • Objective: The pathophysiology of major depressive disorder (MDD) is still not well understood. Conflicting results for surrogate biomarkers in MDD have been reported, which might be a consequence of the heterogeneity of MDD patients. Therefore, we aim to investigate how the severity of depression and various symptom domains are related to the levels of dehydroepiandrosterone sulfate (DHEA-s) in MDD patients. Methods: We recruited 117 subjects from a general practice. Depressive symptoms were assessed using the Beck Depression Inventory (BDI). Depressive symptoms were divided into three subdomains according to BDI items; somatic symptoms, guilt and failure, and mood and inhibition. Results: In subjects with very-mild-to-moderate depression, the DHEA-s level increased as BDI score did. However, the DHEA-s levels in the subjects with severe depression were significantly lower than in subjects with moderate depression (p=0.003). DHEA-s level was correlated with the BDI subscore for guilt and failure in very-mild-to-moderate depression (r=0.365, p=0.006). Conclusion: The DHEA-s level appears to be indicative of MDD severity with respect to depressive symptoms, especially regarding guilt and failure. Our findings suggest that the upregulation of DHEA-s may be a part of a compensatory process in very-mild-to-moderate depression, and the failure of this compensation mechanism may underlie the development of severe depression.

Effect of Dehydroepiandrosterone on Affected and Unaffected Hindlimb Muscles in Rats with Neuropathic Pain Induced by Unilateral Peripheral Nerve Injury (DHEA 투여가 일측성 말초신경 손상에 의해 유발된 신경병증성 통증 쥐의 환측과 정상측 뒷다리근에 미치는 영향)

  • Choe, Myoung-Ae;An, Gyeong-Ju
    • Journal of Korean Academy of Nursing
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    • v.39 no.5
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    • pp.632-640
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    • 2009
  • Purpose: The purpose of this study was to examine the effect of DHEA (Dehydroepiandrosterone) on muscle weight and Type I and II fiber cross-sectional area of affected and unaffected hindlimb muscles in rats with neuropathic pain induced by unilateral peripheral nerve injury. Methods: Neuropathic pain was induced by ligation and cutting of the left L5 spinal nerve. Adult male Sprague-Dawley rats were randomly assigned to one of two groups: The DHEA group (n=10) had DHEA injections daily for 14 days, and the Vehicle group (n=10) had vehicle injections daily for 14 days. Withdrawal threshold, body weight, food intake and activity were measured every day. At 15 days all rats were anesthetized and soleus, plantaris and gastrocnemius muscles were dissected from the both hindlimbs. Body weight, food intake, activity, muscle weight and Type I, II fiber cross-sectional area of the dissected muscles were measured. Results: The DHEA group showed significant increases (p<.05), as compared to the vehicle group for muscle weight of the unaffected plantaris, and in Type II fiber cross-sectional area of the gastrocnemius muscle. The DHEA group demonstrated a higher pain threshold than the vehicle group whereas total diet intake and activity score were not significantly different between the two groups. Conclusion: DHEA administration for 14 days attenuates unaffected plantaris and gastrocnemius muscle atrophy.

Effects of Short-term Thermal Stress on the Mouse Serum Concentrations of Cortisol and Dehydroepiandrosterone Sulphate (단기 고온 스트레스가 마우스 혈청 Cortisol, Dehydroepiandrosterone Sulphate 농도에 미치는 영향)

  • 차정호;최광수;최형송
    • Korean Journal of Animal Reproduction
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    • v.24 no.1
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    • pp.109-113
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    • 2000
  • This study was carried out to investigate the effect of short-term thermal stress on the serum concentrations of cortisol and DHEAS in BALB / c male mice. Cortisol and DHEAS concentrations in serum were measured by radioimmunoassay(RIA). We found there were significantly increased in the cortisol levels in 30 min-stressed group(T30) compared with control group(p<0.01), and then declined without significance in 120 min-stressed group (T120) compared with T30. By contrast, DHEAS levels were decreased without significance in both T30 and T120 compared with control group. Though short-term thermal stress, the continuous decline of DHEAS levels were observed. These results show that short-term thermal stress affects the serum levels of cortisol and DHEAS in mice. Furthermore, we found that DHEAS is a stress-related hormone and will be able to utilize as a stress marker.

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Induction of Integrin Signaling by Steroid Sulfatase in Human Cervical Cancer Cells

  • Ye, Dong-Jin;Kwon, Yeo-Jung;Shin, Sangyun;Baek, Hyoung-Seok;Shin, Dong-Won;Chun, Young-Jin
    • Biomolecules & Therapeutics
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    • v.25 no.3
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    • pp.321-328
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    • 2017
  • Steroid sulfatase (STS) is an enzyme responsible for the hydrolysis of aryl and alkyl sulfates. STS plays a pivotal role in the regulation of estrogens and androgens that promote the growth of hormone-dependent tumors, such as those of breast or prostate cancer. However, the molecular function of STS in tumor growth is still not clear. To elucidate the role of STS in cancer cell proliferation, we investigated whether STS is able to regulate the integrin signaling pathway. We found that overexpression of STS in HeLa cells increases the protein and mRNA levels of integrin ${\beta}1$ and fibronectin, a ligand of integrin ${\alpha}5{\beta}1$. Dehydroepiandrosterone (DHEA), one of the main metabolites of STS, also increases mRNA and protein expression of integrin ${\beta}1$ and fibronectin. Further, STS expression and DHEA treatment enhanced phosphorylation of focal adhesion kinase (FAK) at the Tyr 925 residue. Moreover, increased phosphorylation of ERK at Thr 202 and Tyr 204 residues by STS indicates that STS activates the MAPK/ERK pathway. In conclusion, these results suggest that STS expression and DHEA treatment may enhance MAPK/ERK signaling through up-regulation of integrin ${\beta}1$ and activation of FAK.