Effects Of Stanozolol Research Articles

Effects of stanozolol on apoptosis mechanisms and oxidative stress in rat cardiac tissue

Stanozolol is a widely used 17α-alkylated anabolic androgenic steroid (AAS) derivative. Despite stanozolol’s adverse effects, its effect on oxidative stress parameters and mitochondrial apoptosis pathway is not clearly defined. In our study, thirty four male Sprague-Dawley rats were divided into 5 groups as control (C), vehicle control (VC), steroid (ST), vehicle control-exercise (VCE), and steroid-exercise (STE). Animals were subcutaneously administered stanozolol 5 mg/kg in steroid groups and propylene glycol 1 ml/kg in the vehicle-control groups. On the 28th day-after sacrification, oxidative stress (MDA, GSH, PC, SOD, CAT) and apoptosis parameters (TUNEL, Cytochrome-c) in cardiac tissue were evaluated. Also, blood vessel morphology of cardiac tissue was evaluated with Verhoeff-van Giesen staining. It has been demonstrated that stanozolol administration triggers apoptosis by using TUNEL assay and cytochrome-c immunohistochemical staining intensity, while this effect is significantly reduced in the presence of exercise. In conclusion, the present study demonstrated that stanozolol administration induces apoptosis with increasing PC and CAT levels, while GSH, MDA and SOD parameters do not reveal any significant change. Exercise has a protective role in stanozolol induced oxidative stress and apoptosis. According to Verhoeff–van Giesen staining results for blood vessel morphology assessment, it has been seen that exercise has a protective role on cardiac blood vessels. This mechanism needs further investigations with long term exposure studies for clarifying possible pathways.

Effects of stanozolol on apoptosis mechanisms

Effects of stanozolol on apoptosis mechanisms

Determination of genotoxic effects of stanozolol in rats

Determination of genotoxic effects of stanozolol in rats

High-intensity Exercise Modifies the Effects of Stanozolol on Brain Oxidative Stress in Rats

We analyzed the effects of high-intensity exercise (HIE) and anabolic androgenic steroids (AAS) on brain redox status. 40 male Wistar rats were randomly distributed in 4 experimental groups (n=10) with or without HIE and with or without weekly Stanozolol administration. Thiobarbituric acid-reactive substances (TBARs) and protein carbonyl content (PCC) were assessed. Total superoxide dismutase (tSOD), manganese superoxide dismutase (Mn-SOD), copper/zinc superoxide dismutase (CuZn-SOD) and catalase (CAT) activities were measured. Finally, protein expression levels of glutathione peroxidase (GPx), NAD(P)H dehydrogenase, Quinone 1 (NQO1), NF-E2-Related Factor 2 (Nrf2), glial fibrillary acidic protein (GFAP), nuclear factor kappa β p65 (NF-κβ) and signal transducer and activator of transcription 3 were determined. Brain PCC concentrations were lower in the HIE groups compared to the untrained controls, whereas CAT activity was higher (both, p<0.01). Both HIE and AAS groups exhibited higher expression levels of GFAP and GPx, but lower NQO1 levels (all, p<0.05). There were increased expression levels of NF-κβ in the AAS groups (p<0.01). In addition, there was increased expression of Nrf2 in the HIE groups (p<0.001). HIE*AAS interactions were found on TBARs content and GFAP expression, with HIE downregulating and upregulating AAS-mediated increases in TBARs and GFAP, respectively (p<0.05). Overall, HIE appeared to reduce the AAS-mediated negative effect on brain redox status.

Effects of stanozolol on collagen synthesization of cultured growth plate chondrocytes from pubertal female rat treated with GnRHa in vitro

Objective To observe the effects of stanozolol on collagen I1 and X synthesization of cul- tured growth plate ehondrocytes from pubertal female rat treated with GnRHa in vitro. Methods Primary Chon-drocytes from 6 female rats were divided into two groups ( time-effect groups and concentration-effect groups). immunohistochemical staining of collagen Ⅱ, X were conducted. Results the results of type Ⅱ collagen synthe- sization demonstrated stanozolol enhanced the proliferation of the chondrocytes, time-course studies had shown that the proliferation were maximally stimulated by stanozolol after 3 days of incubation and decreased again after longer periods of incubation. Stanozolol did not stimulated type X collagen synthesization from 10-11 M-10-8 M, but experiments showed that type X collagen was already stimulated after incubation in stanozolol (10-7-10-5 M). Time-course studies had shown those type X collagen synthesizations were stimulated by stanozolol after 4-5 days of incubation. Conclusion Stanozoiol enhances the proliferation of ehondrocytes of pubertal female rat treated with GnRHa in vitro( time-course-dependent and concentration-dependent). Key words: Chondrocyte; Epiphyseal growth plate; Stanozolol; Collagen

Comparison of the effects of stanozolol, oxymetholone, and testosterone cypionate on the sexual behavior of castrated male rats.

In 3 experiments, adult male Long-Evans rats were castrated and treated daily with an anabolic-androgenic steroid (AAS) compound (either stanozolol, oxymetholone, or testosterone cypionate) for 6 weeks. Subjects were assigned to 5 groups that received injections of a high, medium, or low dose of the AAS, testosterone propionate, or the oil vehicle. Stanozolol failed to maintain ejaculation at any dose tested. Although some subjects receiving the low dose of oxymetholone ejaculated, oxymetholone generally failed to stimulate ejaculation above the levels of the oil group. Testosterone cypionate sustained ejaculation at all doses tested. The relative potency of the medium dose of each AAS in the sex accessory tissues was (from most potent to least potent): testosterone cypionate > stanozolol = oxymetholone = oil. Thus, these 3 AAS compounds produced a range of behavioral and endocrine responses in castrated male rats.

Effects of stanozolol and L-carnitine on erythrocyte osmotic fragility during aerobic exercise in rats

The effect on erythrocyte osmotic fragility of two anabolic agents, widely used to improve physical performance, has been studied. These agents, the steroid derivative, stanozolol, and a quaternary amine,l-carnitine, were administered to rats at rest and while performing running exercises, for 12 weeks. The results show that exercise does not alter the haemolysis curve. Administration of both agents in resting condition does increase the osmotic resistance of the erythrocytes. The combined effect of drug administration and physical exercise further increases the osmotic resistance in the case of stanozolol, presumably due to the steroid-erythrocyte membrane interaction as well as by an erthyropoietic effect.

The effects of stanozolol and boldenone undecylenate on plasma testosterone and gonadotropins and on testis histology in pony stallions

Fifty 2- to 16- yr old pony stallions were randomly assigned to one of five treatments: Group 1, controls (no treatment); Group 2, 0.55 mg/kg stanozolol weekly for 13 treatments; Group 3, 1.1 mg/kg stanozolol every 3 wk for 5 treatments; Group 4, 1.1 mg/kg boldenone undecylenate every 3 wk for 5 treatments; and Group 5, 0.55 boldenone undecylenate weekly for 13 treatments. Mean plasma testosterone levels for Groups 2, 4, and 5 were elevated over controls (P < 0.01) at 2, 8, and 9 wk, respectively. Testosterone levels for ponies in Group 3 did not differ from controls (P > 0.05). There were no differences in mean plasma luteinizing hormone (LH) and follicle stimulating hormone (FSH) levels among groups (P > 0.05). Daily spermatid production per gram of testicular parenchyma (DSP/gm) in Group 5 was lower than in controls (P < 0.05), whereas DSP/gm was not different among groups 1 to 4 (P > 0.05). There were no differences among groups (P > 0.05) in the percentage of Stage 8 tubules or relative number of Leydig cells. The mean diameter of Leydig cells was less for Group 5 than for controls (P < 0.05), but was not different for Groups 1 to 3 (P > 0.05).

Stanozolol-Induced Changes in Fibrinolysis and Coagulation in Healthy Adults

The effect of orally-administered stanozolol, 5 mg b.d. on fibrinolysis, coagulation and on various haematological and biochemical parameters have been studied in 16 healthy adults, 8 males and 8 females. Statistically significant enhancement of extrinsic (tissue-type) plasminogen activator activity was detected in all subjects studied. This was associated with significant increases in plasma plasminogen and a concomitant reduction in histidine-rich glycoprotein. There were no changes in plasma urokinase activity. Changes in the coagulation system included significant reduction in plasma fibrinogen and elevation of protein C and antithrombin III. Changes in plasma lipids included significant reduction of HDL cholesterol associated with an increase in LDL triglycerides. No change occurred in total cholesterol. There were no major differences between the sexes, nor were there serious side effects. The effects of stanozolol on extrinsic (tissue-type) plasminogen activator activity, "free" plasminogen, protein C and antithrombin III, argue strongly in favour of its therapeutic potential.

The effects of stanozolol and boldenone undecylenate on scrotal width, testis weight, and sperm production in pony stallions

Fifty mature pony stallions were randomly assigned to one of five treatment groups: Group 1- controls (no treatment), Group 2 - 0.55 mg/kg stanozolol weekly for 13 treatments, Group 3 - 1.1 mg/kg stanozolol every 3 weeks for 5 treatments, Group 4 - 1.1 mg/kg boldenone undecylenate every 3 weeks for 5 treatments, and Group 5 - 0.55 mg/kg boldenone undecylenate weekly for 13 treatments. Scrotal widths (SW), combined testis weights (CTW), and daily sperm productions (DSP) were not different between Groups 1 and 2. Ponies in Group 5 had smaller SW (P<0.01), smaller CTW and decreased DSP compared to controls (P < 0.05). Although SW for ponies in Groups 3 and 4 were less than for controls (P < 0.01), CTW and DSP were not different. The only treatment regime that did not alter SW, CTW, and DSP was Group 2 (0.55 mg/kg stanozolol weekly for 13 treatments).

Reduction in high density lipoproteins by anabolic steroid (stanozolol) therapy for postmenopausal osteoporosis

The effects of stanozolol, 17-methyl-2H-5α-androst-2-eno[3,2- c ]pyrazol-17β-ol, on lipoprotein levels were assessed in a short-term (6 wk) prospective study of 10 normolipidemic, postmenopausal, osteoporotic women. While total cholesterol and triglyceride levels remained constant, equal and offsetting responses were seen in low density lipoprotein (LDL) cholesterol (+30.9 ± 28.1 mg/dl [mean ± S.D.], p < 0.01, a 21% increase) and high density lipoprotein (HDL) cholesterol (−32.5 ± 11.9 mg/dl [mean ± S.D.], p < 0.001, a 53% decline). Hence the LDL HDL ratio increased dramatically, from 2.5 ± 0.7 to 6.8 ± 2.5. Within HDL, stanozolol was associated with a greater decline in HDL 2 (from 26.0 ± 7.4 mg/dl to 3.8 ± 1.9 mg/dl, p < 0.001, an 85% decrease) than HDL 2 (which diminished from 35.7 ± 3.2 to 24.1 ± 5.8 mg/dl, p < 0.001, a 35% decrease). The major HDL apolipoproteins also declined (A-I by a mean of 41% and A-II by 24%, both p < 0.001). Postheparin hepatic triglyceride lipase increased (off treatment 74 ± 42 nmole free fatty acid min −1 mole −1, on treatment 242 ± 110, n = 6, p = 0.06). All changes were reversed by 5 wk following termination of the drug. These lipoprotein changes suggest caution in the long term prescription of stanozolol, particularly in those without overriding clinical indications for its use.