Effect Of Stanozolol Research Articles

Direct effects of the anabolic/androgenic steroids, stanozolol and 17α-methyltestosterone, on benzodiazepine binding to the γ-aminobutyric acid A receptor

Various exogenous and endogenous steroids have been demonstrated to have both enhancing and inhibiting effects on ligand binding to the γ-aminobutyric acid A receptor (GABA A receptor) in previous studies. In the present study we have explored the possibility that an additional class of synthetic steroidal compounds, anabolic/androgenic steroids (AAS), mediate some of their CNS effects through direct interaction with the GABA A receptor. At micromolar concentrations, two AAS, stanozolol and 17α-methyltestosterone (17α-MT), significantly inhibited 1 nM [ 3H]flunitrazepam ([ 3H]Fln) binding to rat brain cerebrocortical membranes. Inhibition of 1 nM [3H]Fln binding by stanozolol was similar for both males and females (∼50% inhibition at 50 μM stanozolol). 17α-MT was much less efficacious, but did significantly inhibit 1 nM [ 3H]Fln binding at concentrations >10 μM. In equilibrium binding assays, stanozolol (50 μM) raised the apparent K D for [ 3H]Fln binding. The observed changes in the [ 3H]Fln binding curve, when analyzed by Rosenthal analysis, reveal complex equilibrium binding behavior. In females, the Rosenthal plot was best fit by a two site binding model. Stanozolol (50 μM) inhibited binding to the higher affinity site in a manner consistent with competitive inhibition, increasing the K D without changing the B max. However, the effect of stanozolol on the binding to the low affinity site was more complex, with an increase in both the K D and the B max. In males the data were best fit by a single binding site model. This single site exhibited a slight increase in the K D and a decrease in the B max in the presence of 50 μM stanozolol. Our results demonstrate that the AAS, stanozolol and 17α-MT, directly interact with the GABA A receptor and that their effects on ligand binding to the GABA A receptor are different between the sexes.

THE EFFECT OF STANOZOLOL ON FINAL HEIGHT AND SKELETAL MATURATION IN TURNER'S SYNDROME

<Aims and Methods> The effect of stanozolol on the final height and the skeletal maturation was studied in 35 patients with Turner's syndrome without spontaneous genital bleeding. All patients received stanozolol (1mg/day), estrogen and progesterone therapy. Bone age was evaluated by TW2 RUS method. Height SD score for Japanese Turner standard was used. <Results> The final height (142. 42 = 3.93cm) was significantly higher than that in untreated group (139.1 ± 5.6cm). ΔHeight SD score (Δ HSDS) which means the difference between height SD score at the start of stanozolol therapy and final height SD score was 1.00 ± 0.53. There were no significant differences in final height and Δ HSDS between the patients with 45, X karyotype (n=11) and those with other chromosomal variants (n=24). The final height in SFD group (n=10) was significantly shorter than that in AFD group (n = 19). Δ Bone age/Δ chronological age ratio during stanozolol therapy in patients whose bone ages were above 12 years old (n=27, 0. 31±0.18) was significantly lower than that in patients whose bone ages were below 12 years old (n=7. 1.08±0.23)(p<0. 005). <Conclusions> Stanozolol didn't accelerate bone maturation after 12 years of bone age. The final height was improved by stanozolol.

Effect of stanozolol on itching in primary biliary cirrhosis: Author's reply

Effect of stanozolol on itching in primary biliary cirrhosis: Author's reply

The effect of stanozolol on various types of defective fibrinolysis

Defective fibrinolysis is a common finding in patients who have had thrombosis. In this communication is reported 11 male patients all with decreased fibrinolytic activity on fibrin plates after stimulation with venous occlusion. The plasminogen activator (PA) concentration according to immunoradiometric assay was normal in all of them; the PA inhibitor of the endothelial cell type (PAI1) was increased in nine patients but two had a normal PAI 1 activity. Stanozolol produced a pronounced biochemical effect in normalising, or nearly normalising, the fibrinolytic activity on fibrin plates in all the patients. In six of the nine patients with increased PAI 1 also values in the reference range were reached and in the remaining three borderline values were found indicating a marked improvement on stanozolol. One patient in addition to defective fibrinolysis had decreased protein C activity (PCa). It is known that activated protein C stimulates the fibrinolytic system. In the presented case stanozolol had no effect on PCa; therefore it is suggested that the increased fibrinolysis is not mediated via the protein C system.

Effect of Stanozolol on Factors VIII and IX and Serum Aminotransferases in Haemophilia

The treatment of haemophilia has been dramatically improved since the introduction of factor VIII and IX concentrates, however these concentrates have brought new problems such as hepatitis and A.I.D.S. An oral agent which could raise endogenous levels of factor VIII and IX would be of great benefit. Danazol, an anabolic steroid, has recently been shown to increase levels of factors VIII and IX in haemophilia. We therefore studied the effect of stanozolol, a closely related anabolic steroid, in 15 patients with haemophilia A or Christmas disease over a 2-4 week period. There was no consistent change in factor VIIIc or factor IX, and fibrinolysis was significantly enhanced. No effect was apparent on the incidence of spontaneous bleeds. However serum aminotransferases which were abnormal in 11 of the 15 patients at the start of the study fell significantly with stanozolol therapy. This raises the interesting possibility that anabolic steroids may be beneficial in patients with chronic liver diseases.

Effect of stanozolol on delta-aminolaevulinic acid synthase and hepatic monooxygenase activity in man and rat.

Stanozolol is an anabolic steroid which is used in the treatment of aplastic anaemia and has been recently advocated for the prophylaxis of vascular thrombosis. Similar steroid substances stimulate the activity of delta-aminolaevulinic acid synthase (ALA S), the rate limiting enzyme of haem biosynthesis, in rat hepatocytes and chick embryo liver cell cultures and activate acute hepatic porphyria. In the present study stanozolol (10 mg daily for 14 days) has been shown to increase significantly leucocyte ALA S activity in 9 healthy male subjects. There was a concomitant rise in urinary ALA and total porphyrin excretion but no change in antipyrine kinetics or urinary 6 B hydroxycortisol excretion. In a complementary study in male Sprague Dawley rats, stanozolol administered intraperitoneally, produced a dose-dependent increase in hepatic ALA S activity without changing hepatic cytochrome P 450 content. Stanozolol has been clearly shown to elevate ALA S activity, probably directly, and thereby, porphyrin production without affecting hepatic monooxygenase activity. This porphyrinogenic effect may be relevant to the successful treatment of aplastic anaemia with anabolic steroids. Leucocyte ALA S activity may provide a human system for the study of drug porphyrinogenicity in vivo.

Endothelial Fibrinolytic Activity in Hypercholesterolemic and Diabetic Rats; Effect of Stanozolol, Streptozotocin, Dexamethasone and Hypophysectomy

In genetically hypercholesterolaemic rats (RICO) the intimal plasminogen activator activity (PAA) at the nonbranching regions of the aorta, but not at the branching regions, was markedly lower than in controls. In alloxan-induced diabetes in rats, the pattern of changes in tissue PAA was different in different tissues. The anabolic steroid stanozolol induced in male rats a dose and time dependent increase in the tissue PAA; this increase was varying from one tissue to another. The antibiotic streptozotocin, at a diabetogenic dose, induced a 200% increase in the intimal PAA of the aorta in RICO rats and by 100% in controls ( normal rats) ten weeks after a single injection. Administration of dexamethasone in normal rates 24 hours and 3 hours before streptozotocin injection prevented the enhancement of PAA. However, administration of dexamethasone simultaneously with streptozotocin did not affect the enhancement of the intimal PAA. The hypophysectomy induced in rats significantly increased PAA in the intima of the aorta.

The Effect of Stanozolol on the Fibrinolytic Enzyme System in Normal Subjects

In a volunteer study stanozolol was given in a dosage of 5mg twice per day for six weeks. A variety of parameters in blood coagulation and fibrinolysis were measured. Significant stimulation of the fibrinolytic system was found in seven days and this was associated with a significant fall in the levels of fibrinogen and alpha 2-macroglobulin. No major side effects were observed.

The fibrinolytic response to stanozolol in normal subjects

The effect of stanozolol (17-β-hydroxy-17α-methyl androstano {3.2,-c} pyrazole) has been studied on various components of the fibrinolytic and coagulation systems in normal adult subjects. Statistically significant increases in plasminogen activator activity, measured by the euglobulin clot lysis time, and plasma plasminogen were observed two days and ten days respectively after administration of stanozolol; these remained elevated throughout the study. Also, statistically significant reductions of plasma fibrinogen and a2 macroglobulin occurred within seven days of commencement of the drug and these changes persisted throughout the six week period of the trial. These changes, shown in normal individuals, indicate the potential value of stanozolol in clinical situations where fibrinolytic enhancement is considered beneficial.

Effect of Stanozolol on Liver Function

Effect of Stanozolol on Liver Function