Nandrolone Treatment Research Articles

Nandrolone Decanoate Causes Pathologic Changes in the Uterus of Surgically Postmenopausal Female Cynomolgus Macaques

To determine the effects of the androgenic anabolic steroid nandrolone decanoate on uterine endometrium and myometrium and on the mammary gland of female cynomolgus macaques by using morphologic, histomorphometric, and histopathologic determinations. Histologic and histomorphometric measurements were performed on uteri and mammary glands that were collected at necropsy from animals that had been used in a long-term experiment to examine the effects of nandrolone decanoate on bone and coronary arteries. The animals were surgically postmenopausal cynomolgus macaques randomized into four treatment groups: (a) intact sham ovariectomized (sham; n = 12), (b) ovariectomized (OVX; n = 15), (c) ovariectomized + nandrolone decanoate for 2 years (OVX + ND; n = 14), and (d) ovariectomized + nandrolone decanoate for 1 year, beginning 1 year after ovariectomy (OVX + NDdelay; n = 11). Intramuscular injections of nandrolone decanoate (25 mg every 3 weeks) were given to the two nandrolone-treated groups of animals (OVX + ND and OVX + NDdelay): one starting 3 weeks after ovariectomy and continuing for 2 years and the other group 1 year after ovariectomy. The sham and OVX groups were given an intramuscular injection of sterile vehicle every 3 weeks. Nandrolone treatment was moderately uterotropic in all treated versus ovariectomized animals. Changes induced were an increase in uterine weight, endometrial thickness, and glandular area, and a high incidence of mucometra. Glandular architecture was altered by nandrolone treatment such that glands extended into the myometrium (producing an adenomyosis-like lesion). Mammary gland changes were mild and equivocal. Nandrolone induced pathologic changes in ovariectomized monkeys similar to adenomyosis in the uterus.

Exercise performance indices in normal and anabolic steroid treated trotters

SummarySix adult Finnhorse trotters performed a standardised exercise test (SET) on a treadmill and a 4000 m maximal exercise test (MET) on a racetrack before, immediately and 13 weeks after a 14 week treatment with nandrolone laurate. Six other trotters served as controls. All horses were trained during the whole experiment. Blood lactate concentration, V200 VLa4 and red cell volume (CV) were determined in connection to the SET and blood lactate concentration, heart rate and performance time in the MET. All horses significantly improved their performance in the MET, but no differences were observed between the 2 groups. Nandrolone treatment caused a significant (P<0.05) increase in the CV and in the percentage of the oxidative type IIA fibres in the middle gluteal muscle. During the experiment V200 and VLa4 did not change (P>0.05) in either of the groups. The results indicate that CV was the only variable that predicted performance during the last 1000 m of the maximal test, whereas indicators of aerobic capacity, like V200 and VLa4, were of minor value. In the control group, the increase in the blood lactate concentration in the SET correlated positively with the total performance time (r=635; P<0.01) and the time of the last 1000 m (r=0.727; P<0.001) in the MET, but no correlation was found in the nandrolone group. The differences between the control and nandrolone groups suggest that both aerobic and anaerobic energy production in muscle are affected by nandrolone treatment.

Chronic treatment with the anabolic steroid, nandrolone, inhibits vasodilator responses in rabbit aorta

The effect of chronic treatment of rabbits for 4, 8 and 12 weeks with the anabolic steroid, nandrolone, on vasodilator responses was studied in segments of different arteries. The treatment abolished endothelium-dependent relaxation caused by acetylcholine and the Ca 2+-ionophore, A23187, in thoracic aorta, and reduced endothelium-independent relaxations induced by exogenous nitric oxide (NO) or sodium nitroprusside. The inhibitor of NO synthesis, N G-monomethyl- l-arginine, abolished vasodilator responses to acetylcholine and A23187. In contrast, relaxation induced by acetylcholine, NO or sodium nitroprusside in mesenteric and femoral arteries was unaltered by nandrolone treatment. Bioassay experiments using donor segments and endothelium-denuded bioassay rings from thoracic aorta show that acetylcholine, applied either through control or treated (12 weeks) donor segments, produced similar relaxation in bioassay rings from control rabbits, but this relaxation was markedly reduced in rings from treated rabbits. The increases of cyclic GMP levels induced by acetylcholine or sodium nitroprusside in segments from thoracic aorta were abolished by nandrolone treatment. These results suggest that the treatment with nandrolene reduces NO-mediated relaxation only in thoracic aorta by inhibition of guanylate cyclase, endothelial NO production and vasodilator machinery being unaltered.

Lack of demonstrated effect of nandrolone on serum lipids

Numerous prior studies of serum lipid levels during anabolic steroid (AS) use have uniformly demonstrated dramatic adverse lipid profiles (eg, average high-density lipoprotein [HDL] depression of 50%) during administration of 17α-alkylated AS. In contrast, the existing studies of 17β-esterified AS have shown mild or absent lipid effects (eg, HDL depression 0% to 16%) with these agents. Thus, the potential effects on serum lipids of individual AS are an important clinical consideration. The present study was therefore designed to investigate the lipid effects of nandrolone, a 17β-esterified AS. Twenty-one men and three women had lipid profiles measured before and after administration of nandrolone decanoate 100 mg intramuscularly (IM) once a week for 6 weeks. No significant change was noted in HDL cholesterol (HDL-C), low-density lipoprotein cholesterol (LDL-C), total cholesterol, triglycerides, the total cholesterol to HDL-C ratio, or the LDL-C HDL-C ratio from nandrolone treatment. Moreover, observed trends toward HDL-C depression (−2.00 ± 8.83 mg/dL; values reported are for men only unless noted otherwise) and LDL elevation (+5.05 ± 20.45 mg/dL) were small. In power analysis, HDL-C depressions of 6.3, 7.6, or 8.7 mg/dL during nandrolone were ruled out with powers of 80%, 95%, and 99%, respectively.

Anabolic steroid (nandrolone) treatment during adolescence decreases the number of glucocorticoid and estrogen receptors in adult female rats.

The density of thymic glucocorticoid receptors and the density of uterus estrogen receptors (I) decreased significantly in adult female Wistar rats following nandrolone treatment at the age of six and seven weeks. There was no significant alteration of thymic glucocorticoid receptor density in males. Affinity of glucocorticoid and estrogen receptors did not differ from the controls significantly. The results demonstrate that the receptors of immature cells can be imprinted in adolescence similarly to those in the perinatal period and chemical substances capable of binding to the immature receptors can result in prolonged alteration of their binding character. This phenomenon should be taken into consideration especially in the case of nandrolone administration which can be used as a doping substance.

Effects of the rate of acetylcholine receptor synthesis on the severity of experimental autoimmune myasthenia gravis

The effect of target organ manipulation by means of denervation and treatment with anabolic steroids on the severity of disease in EAMG was assessed in inbred rats. Unilateral limb denervation, a procedure known to increase the AChR content of muscle, 'protected' the denervated leg against antibody-mediated AChr loss in acute EAMG induced by passive transfer of mAb 35 directed against the main immunogenic region. Also in chronic EAMG, brought about by immunizing rats with AChR in complete Freund's adjuvant, the AChR loss of the denervated leg was about one fourth (13.5 vs. 53%) of the control leg. In both acute and chronic EAMG the amount of AChR complexed with antibody was lower in the denervated leg. This lower AChR occupancy with antibody in the denervated leg occurred also in conditions of marked antibody excess and was therefore due to enhanced AChR synthesis. Next the effect of treatment with a weakly virilizing anabolic steroid nandrolone in chronic and acute EAMG was examined in order to examine whether a hypothesized enhanced synthesis of AChR would protect animals from disease. In the absence of an immunosuppressive effect, in terms of concentration of antibodies to AChR, nandrolone treatment protected the rats from severe disease in the chronic EAMG model as shown by the fact that of the 9 rats 6 showed mild (1+) disease and 3 no disease at all; conversely 6 out of 9 control rats showed severe (3+) disease. Rats treated with nandrolone showed a 48 +/- 1.7% loss of AChR compared to a loss of 58 +/- 3.6% in the control rats, suggesting enhanced AChR synthesis. When nandrolone-pretreated rats were given acute EAMG by passive transfer of mAb 35 a paradoxical effect was seen. In contrast to the controls all of the rats pretreated with nandrolone showed severe signs of EAMG; this was associated with a higher loss of AChR and increased consumption of complement C4 as suggested by decreased concentrations of C4 in the serum. Results show increased AChR synthesis to protect against chronic EAMG both in terms of clinical disease (nandrolone) as well as AChR loss (nandrolone, denervation). In addition it was shown that nandrolone increases serum C4 consumption which in the complement-dependent acute EAMG model causes enhancement of the severity of clinical disease and increased AChR loss.

Changes in cadaverine and putrescine metabolism in the mouse kidney induced to growth by an anabolic steroid.

The formation of cadaverine and putrescine was studied in the kidneys of gonadectomized male mice stimulated to growth by nandrolone, an anabolic steroid with low androgenic activity. Administration of nandrolone resulted in an increased kidney weight and elevated activities of lysine and ornithine decarboxylase (assayed by measurement of the formation of 14CO2 from the 1-14C-labelled amino acids). The responses were dose and time dependent. The elevated enzyme activities were reflected by an increased endogenous kidney content of cadaverine and putrescine as well as in an increased urinary excretion of the diamines. Further, the kidney content and the urinary excretion of the polyamines spermidine and spermine were elevated on nandrolone treatment. Fractionation of kidney extracts on pore gradient electrophoresis revealed an apparent molecular weight of about 95 000 Daltons of the lysine decarboxylase as well as of the ornithine decarboxylase. On electrofocusing it was evident that both enzymes were present as more than one isoelectric form. However, the main form in both cases focused at a pH of about 5.0.