Nandrolone

Nandrolone administration with or without strenuous exercise increases cardiac fatal genes overexpression, calcium/calmodulin-dependent protein kinaseiidelta, and monoamine oxidase activities and enhances blood pressure in adult wistar rats.[Pubmed:30802539]

Gene. 2019 May 20;697:131-137.

Misuse of anabolic androgenic steroids (AAS) increases prevalence of cardiovascular abnormalities in athletes, and the underlying molecular mechanism involved in those abnormalities continues to be investigated. The aim of this study was to investigate the effect of chronic Nandrolone exposure on alpha and beta-myosin heavy chain (MHC) isoforms gene expression transition, blood pressure related parameters, calcium/calmodulin-dependent protein kinaseIIdelta (CaMKIIdelta), and monoamine oxidase (MAO) activities in rats' hearts. It was also planned to evaluate the effect of strenuous exercise on cardiac abnormalities induced by Nandrolone. Thirty-two male wistar rats were assigned into four groups, namely control, Nandrolone, Nandrolone with strenuous exercise, and strenuous exercise groups. Nandrolone consumption significantly increased systolic, diastolic, pulse and dicrotic pressure, mean arterial pressure, as well as the amplitude of first peak (H1). Moreover, exercise combined with Nandrolone completely masked this effect. The mRNA expression of beta-MHC and the ratio of beta -MHC/alpha -MHC showed a significant increase in the Nandrolone and Nandrolone with strenuous exercise groups compared to those in the control group. The values of heart tissue calcium/calmoldulin-dependent protein kinase IIdelta (CaMKIIdelta), and monoamine oxidase (MAO) in the Nandrolone, Nandrolone with strenuous exercise and exercise groups were significantly higher than those values in the control group. These findings indicate that Nandrolone-induced heart and hemodynamic abnormalities may in part be associated with MHC isoform changes and Ca(2+) homeostasis changes mediated by increased CaMKIIdelta and MAO activities and that these effects can be provoked via strenuous exercise.

Simple and Accurate HPTLC-Densitometric Method for Assay of Nandrolone Decanoate in Pharmaceutical Formulation.[Pubmed:30691078]

Molecules. 2019 Jan 25;24(3). pii: molecules24030435.

This study reports the development and validation of a new, simple, and accurate high-performance thin-layer chromatography (HPTLC)-densitomeric method for the determination of Nandrolone decanoate in a commercially available injection formulation. Chromatographic analysis was performed on glass CN modified silica gel 60F254 plates developed using n-hexane-ethyl acetate in volume ratio 42.5:7.5 as the mobile phase. Densitometric scanning was carried out at the wavelength of 245 nm. This chromatographic system gave compact spot and a symmetrical peak of Nandrolone decanoate with retardation factor (RF) value at 0.57 (+/-0.02). The linearity of this method with the high correlation coefficient of calibration plot ranges from 0.780 to 12.500 mug/spot. The developed method is characterized by good precision (coefficient of variation CV < 2%) and high accuracy close to 100.3% (R = 99.0%). Values of limits of detection and quantification equal to 0.231 and 0.700 mug/spot, respectively, confirm the sensitivity of the developed method. The analysis of the pharmaceutical formulation of Nandrolone decanoate indicates drug content of 50.5 mg/mL and 101.0% in relation to the label claim. This is in good agreement with the recommendation of the International Council for Harmonisation (ICH) guidelines as well as the pharmacopoeial requirements. The low CV value (<1%) of Nandrolone decanoate content in the tested injection formulation confirms the suitability of the proposed HPTLC-densitometric method for routine control of this compound in examined pharmaceuticals.

Nandrolone decanoate administration does not attenuate muscle atrophy during a short period of disuse.[Pubmed:30689637]

PLoS One. 2019 Jan 28;14(1):e0210823.

BACKGROUND: A few days of bed rest or immobilization following injury, disease, or surgery can lead to considerable loss of skeletal muscle mass and strength. It has been speculated that such short, successive periods of muscle disuse may be largely responsible for the age-related loss of muscle mass throughout the lifespan. OBJECTIVE: To assess whether a single intramuscular injection of Nandrolone decanoate prior to immobilization can attenuate the loss of muscle mass and strength in vivo in humans. DESIGN, SETTING AND PARTICIPANTS: Thirty healthy (22 +/- 1 years) men were subjected to 7 days of one-legged knee immobilization by means of a full leg cast with (NAD, n = 15) or without (CON, n = 15) prior intramuscular Nandrolone decanoate injection (200 mg). MEASURES: Before and immediately after immobilization, quadriceps muscle cross-sectional area (CSA) (by means of single-slice computed tomography (CT) scans of the upper leg) and one-legged knee extension strength (one-repetition maximum [1-RM]) were assessed for both legs. Furthermore, muscle biopsies from the immobilized leg were taken before and after immobilization to assess type I and type II muscle fiber cross-sectional area. RESULTS: Quadriceps muscle CSA decreased during immobilization in both CON and NAD (-6 +/- 1% and -6 +/- 1%, respectively; main effect of time P<0.01), with no differences between the groups (time x treatment interaction, P = 0.59). Leg muscle strength declined following immobilization (-6 +/- 2% in CON and -7 +/- 3% in NAD; main effect of time, P<0.05), with no differences between groups (time x treatment interaction, P = 0.55). CONCLUSIONS: This is the first study to report that Nandrolone decanoate administration does not preserve skeletal muscle mass and strength during a short period of leg immobilization in vivo in humans.

Nandrolone administration abolishes hippocampal fEPSP-PS potentiation and passive avoidance learning of adolescent male rats.[Pubmed:30562047]

Can J Physiol Pharmacol. 2019 Feb;97(2):130-139.

Despite the chronic effects of Nandrolone decanoate (ND), the acute effects of ND on passive avoidance learning (PAL) and memory and its mechanism have not been investigated. This research examines the acute effect of ND on PAL, CA1 synaptic plasticity, testosterone and corticosterone serum levels, and the role of androgenic receptors (ARs). Adolescent male rats were treated with ND, 30 min before training and retention and after training test. AR antagonist was applied 15 min before ND. Hippocampal slices were perfused by ND. ND administration had an inverted U-shape effect on acquisition of PAL and on testosterone and corticosterone serum levels. The consolidation was only affected by high dose of ND. ND significantly decreased the retention of PAL across all doses. The magnitude of field excitatory postsynaptic potential long term potentiation was lower than that of control slices. In addition, an attenuation of field excitatory postsynaptic potential population spike coupling was also observed. Nilutamide could nullify the ND impairment effect. We concluded although a single dose of ND could affect all stages of PAL, its effects were more potent on retrieval, possibly arising from the acute effect of ND on the alterations of CA1 synaptic plasticity. In addition, ND may induce its effects directly through ARs and indirectly through plasma testosterone and corticosterone.

Toxic Impact of Anabolic Androgenic Steroids in Primary Rat Cortical Cell Cultures.[Pubmed:30500611]

Neuroscience. 2019 Jan 15;397:172-183.

The use of anabolic androgenic steroids (AASs) among non-athletes is a public health-problem, as abusers underestimate the negative effects associated with these drugs. The present study investigated the toxic effects of testosterone, Nandrolone, stanozolol, and trenbolone, and aimed to understand how AAS abuse affects the brain. Mixed cortical cultures from embryonic rats were grown in vitro for 7days and thereafter treated with increasing concentrations of AASs for 24h (single-dose) or 3days (repeated exposure). Cells were co-treated with the androgen-receptor (AR) antagonist flutamide, to determine whether the potential adverse effects observed were mediated by the AR. Cellular toxicity was determined by measuring mitochondrial activity, lactate dehydrogenase (LDH) release, and caspase-3/7 activity. Nandrolone, unlike the other AASs studied, indicated an effect on mitochondrial activity after 24h. Furthermore, single-dose exposure with testosterone, Nandrolone and trenbolone increased LDH release, while no effect was detected with stanozolol. However, all of the four steroids negatively affected mitochondrial function and resulted in LDH release after repeated exposure. Testosterone, Nandrolone, and trenbolone caused their toxic effects by induction of apoptosis, unlike stanozolol that seemed to induce necrosis. Flutamide almost completely prevented AAS-induced toxicity by maintaining mitochondrial function, cellular integrity, and inhibition of apoptosis. Overall, we found that supra-physiological concentrations of AASs induce cell death in mixed primary cortical cultures, but to different extents, and possibly through various mechanisms. The data presented herein suggest that the molecular interactions of the AASs with the AR are primarily responsible for the toxic outcomes observed.

Possible Protective Role of Whey Protein on the Rat's Liver Tissues Treated with Nandrolone decanoate.[Pubmed:30311477]

Pak J Biol Sci. 2018 Jan;21(6):262-274.

BACKGROUND AND OBJECTIVE: Nandrolone and whey protein are used as supplementary food and athletic food. The aim of this study was to evaluate the possible histological and ultrastructural alterations in the liver of adult rats after treatment of the anabolic androgenic steroids (Nandrolone decanoate) and whey protein. MATERIALS AND METHODS: Twenty eight Wistar Albino male rats were used in the present study divided into 4 groups: Control group received 0.5 mL of saline solution by oral, Nandrolone group injected intramuscular (10 mg kg-1 b.wt./week for 3 months), whey protein group treated by oral (5 mg kg-1 b.wt./week for 3 months) and Nandrolone and whey protein group. At the end of the experimentation, all the rats were sacrificed and liver samples were processed for histological and ultrastructural examination. Haematoxylin and eosin stains for general histological examination and Mallory trichrome stain for collagen fibers. RESULTS: Light microscopy examination of the liver of the Nandrolone group showed bleeding and widening of the blood sinusoids. Degeneration, vacuolation, coagulative necrosis and pyknotic nuclei were observed. In addition, increased collagen fibers were detected. Whey protein group showed more or less normal hepatocytes, blood sinusoids and collagen fibers. The Nandrolone and whey protein group illustrated normal appearance of hepatocytes with vacuolation in some of the hepatocytes and normal blood sinusoids and collagen fibers were noticed. Electron microscopic examination of the Nandrolone group showed depletion of the nuclear chromatin, damaged mitochondria, increased of lysosomes, some lipid droplets, damaged blood sinusoids and space of Disse and increased of Kupffer cells, whereas the whey protein group appeared normal. The Nandrolone and whey protein group showed well developed hepatocytes, regular space of Disse and normal hepatic sinusoids. CONCLUSIONS: Whey protein may be ameliorate the hepatic architecture after treatment with Nandrolone.