The illicit use of anabolic androgenic steroids (AAS) to enhance physical strength, performance, and appearance is associated with severe physical and psychological adverse effects. Long-term AAS use has been associated with altered behavior and cognitive impairments. Nevertheless, the neurobiological effects of AAS use remain underexplored, especially in terms of brain neurotransmitter and lipid profiles. This study applied advanced Fourier-transform ion cyclotron resonance matrix-assisted laser desorption/ionization mass spectrometry imaging (FTICR-MALDI-MSI) to investigate the effects of three AAS decanoate prodrugs, nandrolone, testosterone, and trenbolone, on brain monoamine neurotransmitter systems and lipid composition in male rats (n = 32). The AAS administration was found to alter dopamine and serotonin levels, as well as the metabolism of these molecules across multiple brain regions; significant effects on neurotransmitter levels, associated metabolites, and turnover ratios were observed. Additionally, AAS treatment affected brain lipid composition, with nandrolone and testosterone increasing the levels of phosphatidylethanolamines, ether-linked phosphatidylethanolamines, and phosphatidylserines; in contrast, trenbolone demonstrated an opposite trend. The presented findings revealed distinct, steroid-specific alterations in brain neurotransmitters and lipid profiles; these changes were particularly strong in the tail of the striatum, where lipid dysregulation was linked to neurotransmitter dynamics. The potential neurotoxic effects further highlight the importance of understanding how steroid-specific mechanisms are linked to behavioral and neurobiological changes. This study advances our knowledge of the neurobiological effects, including the potential risks, of extended AAS use.

Anabolic-androgenic steroids (AAS), such as ND, are commonly used to enhance physical performance and muscle mass. However, its abuse has been associated with numerous adverse health effects, particularly on the hippocampus, affecting learning, working memory, and cognitive functions. The current study aims to investigate the potential effects of ND, aerobic exercise, resistance exercise, and the combination of ND with aerobic or resistance exercise on memory and cognitive functions. Moreover, the study aims to explore the possible underlying mechanisms of changes in memory and cognitive function. Adult male rats were divided into four groups: control (GI), only ND-treated (GII), only exercise (GIIIa & GIIIb), and combined exercise + ND-treated (GIVa & GIVb). Exercise included aerobic treadmill training and ladder-climbing modalities for 8 weeks, either alone or with ND. Cognitive function was evaluated using the Modified Barnes Maze and T-maze tests. Hippocampal integrity was assessed through oxidative stress markers, hippocampal brain-derived neurotrophic factor (BDNF) levels, hippocampal nerve growth factor (NGF) expression, and histological examination. ND significantly impaired spatial learning and memory, increased oxidative stress, lowered hippocampal BDNF levels, and reduced NGF expression in the hippocampus. Exercise markedly attenuated these harmful effects. Aerobic exercise gave the most pronounced improvements. It restored cognitive function, enhanced antioxidant defenses, increased hippocampal BDNF levels, increased hippocampal NGF expression, and preserved hippocampal structure. Resistance training also had neuroprotective effects, but to a lesser extent than aerobic exercise. In brief, both aerobic and resistance exercise have been shown to exert protective effects against ND-induced neurotoxicity by enhancing antioxidant defenses and promoting neuronal integrity. The monitored neuroprotective benefits suggest that physical exercise could serve as a possible non-pharmacological approach to prevent or decrease cognitive impairments associated with anabolic steroid abuse.

To evaluate whether cumin (Cuminum cyminum) oil attenuates nandrolone decanoate (ND)-induced hepatic alterations in rats. Eighty male Sprague-Dawley rats were randomized into six groups: control, cumin oil alone, ND low dose (10 mg/kg/week), ND high dose (20 mg/kg/week), ND low dose + cumin oil, and ND high dose + cumin oil. Cumin oil was administered orally at 400 mg/kg/day for 4 weeks. Outcomes included relative liver weight index, serum ALT/AST, total bilirubin, lipid profile, and blinded histopathology. Both ND doses increased ALT/AST and bilirubin levels and worsened the lipid profile compared with controls, with more pronounced and significant alterations in the high-dose ND group. Co-administration of cumin oil attenuated ND-associated elevations in liver enzymes and bilirubin, improved lipid parameters, and was associated with reduced histological damage compared with ND alone. Interestingly, cumin oil alone increased ALT/AST and lipid parameters compared with controls, although liver architecture remained unremarkable on H&E. In this rat model, cumin oil co-administration partially attenuated ND-induced hepatic biochemical, lipid, and histological alterations. However, cumin oil alone increased ALT/AST and lipid parameters despite unremarkable H&E morphology. Therefore, the present findings should be interpreted as evidence of context-dependent attenuation during ND exposure, not as proof of an independent hepatoprotective or lipid-lowering effect of cumin oil in healthy rats. Dose-ranging, safety evaluation, batch-specific chemical profiling, preparation standardization, and mechanistic studies incorporating antioxidant/oxidative stress markers such as MDA, GSH, SOD, CAT, GPx, and molecular endpoints are needed to clarify pathways and translational relevance.

This study examined the effects of resistance training (RT) and supraphysiological nandrolone decanoate (ND) administration on hippocampal neurogenesis, neurotrophic signaling, and behavior. Forty 3-month-old male C57BL/6 J mice were randomized to RT or sedentary (SED) conditions. Each group was further divided into sham (S) or ND (38 mg·kg[-1]·wk.[-1]) treatment groups. All interventions lasted 7 wk. Adult hippocampal neurogenesis was quantified in the dentate gyrus using BrdU[+]/NeuN[+] immunolabeling. Hippocampal expression of brain-derived neurotrophic factor (BDNF), androgen receptor (AR), estrogen receptor-β (ER-β), insulin-like growth factor-1 (IGF-1), and irisin was assessed by western blot analyses. No significant exercise × treatment interactions were observed for any of the behavior measures. When collapsed across treatments, RT exhibited a greater number of open-arm entries (p = 0.006) and reduced average latency times (p = 0.002) than SED. ND administration did not alter behavioral outcomes. RT (p = 0.001) and ND (p = 0.032) each independently increased hippocampal BrdU[+]/NeuN[+] cell numbers, with no additive effects. AR expression for SED-S was significantly lower (p's < 0.05) than all other groups and IGF-1 expression for RT-S was significantly greater (p's < 0.05) than all other groups. Main effects revealed that RT and ND resulted in significant elevations in AR, ER-β and BDNF expressions. In conclusion, RT enhanced hippocampal plasticity and behavioral performance, whereas supraphysiological ND administration produced distinct molecular changes without conferring additive behavioral or neuroplastic benefit.

The manufacture and distribution of illicit drugs in the Republic of Korea are an increasing problem. We aimed to develop a rapid and reliable simultaneous analytical method for monitoring the illegal presence of anabolic androgenic steroids (AAS) in foods and drugs. Forty-five AAS compounds were analyzed using a validated liquid chromatography-tandem mass spectrometry (LC-MS/MS) method in accordance with international standards. Liquid chromatography-quadrupole time-of-flight mass spectrometry (LC-QTOF/MS) has enabled the determination of representative fragment ion patterns. The validated method was applied to 95 real samples, including 11 foods, 40 dietary supplements, and 44 counterfeit drugs. The overall detection rate was 38.9%, with the highest rate observed in counterfeit drugs (81.8%), followed by dietary supplements (2.5%), whereas no AAS were detected in foods. When classified by formulation, injectables showed the highest detection rate (100.0%), followed by liquids (78.6%), tablets (58.3%), powders (20.0%), and capsules (3.3%). Frequently detected compounds included testosterone-17-propionate (0.001-119, 850.0 μg/g), testosterone-17-isocaproate (0.002-1442.7 μg/g), and nandrolone decanoate (0.01-120,023.0 μg/g). Anastrozole and exemestane, which are not currently included as LC-MS/MS target compounds, were also identified through LC-QTOF/MS. Furthermore, LC-QTOF/MS results revealed the presence of nonsteroidal compounds, including phosphodiesterase-5 inhibitors and weight-loss compounds, indicating potential health risks associated with the combined pharmacological effects of these substances. The analytical method developed in this study can be effectively used for both screening and quantification and offers practical applicability to regulatory monitoring and enhancement of public health protection.

Illicit use of nandrolone can result in apoptosis in the hippocampus tissue but the underlying mechanism is unknown. The present study evaluated the role of S1P1/Akt/FOXO3a pathway in hippocampus cell apoptosis following exposure to nandrolone decanoate either alone or in combination with N-acetyl-cysteine. Twenty-four male Wistar rats were randomly divided into three groups (n = 8): control, nandrolone (10 mg/kg; intramuscularly; three times per week), and nandrolone + N-acetyl-cysteine (150 mg/kg; intraperitoneally). After six weeks of treatment, the number of apoptotic cells was significantly increased in the nandrolone treated group compared with the control group. Compared to control group, nandrolone group showed significant upregulation of NOX2, iNOS, 8-OHdG, P-FOXO3a/FOXO3a and lactate dehydrogenase (LDH) protein expression in rat hippocampus cells. Conversely, the protein expressions of P-Akt/Akt and S1P1 were significantly downregulated in hippocampus tissue of rats treated with nandrolone compared with control rats. Co-administration of N-acetyl-cysteine with nandrolone significantly reduced the apoptotic index and reversed the expressions of S1P1, P-Akt/Akt and P-FOXO3a/FOXO3a in the hippocampus neurons compared with the nandrolone group. These findings suggest that S1P1/Akt/FOXO3a signaling pathway may at least in part play an important role in the progression of apoptosis induced by nandrolone exposure, providing new insights into the pathogenesis and potential treatment of nandrolone-induced hippocampal damage.

Postmenopausal osteoporosis is often accompanied by reduced muscle mass and chronic bone pain, amplifying fracture risk and functional decline. Nandrolone decanoate (ND), a synthetic anabolic steroid, has been proposed as a dual-acting agent that may benefit both bone and muscle through osteoanabolic and myoanabolic mechanisms, yet its therapeutic value in osteoporosis remains uncertain. We conducted a systematic review and meta-analysis of randomized controlled trials comparing ND with placebo in postmenopausal women with primary osteoporosis. The review followed Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) 2020 guidelines and was prospectively registered in the International Prospective Register of Systematic Reviews (PROSPERO; CRD420251147647). Seven trials with 293 participants were included, with sample sizes varying by outcome. ND reduced fracture risk compared with placebo (moderate-certainty evidence). It produced modest increases in bone mineral density (BMD; low certainty) and more substantial gains in forearm bone mineral content (BMC; moderate certainty). ND also reduced pain (moderate certainty) and increased muscle mass (moderate certainty). However, ND was associated with a higher incidence of mostly mild virilizing adverse events (hirsutism, acne, voice changes; low certainty). Given the small sample sizes and methodological limitations of older trials, ND may be considered as a potential adjuvant option for selected postmenopausal women, particularly when muscle loss or refractory bone pain is present, provided treatment occurs under close clinical and laboratory monitoring. Larger, contemporary randomized trials are needed to define ND's role within modern osteoporosis management.

This paper describes the detection of nandrolone decanoate and its metabolites in mane hair collected from horses that have been treated with nandrolone decanoate (Deca-Durabolin). The intramuscular administration study of nandrolone decanoate in three Thoroughbred castrated horses (each received 800 mg weekly for 3 consecutive weeks) was previously conducted to investigate its metabolism and detection time in plasma and urine for doping control purposes. In this work, segmental analysis of the post-administration hair has revealed that (i) nandrolone decanoate and its metabolites, nandrolone and 4-estrene-3,17-dione, could be detected in horse mane after intramuscular administration, and (ii) the spreading of these substances along the entire hair strand was observed, which suggested the involvement of sweat or sebum incorporation.

Anabolic-androgenic steroid (AAS) abuse is associated with damage to various organs, including the liver. However, the underlying molecular mechanisms remain unclear. This study was conducted to elucidate the effect of nandrolone decanoate on liver injury, both alone and in combination with N-acetylcysteine (NAC), and its related mechanisms. Twenty-four male Wistar rats were randomly subdivided into three groups: Control (Con), Nandrolone (10 mg/kg) (ND), and Nandrolone + NAC (ND+NAC: 150 mg/kg daily). After 6 weeks, nandrolone treatment led to increased levels of triglycerides, cholesterol, LDL, AST, ALT, and ALP, along with a decreased HDL level compared to the control group. ND administration also elevated the expression of PTP1B, HNF4A, and FAT/CD36 genes, as well as protein levels of MMP-2, MMP-9, TGF-β1, SMAD-3, and SREBP-1. miRNA-29b levels decreased in liver tissue following nandrolone exposure, as determined by RT-PCR. Moreover, histopathological examination showed increased fibrosis after ND treatment. Consumption of NAC along with ND partially ameliorated gene and protein expression alterations and fibrotic changes, and improved the undesirable lipid profile and liver enzyme levels compared to the ND group. These findings indicate that ND-induced liver abnormalities may be partly associated with lipid homeostasis changes mediated by overexpression of the aforementioned genes and proteins. They also demonstrate that these effects can be reduced by using NAC as an antioxidant and anti-inflammatory agent.

Although the misuse of androgenic-anabolic steroids is increasing, not much research has been done to determine how it affects renal function. Our research sought to ascertain how Nandrolone decanoate (ND) treatment affected kidney function and histological changes in adult male albino rats. Additionally, we sought to evaluate the impact of combining ND therapy with anaerobic exercise. A total of 39 male rats were divided into three groups (n = 13 each): control, ND treated (15mg/kg/day for 8 weeks; SC), and trained-ND treated (8-12 ladder climbs, three times per week for eight weeks). Blood and kidney samples were taken after eight weeks of anaerobic exercise and therapy. The study assessed organ weight, serum urea, and creatinine levels, inflammation (TNF-α, IL-6), oxidative stress markers (MDA, SOD, TAC), kidney histology, and collagen content. Caspase3 and BAX immunohistochemistry were performed, whereas Sirt1, Beclin-1, and microtubule-associated protein light chain 3 (LC3) mRNA were analyzed using RT-PCR. The current study illustrated that exercise significantly improved kidney function, histological results, and damage score while reducing collagen deposition, inflammation, and oxidative stress. Apoptosis proteins (CASPASE3 and BAX) were dramatically reduced, whereas Sirt1 and autophagy proteins (Beclin-1 and LC3) mRNA levels were increased. In our conclusion, because of its anti-inflammatory, antioxidative, and antiapoptotic properties as well as its modification of autophagy protein mRNA, anaerobic exercise in conjunction with ND administration in rats led to a reduction in renal damage and kidney fibrosis.

Sr2NiCoAl0.3Fe27.7O46 X-Type hexa-nano-ferrites were prepared using a co-precipitation route, coated with Chitosan, and synthesized into a ferrite chitosan curcumin nanoparticle system. This combination enhances curcumin's therapeutic properties, chitosan's bioavailability, and ferrite's magnetic targeting potential, offering improved cellular uptake and diagnostic applications. Nandrolone decanote (ND), one of the class II anabolic androgenic steroids (AASs), quickly spreading as a class of medications used in both clinical and illegal settings. AAS can enhance tolerance to exercise, so they are taken illegally by bodybuilders and adolescents. However, the abuse of AASs can lead to serious and irreversible organ toxicity. This study designed to investigate the therapeutics effect of nano ferrite chitosan curcumin nanoparticles (NF-CH-CurNPs) against ND induced hepatic toxicity, proliferation, inflammation, oxidative stress, and DNA damage in male rats. 48 adult male rats assigned to 6 groups [1st Gp, control; 2nd Gp, CurNPs; 3rd Gp, NF-CH-CurNPs; 4th Gp, ND; 5th Gp, ND + CurNPs; 6th Gp. ND + NF-CH-CurNPs]. Current results revealed, a significant elevation in the levels of aspartate transaminase (AST), alanine transaminase (ALT), total proteins, liver DNA damage, injury, malondialdehyde (MDA), proliferating cell nuclear antigen (PCNA), tumor necrosis factor alpha (TNFα) and a significant depletion in albumin, catalase, superoxide dismutase (SOD), reduced glutathione (GSH) after ND administration as compared to control and CurNPs groups. Treatment of ND with CurNPs or NF-CH-CurNPs significantly improved liver functions, structure, oxidative stress, DNA damage, PCNA, and TNFα expressions, with NF-CH-CurNPs showing potential for scavenging free radicals.

Nandrolone, is an anabolic androgenic steroid (AAS) used by adolescents and young adults. Supraphysiologic doses of AAS are correlated with dysfunctions in anxiety and reward. This study examined whether exposure to nandrolone before puberty altered anxiety- and addictive-like behaviors. Dopamine type 2 receptors (D2DR) in the nucleus accumbens (NAc) and medial prefrontal cortex (mPFC) were also analyzed. Beginning on day 28 and ending on day 37, male rats received a daily injection of nandrolone decanoate (20 mg/kg) and were subsequently evaluated for anxiety. Their locomotor response (sensitization) and preference (conditioned place preference (CPP) to cocaine (15 mg/kg) were also assessed. Nandrolone reduced anxiety and ambulation, accelerated the development of sensitization to cocaine, and reduced CPP to cocaine by 27%. Expression of D2DR in the NAc and the PFC of males was increased by nandrolone, whereas treatment with cocaine reduced accumbal D2DR. We hypothesize that nandrolone accelerated the development of the neural circuitry that participates in behavioral sensitization and reduced the rewarding properties of cocaine. The observed increase in accumbal D2DR may have potentially mediated the reduction in anxiety and ambulation and hastened the maturation of the neural circuitry responsible for the sensitized response to cocaine.