Abuse of Anabolic-Androgenic Steroids (AAS) by professional and recreational athletes for endurance performance and physique is increasing globally, consequently resulting in secondary pathophysiological effects. The present investigation aims to determine the effect of one of the AAS, stanozolol (ST), on uterine physiology and histology. A total of 15 female mice were assigned to three experimental groups (n = 5). ST was dosed subcutaneously (low-dose, 0.5 mg/kg bwt; high-dose, 5.0 mg/kg bwt or 1% alcohol-baseline control) for 30 days, and treatment was withdrawn on the 31st day. In this study, we evaluated histomorphometry of the uterus, immunoexpression of the estrogen receptor α (ERα), the androgen receptor (AR), and the prolactin receptor (PRLR), after ST treatment. In addition, we measured serum levels of testosterone (T), estradiol (E2), and prolactin (PRL). Morphometric evaluation of uterus demonstrated aberrant endometrial luminal epithelial proliferation, marked by irregular branching with papillary formations. Prolonged administration of ST resulted in disruption of uterine organization, reflecting its deleterious impact on uterine histoarchitecture. In the high-dose treated group, divergent ERα immunoexpression-characterized by endometrial downregulation and myometrial upregulation-correlated with increased myometrial thickness and subsequent hyperplasia. ST, being a derivative of Dihydrotestosterone (DHT), an anabolic steroid, may exert its androgenic-to-enhanced anabolic efficacy through non-genomic actions in the myometrium, while inducing distinct pathologic changes in the endometrium, suggesting a compartment-specific effect in the murine uterus. Prolonged treatment of ST augmented stromal immunoexpression of AR in the endometrium, suggesting AR-dependent mechanisms in this compartment. Substantial hyperexpression of prolactin receptor (PRLR) in both endometrium and myometrium suggests a potential stimulatory effect of ST on PRLR. High-dose ST administration significantly elevated circulating T and PRL levels while suppressing E2 concentrations, indicating interference with the hypothalamic-pituitary-gonadal (HPG) axis, reflecting an altered hormonal milieu. It is inferred that prolonged treatment of ST resulted in aberrant endometrial proliferation, histoarchitectural anomalies, compartment-specific differential immunoexpression of hormone receptors in the endometrium and myometrium, and altered serum hormonal milieu.

BACKGROUND: Stano is an anabolic androgenic steroid (AAS) with various adverse cardiovascular effects because it induces ventricular dysfunction. The objective of this study was to evaluate and demonstrate how Empagliflozin (EP) and platelet-rich plasma (PRP) can reduce the cardiotoxic effects linked to Stano administration in albino rats. METHODS: Fifty-four (n = 54) rats were involved in this research, the animals were randomly divided into six groups: (C, EP, PRP, Stano, SEP, and SPRP). Various cardiovascular health markers, focusing on the relationship between oxidative stress and inflammation in cardiomyopathy were evaluated. RESULTS: There was extensive myocardial injury and damage in the Stano group, as reflected by induction of oxidative stress by increase in the level of MDA, along with significantly reduced level of GSH and CAT. Increased expression of inflammatory markers like IL-1β, and NF-κB/P65 pathway, with strong immunoreactivity of caspase-3-an apoptosis marker in cardiac tissue were observed. Evidence of left ventricular hypertrophy with pathological changes in cardiac tissues was also noted, together with functional impairments. Hypertrophy acts as a compensatory mechanism against injury and stress, since it may cause various complications in case of a lack of intervention. CONCLUSION: Stano activates the initiation of some apoptotic and inflammatory signaling pathways to cause serious aggravated cardiovascular health threats. On the other hand, all the structural function and antioxidant parameters related to cardiovascular health showed improvement after both EP and PRP treatments. Intriguingly, EP and PRP have emerged as effective promising agents against the deleterious cardiac damage linked to Stano use. Nevertheless, more research is actually needed to explain the mechanisms and optimize clinical application or management of those exposed to ASS.

Polydrug use among teenagers is widespread and emergent either among athletes or non-athletes. It is reported that stanzolol (Stanz) is commonly abused with cannabis (Cann), this combination probably affects the testicular functions negatively. Aim The present study aimed to evaluate the toxic effects of Stanz and or Cann on reproductive hormones and testicular enzymes. Male Wistar rats were administered Stanz (5 mg/kg, s.c., once per week) and Cann (20 mg/kg, i.p., daily) either alone or in combination for two months, in exercise or sedentary conditions. Swimming exercise protocol was applied. Administration of both Stanz and Cann induced testicular damage, as evidenced by altered hormones, oxidative stress, and testicular enzymes. The testis tissue was significantly injured by the combined administration. In serum, levels of free testosterone, follicular stimulating hormone (FSH), lutenizing hormone (LH) were markedly reduced, while sorbitol dehydrogenase level increased. Moreover, tissue malondialdehyde (MDA) was significantly increased, glutathione (GSH) content decreased, testicular N-acetyl-β-glucosaminidase (NAG) and Myeloperoxidase (MPO) were increased. SIRT1 and STS mRNA expression were downregulated. Besides, distinct histopathological changes were detected in testis of Stanz and Cann injected rats. Nevertheless, Stanz, Cann or combined treatment showed a considerable up-regulation of immunoexpression of inducible nitric oxide synthase (iNOS) and caspase-3 in testes tissue. Oxidative stress and inflammation played a significant role in the observed pathological changes. Training was partially ameliorating for the observed effects. Use of the drugs in sedentary rats had more detrimental effects on testes. Although exercise could palliate the damage partially, it was not fully protective.

In this study, we assess the feasibility of wastewater sampling from manholes as a potential monitoring tool for performance and image-enhancing drugs (PIEDs) at local gyms and general sports centers in Denmark. Wastewater samples from two gyms and two sports centers were analyzed using two LC-MS-based analytical methods (UPLC-MS/MS and UPLC-TOF-MS) to detect the presence of PIEDs. Samples were collected at 3-h intervals during the opening hours on three selected days of the week for each location. The study showed the presence of anabolic agents such as oxandrolone, stanozolol, and ostarine in wastewater sampled from the gyms. All three compounds are class C drugs in the United States, and likewise, illegal to sell and possess in Denmark. Other PIEDs, such as aromatase inhibitors and psychoactive drugs, were detected in several samples from both gyms and sports centers. However, gyms showed a higher occurrence of PIEDs, whereas general sports centers showed a lower occurrence. Although it cannot be used as a traditional prevalence measure, wastewater sampling from manholes is a useful tool for studying the occurrence of PIEDs among recreational athletes at specific locations or events. Wastewater analysis may be used as an easy and cost-effective tool to complement both preventive and control measures, such as information campaigns, surveys, or personal testing. However, not all locations are suitable for manhole sampling, and it is necessary to consider the legal, ethical, and practical aspects before using wastewater analysis to monitor communities or specific populations.

The abuse of anabolic-androgenic steroids (AAS) is associated with numerous adverse cardiovascular effects, including ventricular hypertrophy, myocardial fibrosis, and sudden cardiac death (SCD), which is a term that identifies a sudden death occurred due to cardiac conditions, congenital or acquired, particularly among young athletes and bodybuilders. This systematic review examines cases of AAS-related deaths, with a particular focus on autoptic, histopathological, immunohistochemical, and toxicological findings that highlight cardiac remodeling and myocardial damage. Numerous fatal cases were analyzed, primarily involving young men with a history of AAS abuse. Autopsy examinations revealed significant cardiac abnormalities such as left ventricular hypertrophy, coronary thrombosis, and dilated cardiomyopathy. Histopathological analyses showed focal myocardial necrosis, myocardial fiber disarray, and interstitial fibrosis, while immunohistochemical studies confirmed the presence of markers such as troponin T, fibronectin, and the C5b-9 complement complex, indicating inflammation, fibrosis, and necrosis. Toxicological analyses frequently detected testosterone, stanozolol, trenbolone, and nandrolone in blood, urine, and hair samples, confirming prolonged use of these substances. The results suggest that AAS-induced hypertrophy and fibrosis contribute to the pathogenesis of fatal arrhythmias and sudden cardiac death, even in the absence of pre-existing coronary artery disease. This review highlights the importance of integrating histopathological, immunohistochemical, and toxicological analyses with autopsy findings in forensic investigations to accurately identify AAS-related deaths and develop prevention strategies to reduce the abuse of these substances, particularly among young athletes and bodybuilders.