Anabolic-Androgenic Steroid-Induced Toxicity in Primary Neonatal Rat Myocardial Cell Cultures

Welder, Allison A.; Robertson, John; Fugate, Robert D.; Melchert, Russell B.

doi:10.1006/taap.1995.1158

Cited by 25 publications

(23 citation statements)

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“…Although sudden death of unknown origin is sometimes reported, it is possible that this may be due to AAS-induced cardiac damage. In light of our current findings, and those in previous reports regarding the serious deleterious effects of AAS on the myocardium, this is a logical conclusion [37][38][39][40]. Furthermore Marsh et al reported that androgen receptors were present in cardiac muscle [41].…”

Section: Discussionsupporting

confidence: 84%

Endocrinological and Pathological Effects of Anabolic-androgenic Steroid in Male Rats

2004

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Abstract. Many athletes use drugs, especially anabolic androgenic steroids (AAS), but there are few reports on the endocrinological and pathological changes in AAS abusers. In this study we reported the results of endocrinological examinations in rats administered AAS and also physical changes. We separated 37 male Wistar rats (7 weeks old) into 3 groups: Group A was medicated with nandrolone decanoate, metenolone acetate, and dromostanolone; Group B with nandrolone decanoate and saline; and Group C was given only saline. They were given subcutaneous injections of the medications or the control vehicle once a week for 6 weeks. Medications were stopped for 4 weeks, and then resumed for another 6 weeks. After that, rats were sacrificed. Serum testosterone level in Group A was significantly higher than that in Group C. Serum dihydrotestosterone in Group A was significantly higher than that in both Groups B and C. Serum estradiol-17b levels in Groups A and B were significantly higher than that in Group C. In pathological evaluation, heart, testis, and adrenal gland were severely damaged. These findings indicate that there is a high degree of risk related to the use of AAS.

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Section: Discussionsupporting

confidence: 84%

Endocrinological and Pathological Effects of Anabolic-androgenic Steroid in Male Rats

2004

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“…22,29 Nongenomic effects of androgens have been described, including alterations in calcium flux, 37 that possibly could contribute to the hypertrophic response as well. Of note, testosterone and dihydrotestosterone in the concentrations studied had no adverse affect on cell morphology or viability, unlike the findings of Melchert and Welder 38 and Welder et al, 39 who studied much higher concentrations and reported a toxic effect. DHT augmented ANP secretion (*PϽ0.02; nϭ9), whereas T was without effect (PϭNS; nϭ9).…”

Section: Discussioncontrasting

confidence: 62%

Androgen Receptors Mediate Hypertrophy in Cardiac Myocytes

et al. 1998

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Background-The role of androgens in producing cardiac hypertrophy by direct action on cardiac myocytes is uncertain.Accordingly, we tested the hypothesis that cardiac myocytes in adult men and women express an androgen receptor gene and that myocytes respond to androgens by a hypertrophic response. Methods and Results-We used reverse transcription-polymerase chain reaction methods to demonstrate androgen receptor transcripts in multiple tissues and [ 3 H]phenylalanine incorporation and atrial natriuretic peptide secretion as markers of hypertrophy in cultured rat myocytes. Messenger RNA encoding androgen receptors was detected in myocytes of male and female adult rats, neonatal rat myocytes, rat heart, dog heart, and infant and adult human heart. Both testosterone and dihydrotestosterone produced a robust receptor-specific hypertrophic response in myocytes, determined by indices of protein synthesis and atrial natriuretic peptide secretion. Conclusions-Androgen receptors are present in cardiac myocytes from multiple species, including normal men and women, in a context that permits androgens to modulate the cardiac phenotype and produce hypertrophy by direct, receptor-specific mechanisms. There are clinical implications for therapeutic or illicit use of androgens in humans.(Circulation. 1998;98:256-261.)

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“…For example, the microscopic lesions seen after administration of oxymetholone to female rats, and mechanistic studies with oxymetholone suggest a vasoactive mechanism. However, cell culture studies with cardiomyocytes indicate oxymetholone may have a direct toxic effect on cardiomyocytes (Welder et al 1995). Additionally, mechanisms may vary between different species.…”

Section: Discussionmentioning

confidence: 99%

Morphologic Aspects of Rodent Cardiotoxicity in a Retrospective Evaluation of National Toxicology Program Studies

et al. 2011

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The heart is increasingly recognized as a target for toxicity. As studies in laboratory rodents are commonly used to investigate the potential toxicity of various agents, the identification and characterization of lesions of cardiotoxicity is of utmost importance. Although morphologic criteria have been established for degenerative myocardial lesions in rats and mice, differentiation of spontaneously occurring lesions from toxin-induced or toxin-related lesions remains difficult. A retrospective light microscopic evaluation was performed on the hearts of F344 rats and B6C3F 1 mice from National Toxicology Program (NTP) studies of six chemicals identified in the NTP database in which treatment-induced myocardial toxicity was present. Two previously defined myocardial lesions were observed: ''cardiomyopathy'' that occurred spontaneously or as a treatment-related effect and ''myocardial degeneration'' that occurred as a treatment-related effect. Both lesions consisted of the same basic elements, beginning with myofiber degeneration and necrosis, with varying amounts of inflammation, interstitial cell proliferation, and eventual fibrosis. This observation is indicative of the heart's limited repertoire of responses to myocardial injury, regardless of the nature of the inciting agent. A prominent differentiating factor between spontaneous and treatment-induced lesions was distribution and lesion onset. Once the respective lesions had undergone fibrosis, however, they generally appeared morphologically indistinguishable.

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Anabolic-Androgenic Steroid-Induced Toxicity in Primary Neonatal Rat Myocardial Cell Cultures

Cited by 25 publications

References 0 publications

Endocrinological and Pathological Effects of Anabolic-androgenic Steroid in Male Rats

Endocrinological and Pathological Effects of Anabolic-androgenic Steroid in Male Rats

Androgen Receptors Mediate Hypertrophy in Cardiac Myocytes

Morphologic Aspects of Rodent Cardiotoxicity in a Retrospective Evaluation of National Toxicology Program Studies

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