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- Oct 11, 2010
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Old news for some but for those of you who are doing your research.
Simple if you do ECA's and are taking hcg for pct or just to keep the old testes up to par for pct than leave the asprin out.
peace.
Aspirin inhibits androgen response to chorionic gonadotropin in humans
Domenico Conte1, Francesco Romanelli1, Silvia Fillo1, Laura Guidetti2, Aldo Isidori1, Francesco Franceschi3, Maurizio Latini1, and Luigi di Luigi2
1 Division of Andrology, Department of Medical Pathophysiology, University "La Sapienza," 00161 Rome; 2 Laboratory of Endocrinological Research, University Institute of Motor Sciences, 00194 Rome; and 3 Department of Orthopedics, Libera Universitá, Campus Biomedico, 00155 Rome, Italy
Eicosanoids play an important role in the regulation of the hypothalamic-pituitary axis; less clear is their role in testicular steroidogenesis. To evaluate the involvement of cyclooxygenase metabolites, such as prostaglandins, in the regulation of human testicular steroidogenesis, we examined the effects of a prostaglandin-blocker, aspirin, on plasma testosterone, pregnenolone, progesterone, 17OH-progesterone, androstenedione, dehydroepiandrosterone, and 17beta -estradiol response to human chorionic gonadotropin (hCG) in normal male volunteers in a placebo-controlled, single-blinded study. To test the efficacy of aspirin, seminal prostaglandin E2 levels were also determined. hCG stimulation increased peripheral levels of testosterone, 17OH-progesterone, androstenedione, dehydroepiandrosterone, and 17beta -estradiol, without affecting circulating pregnenolone and progesterone values. Aspirin significantly lowered seminal prostaglandin E2 levels, whereas it did not modify steroid concentrations not exposed to exogenous hCG. Moreover, the drug significantly reduced the response of testosterone, 17OH-progesterone, androstenedione, and dehydroepiandrosterone to hCG, as assessed by the mean integrated area under the curve, whereas it did not influence 17beta -estradiol response. In conclusion, aspirin treatment inhibits androgen response to chorionic gonadotropin stimulation in normal humans. The action of aspirin is probably mediated via an effective arachidonate cyclooxygenase block.
Simple if you do ECA's and are taking hcg for pct or just to keep the old testes up to par for pct than leave the asprin out.
peace.
Aspirin inhibits androgen response to chorionic gonadotropin in humans
Domenico Conte1, Francesco Romanelli1, Silvia Fillo1, Laura Guidetti2, Aldo Isidori1, Francesco Franceschi3, Maurizio Latini1, and Luigi di Luigi2
1 Division of Andrology, Department of Medical Pathophysiology, University "La Sapienza," 00161 Rome; 2 Laboratory of Endocrinological Research, University Institute of Motor Sciences, 00194 Rome; and 3 Department of Orthopedics, Libera Universitá, Campus Biomedico, 00155 Rome, Italy
Eicosanoids play an important role in the regulation of the hypothalamic-pituitary axis; less clear is their role in testicular steroidogenesis. To evaluate the involvement of cyclooxygenase metabolites, such as prostaglandins, in the regulation of human testicular steroidogenesis, we examined the effects of a prostaglandin-blocker, aspirin, on plasma testosterone, pregnenolone, progesterone, 17OH-progesterone, androstenedione, dehydroepiandrosterone, and 17beta -estradiol response to human chorionic gonadotropin (hCG) in normal male volunteers in a placebo-controlled, single-blinded study. To test the efficacy of aspirin, seminal prostaglandin E2 levels were also determined. hCG stimulation increased peripheral levels of testosterone, 17OH-progesterone, androstenedione, dehydroepiandrosterone, and 17beta -estradiol, without affecting circulating pregnenolone and progesterone values. Aspirin significantly lowered seminal prostaglandin E2 levels, whereas it did not modify steroid concentrations not exposed to exogenous hCG. Moreover, the drug significantly reduced the response of testosterone, 17OH-progesterone, androstenedione, and dehydroepiandrosterone to hCG, as assessed by the mean integrated area under the curve, whereas it did not influence 17beta -estradiol response. In conclusion, aspirin treatment inhibits androgen response to chorionic gonadotropin stimulation in normal humans. The action of aspirin is probably mediated via an effective arachidonate cyclooxygenase block.