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DHEA is transformed into DHEA-S by sulfation at the C3β position via the sulfotransferase enzymes SULT2A1 and to a lesser extent SULT1E1 . [40] [50] [51] This occurs naturally in the adrenal cortex and during first-pass metabolism in the liver and intestines when exogenous DHEA is administered orally. [ citation needed ] Levels of DHEA-S in circulation are approximately 250 to 300 times those of DHEA. [19] DHEA-S in turn can be converted back into DHEA in peripheral tissues via steroid sulfatase (STS). [52] [53]

Apigenin acts as a monoamine transporter activator, one of the few chemicals demonstrated to possess this property. [8] Apigenin is a ligand for central benzodiazepine receptors that competitively inhibited the binding of flunitrazepam with a K i of 4 μM, exerting anxiolytic and slight sedative effects. [9] Apigenin shows second-order positive modulatory activity at GABA A receptors. [10] [11] It has also effects on adenosine receptors [12] and is an acute antagonist at the NMDA receptors ( IC 50 = 10 μM). [11] In addition, like various other flavonoids, apigenin has been found to possess nanomolar affinity for the opioid receptors (K e = 410 nM, 970 nM, and 410 nM for the μ- , δ- , and κ-opioid receptors , respectively), acting as a non-selective antagonist of all three opioid receptors. [13]

Trenbolone hexabol

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