La mia sentenza definitiva sulla DUTASTERIDE
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Citazione:Messaggio inserito da unlocked
gli antiaromatasi che non siano anastrozolo o letrozolo o exemestane ecc non so quanto siano efficaci...lascia xdere i cosiddetti inibitori di origine vegetale xchè sono acqua fresca...
Niente di vegetale. I prodotti di cui parlo sono l'ATD e il 6-bromodione detto anche 6-bromo-adrostenedione.
gli antiaromatasi che non siano anastrozolo o letrozolo o exemestane ecc non so quanto siano efficaci...lascia xdere i cosiddetti inibitori di origine vegetale xchè sono acqua fresca...
Niente di vegetale. I prodotti di cui parlo sono l'ATD e il 6-bromodione detto anche 6-bromo-adrostenedione.
Synthesis and biochemical properties of 6-bromoandrostenedione derivatives with a 2,2-dimethyl or 2-methyl group as aromatase inhibitors.Numazawa M, Handa W, Yamada K.
Tohoku Pharmaceutical University, Sendai, Japan. numazawa@tohoku-pharm.ac.jp
To gain insight into the mechanism for irreversible inactivation of aromatase by 6beta-bromoandrostenedione (1), one of the earliest discovered suicide substrates, in relation to the catalytic function of the enzyme, the 2,2-dimethyl derivative of compound 1, steroid 4, and its 6alpha-isomer 5, as well as 2-methyl-1,4-diene steroid 8 and its 6alpha-bromide 10, were synthesized. All of the steroids inhibited aromatase activity in human placental microsomes with apparent K(i)'s ranging between 10 and 81 nM. The 2,2-dimethyl-6beta- and 6alpha-bromo steroids 4 and 5 were extremely powerful inhibitors (K(i): 14 and 10 nM, respectively), but these two did not cause a time-dependent inactivation of aromatase in the presence of NADPH; in contrast, the 2-methyl-1,4-diene steroids 8 and 10 caused time-dependent inactivation with apparent k(inact) of 0.035 and 0.071 min(-1), respectively, in a suicide manner. These results indicate that the 2,2-dimethyl function of the 6beta-bromide 4 would prevent the inactivation of aromatase caused by inhibitor 1 in a suicide manner, probably through steric activity, whereas the 2-methyl group of steroid 8 did not significantly affect the suicidal inactivation by the parent 1,4-diene steroid, a typical suicide substrate.
Tohoku Pharmaceutical University, Sendai, Japan. numazawa@tohoku-pharm.ac.jp
To gain insight into the mechanism for irreversible inactivation of aromatase by 6beta-bromoandrostenedione (1), one of the earliest discovered suicide substrates, in relation to the catalytic function of the enzyme, the 2,2-dimethyl derivative of compound 1, steroid 4, and its 6alpha-isomer 5, as well as 2-methyl-1,4-diene steroid 8 and its 6alpha-bromide 10, were synthesized. All of the steroids inhibited aromatase activity in human placental microsomes with apparent K(i)'s ranging between 10 and 81 nM. The 2,2-dimethyl-6beta- and 6alpha-bromo steroids 4 and 5 were extremely powerful inhibitors (K(i): 14 and 10 nM, respectively), but these two did not cause a time-dependent inactivation of aromatase in the presence of NADPH; in contrast, the 2-methyl-1,4-diene steroids 8 and 10 caused time-dependent inactivation with apparent k(inact) of 0.035 and 0.071 min(-1), respectively, in a suicide manner. These results indicate that the 2,2-dimethyl function of the 6beta-bromide 4 would prevent the inactivation of aromatase caused by inhibitor 1 in a suicide manner, probably through steric activity, whereas the 2-methyl group of steroid 8 did not significantly affect the suicidal inactivation by the parent 1,4-diene steroid, a typical suicide substrate.
Cancer Res. 1982 Aug;42(8 Suppl):3338s-3341s. Links
Estrogen synthesis in human breast tumor and its inhibition by testololactone and bromoandrostenedione.Dao TL.
A total of 53 tumors have been examined for estrogen synthesis from androstenedione and assayed for estradiol receptors. It was found that of the 40 tumors that metabolized androstenedione to estrogens, 17 tumors were estradiol receptor negative and 23 tumors were estradiol receptor positive. Of the 13 tumors that did not synthesize estrogens, 7 tumors were receptor negative and 6 tumors were receptor positive. No correlation was found between the ability of the tumor to synthesize estrogens and the presence or absence of estradiol receptors. The inhibition of aromatase enzyme in human breast tumors by delta 1-testololactone, testololactone, and 6 alpha- and 6 beta-bromoandrostenedione was investigated. Estrone and estradiol synthesis from androstenedione was reduced in five tumor incubations by the presence of 0.2 mM delta 1-testololactone and testololactone, 6 alpha- and 6 beta-bromoandrostenedione (2.0 microM) were also shown to block estrogen synthesis in 5 tumors. Furthermore, Lineweaver-Burk plots revealed that all four compounds were competitive inhibitors of androstenedione aromatization. An apparent Km of the aromatase enzyme for androstenedione of 0.08 microM and a Vmax of 23 pmol of estrone synthesized per g tumor per hr were determined for one human breast tumor specimen. The use of an aromatase inhibitor such as delta 1-testololactone in the treatment of breast cancer should be reconsidered. Data from one patient with advanced cancer of the breast, responding to previous oophorectomy and adrenalectomy and treated with large doses of delta 1-testololactone, are presented to illustrate the significance of successful treatment by scientific approaches.
PMID: 7083197 [PubMed - indexed for MEDLINE]
Estrogen synthesis in human breast tumor and its inhibition by testololactone and bromoandrostenedione.Dao TL.
A total of 53 tumors have been examined for estrogen synthesis from androstenedione and assayed for estradiol receptors. It was found that of the 40 tumors that metabolized androstenedione to estrogens, 17 tumors were estradiol receptor negative and 23 tumors were estradiol receptor positive. Of the 13 tumors that did not synthesize estrogens, 7 tumors were receptor negative and 6 tumors were receptor positive. No correlation was found between the ability of the tumor to synthesize estrogens and the presence or absence of estradiol receptors. The inhibition of aromatase enzyme in human breast tumors by delta 1-testololactone, testololactone, and 6 alpha- and 6 beta-bromoandrostenedione was investigated. Estrone and estradiol synthesis from androstenedione was reduced in five tumor incubations by the presence of 0.2 mM delta 1-testololactone and testololactone, 6 alpha- and 6 beta-bromoandrostenedione (2.0 microM) were also shown to block estrogen synthesis in 5 tumors. Furthermore, Lineweaver-Burk plots revealed that all four compounds were competitive inhibitors of androstenedione aromatization. An apparent Km of the aromatase enzyme for androstenedione of 0.08 microM and a Vmax of 23 pmol of estrone synthesized per g tumor per hr were determined for one human breast tumor specimen. The use of an aromatase inhibitor such as delta 1-testololactone in the treatment of breast cancer should be reconsidered. Data from one patient with advanced cancer of the breast, responding to previous oophorectomy and adrenalectomy and treated with large doses of delta 1-testololactone, are presented to illustrate the significance of successful treatment by scientific approaches.
PMID: 7083197 [PubMed - indexed for MEDLINE]
: Endocrinology. 1987 Sep;121(3):1010-6. Links
Stereochemistry of the functional group determines the mechanism of aromatase inhibition by 6-bromoandrostenedione.Osawa Y, Osawa Y, Coon MJ.
A selective inhibitor of aromatase (estrogen synthetase) would be a useful pharmacological tool with potential therapeutic application. We have found that 6 alpha-bromoandrostenedione (6 alpha-BrA) is a competitive inhibitor of human placental aromatase with respect to androstenedione, with an apparent Ki of 3.4 nM, while 6 beta-BrA is a mechanism-based irreversible inhibitor with an apparent Ki of 0.8 microM and a kinact of 0.025 min-1. Aromatase activity was measured by tritium release into water from the 1 beta position of [1(-3)H,4(-14)C]androstenedione in reaction mixtures containing NADPH and the aromatase. Time-dependent inhibition was assessed by preincubation of inhibitors with either the 900 X g placental pellet or placental microsomes in the presence of NADPH. Aliquots were taken at intervals, diluted, and assayed for aromatase activity with androstenedione and additional NADPH. The time-dependent inhibition by 6 beta-BrA was dependent on the concentration of this compound and the presence of NADPH, while the addition of excess substrate in the preincubation mixture hindered the inactivation. Both epimers were ineffective in inhibiting rabbit liver microsomal drug-metabolizing activities in a competitive or time-dependent manner. This indicates a high selectivity of 6-BrA inhibition among P-450 cytochromes. These and other 6-substituted androgens may be useful probes into the nature of the active site and mechanism of action of aromatase.
PMID: 3622372 [PubMed - indexed for MEDLINE]
Stereochemistry of the functional group determines the mechanism of aromatase inhibition by 6-bromoandrostenedione.Osawa Y, Osawa Y, Coon MJ.
A selective inhibitor of aromatase (estrogen synthetase) would be a useful pharmacological tool with potential therapeutic application. We have found that 6 alpha-bromoandrostenedione (6 alpha-BrA) is a competitive inhibitor of human placental aromatase with respect to androstenedione, with an apparent Ki of 3.4 nM, while 6 beta-BrA is a mechanism-based irreversible inhibitor with an apparent Ki of 0.8 microM and a kinact of 0.025 min-1. Aromatase activity was measured by tritium release into water from the 1 beta position of [1(-3)H,4(-14)C]androstenedione in reaction mixtures containing NADPH and the aromatase. Time-dependent inhibition was assessed by preincubation of inhibitors with either the 900 X g placental pellet or placental microsomes in the presence of NADPH. Aliquots were taken at intervals, diluted, and assayed for aromatase activity with androstenedione and additional NADPH. The time-dependent inhibition by 6 beta-BrA was dependent on the concentration of this compound and the presence of NADPH, while the addition of excess substrate in the preincubation mixture hindered the inactivation. Both epimers were ineffective in inhibiting rabbit liver microsomal drug-metabolizing activities in a competitive or time-dependent manner. This indicates a high selectivity of 6-BrA inhibition among P-450 cytochromes. These and other 6-substituted androgens may be useful probes into the nature of the active site and mechanism of action of aromatase.
PMID: 3622372 [PubMed - indexed for MEDLINE]
no,infatti faccio questi esami per un controllo di routine,me li ha prescritti Marliani (a parte HIV e EPATITE C):
SIDEREMIA
FERRITINA
ZINCHEMIA
ACIDO FOLICO
VIT B12
fT4
PROLATTINA
DHT
MAGNESIEMIA
HIV
EPATITE C
SIDEREMIA
FERRITINA
ZINCHEMIA
ACIDO FOLICO
VIT B12
fT4
PROLATTINA
DHT
MAGNESIEMIA
HIV
EPATITE C
Oggi sono andato a fare le analisi al distretto sanitario,ma il DHT non me lo hanno potuto fare...e mi hanno detto che devo telefonare all'ospedale centrale (Careggi). Come mai?
Anche a voi è successa una cosa simile?
Anche a voi è successa una cosa simile?
Ho appena telefonato a Careggi e mi hanno detto che il DHT lo fanno solo al Sant'Orsola di Bologna!!!![xx(][xx(]
Ma è possibile?? Sulla ricetta che mi ha fatto il medico c'è scritto DHT-diidrotestosterone
Va bene o l'esame si chiama in un'altra maniera??[:O]
Ma è possibile?? Sulla ricetta che mi ha fatto il medico c'è scritto DHT-diidrotestosterone
Va bene o l'esame si chiama in un'altra maniera??[:O]
Ho telefonato anche a parecchie cliniche private ma niente da fare[V]
Mi hanno detto che fanno il Testosterone Libero,può servire come analisi per valutare il livello di DHT?
Grazie per l'aiuto
Mi hanno detto che fanno il Testosterone Libero,può servire come analisi per valutare il livello di DHT?
Grazie per l'aiuto
ma allora come faccio a sapere se veramente la duta ha qualche efficacia sul mio organismo e in che %?