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Chemical Compound Review

SPECTRUM300034     [(10R,13S,17S)-10,13- dimethyl-3-oxo-1,2,6...

Synonyms: AC1NWAJ3, BSPBio_002784, KBioGR_000428, KBioSS_001739, CCG-39107, ...
 
 
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Disease relevance of testosterone propionate

  • Within 1 week after TP implantation, LNCaP 104-R2 tumors exhibited massive necrosis with severe hemorrhage [1].
  • All 3 prenatal TP treatments administered to females significantly increased mounting frequencies and suppressed lordosis, ovulation, and the positive-feedback effects of estrogen and progesterone on luteinizing hormone release [2].
  • An immobilization response was observed in some, but no all, postpubertally castrated males with high dosages of EB or TP; but the frequency of response did not increase with increasing dosage of TP greater than 250 micrograms/kg body weight [3].
  • Beef tallow significantly increased the development of ventral prostate carcinomas with DMAB alone (from 15 to 45%, P < 0.05), while perilla oil reduced the incidence of prostatic intraepithelial neoplasia (PIN) in the ventral lobe of rats given DMA + TP (from 70 to 10%, P < 0.01), but not in those given DMAB alone [4].
  • CONCLUSIONS: Testosterone-propionate profoundly inhibits the exercise-induced augmented capillarization, whereas (under training conditions) it leads to a mild myocyte hypertrophy [5].
 

Psychiatry related information on testosterone propionate

  • However, the maternal behavior of TP dams, as measured by retrieval and crouching, appeared to be normal [6].
  • This masculinization appears to be complete only in the animals exposed to TP perinatally, suggesting that the critical period for the sexual differentiation of this nucleus may extend into the late prenatal period [7].
  • Masculine sexual behavior was restored and maintained by TP, whereas EC initially activated sexual behavior, including copulation and ejaculation, but was unable to sustain copulatory behavior for the 8- to 18-week periods that were evaluated [8].
  • Males castrated at 1, 6 or 10 days of age but not males castrated in adulthood displayed levels of stereotyped behavior comparable to those of ovariectomized females when all animals were given TP in adulthood [9].
 

High impact information on testosterone propionate

  • TP treatment of mice with LNCaP 104-R2 tumors reduced tumor androgen receptor and c-myc mRNA levels but increased prostate-specific antigen in serum- and prostate-specific antigen mRNA in tumors [1].
  • The effects of TP at doses of 0, 100, 200, and 400 micrograms/day on cell division and cell death in SCC8 tumors of medium size were examined by measurements of the mitotic index and the retention of 5-[125I]iodo-2'-deoxyuridine incorporated into the whole tumor [10].
  • An androgen-dependent tumor (SCC8 tumor) was obtained by inoculating an androgen-responsive cell line derived from the androgen-responsive Shionogi carcinoma 115 (SC115) into mice and then treating the mice with testosterone propionate (TP) at a pharmacological dose (400 micrograms/day) [10].
  • Orchidectomy on day 1 resulted in an approximately 50% decrease in adult SDN-POA volume; however, the influence of the testes on their resulting SDN-POA volume was replaced affectively by the administration of 100 micrograms or 1 mg of TP on postnatal day 2 or by a testicular (but not ovarian) graft on the day of castration [11].
  • E2 replacement in adult TP rats normalized all the mRNA levels, except for PVN GR mRNA which did fall towards the levels of the oil-control animals [12].
 

Chemical compound and disease context of testosterone propionate

  • In androgenized animals clonidine had the opposite effect; it attenuated the inhibitory effect of testosterone propionate (TP) on differentiation of lordosis behavior [13].
  • Prazosin, which was without effect in nonandrogenized animals, also attenuated the inhibitory effect of TP on differentiation of lordosis behavior [13].
  • Body weight was reduced in males exposed to DES, TP or DES + TP, while testicular weight was reduced in animals injected with DES, E2B, TP, DES + TP or DES + progesterone [14].
  • The effects of long-term injections of testosterone propionate (TP), diethylstilbestrol (DES) and TP+DES simultaneously to castrated and sham-operated White Leghorn cocks on feeding, weight gain, obesity, blood lipids and weight of various glands were studied [15].
  • Lordosis did not occur after administration of TP, PCPA, or pargyline, individually or in any other combination [16].
 

Biological context of testosterone propionate

  • In addition, a dose-response study, in which gonadectomized males and females were administered from 25-1000 microg TP, demonstrated a significant linear trend in up-regulation of AR in both males and females, with no sexual dimorphism in the response to hormone treatment [17].
  • All mice that received TP entered constant vaginal estrus, whereas those given vehicle showed variable cytology [18].
  • In castrated males, as well as in females, testosterone propionate (TP, 0.5 mg s.c. in 50 microliters peanut oil) injected on days 1, 3 and 5 postpartum increased mEH and cEH activities at adulthood compared to peanut oil-treated controls [19].
  • No significant sex difference was noted postnatally, and administration of TP 3 h after birth did not change Raf-1 levels examined 24 h later [20].
  • We treated pregnant guinea pigs on Day 50 of gestation with 10 mg testosterone propionate (TP), obtaining fetuses 2, 4, 8, or 18 h later as well as after 5 days of treatment [21].
 

Anatomical context of testosterone propionate

  • Although TP treatment elevated fetal serum T (p less than 0.05), brain cytosolic androgen receptor (ARc) content was unchanged in fetuses of either sex [21].
  • Mice were treated with 0.5 mg of TP or dihydrotestosterone (DHT) or vehicle (oil), and testes were harvested 4, 8, and 16 h after treatment [22].
  • The data are discussed in a mechanistic framework suggesting how TP acts to augment facial nerve regeneration [23].
  • The methodology was verified by confirming the presence of previously characterized TP-regulated genes, including Pem in Sertoli cells and Cyp17a1 in Leydig cells [22].
  • High-androgen groups (control males, Cas+T, TP females) performed better in spatial navigation and exhibited CA3 neurons with longer dendrites, a larger number of dendritic branches, and volumes of influence compared to low-androgen groups (control females, castrated males, OVX) [24].
 

Associations of testosterone propionate with other chemical compounds

  • Perinatal testosterone propionate (TP) treatment of females partially masculinized (enhanced) the LH response to T implant removal, but only if ovariectomy had been performed prior to puberty (at 0 or 25 days of age).(ABSTRACT TRUNCATED AT 250 WORDS)[25]
  • The effects of prolactin (PRL), bromocriptine (Br), testosterone propionate (TP), dihydrotestosterone (DHT), and the combinations of these androgens with PRL/Br on total lipid, total cholesterol, total glyceride glycerols, and total phospholipid and their fractions in cranial and caudal prostates of castrated mature monkeys were studied [26].
  • Simultaneous administration of 19-OH-DHTA and estradiol benzoate (EB) also failed to increase the level of sexual performance, but daily injection (1 mg/kg/day) of testosterone propionate (TP) was very effective in effective in activating sexual behavior [27].
  • The contrasting responses of neonatally feminized subjects to later TP and EB + P treatments suggest that female hamsters retain a greater capacity for heterotypical patterns of ultrasound production than do males [28].
  • In the second experiment, the hormone activity of the implants was increased by using testosterone propionate (TP) or a 50% mixture of estradiol (E2) and cholesterol [29].
 

Gene context of testosterone propionate

  • Neonatal TP treatment did not affect either proTRH mRNA or TRH peptide levels [30].
  • These results indicate that the pituitary GH is involved as one of the major regulatory factors of sex differences in the activities of hepatic AO in mice and TP also contributes to maintaining the higher activity in male mice mainly through the hypothalamus-pituitary system [31].
  • More specifically, EB administration to females resulted in decreased activity of MAO in the corticomedial amygdala and basomedial hypothalamus and an elevation of ChAc activity in the medial preoptic area and corticomedial amygdala while TP administration did not alter enzyme levels in any brain region [32].
  • Androgen treatment (3 mg of testosterone-propionate for 3 days) of gonadectomized animals caused a decrease in the intensity of hepatocyte PRLR-positive staining similarly in both sexes.(ABSTRACT TRUNCATED AT 250 WORDS)[33]
  • 2. The treatment with TP had no effect on the CR activity in liver microsomes of the ovariectomized or hypophysectomized female rat [34].
 

Analytical, diagnostic and therapeutic context of testosterone propionate

  • TP increased the mitotic index dose dependently and at all doses reduced the decrease in the retention of 5-[125I]iodo-2'-deoxyuridine [10].
  • CBA male and female mice received a single subcutaneous injection of 0.5 mg testosterone propionate (TP) in olive oil within 24 h after birth [35].
  • The ability of ovarian steroids to influence the release of LH was examined after ovariectomy in regularly cycling adult female rats and two types of anovulatory persistent estrous rats: rats treated with 10 mug of testosterone propionate (TP) shortly after birth, and normal rats housed under constant illumination [36].
  • To further investigate these issues, the distribution, density, and regulation of neural AR were compared among male and female mice that were intact, gonadectomized, or gonadectomized and given testosterone propionate (TP) through immunocytochemical and Western blot analyses [17].
  • The typical recovery of these two sequences following 5 days of testosterone propionate (TP) replacement therapy was not impaired by the bilateral denervation of the LA [37].

References

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  23. Androgen receptor mRNA regulation in adult male and female hamster facial motoneurons: effects of axotomy and exogenous androgens. Larkowski, T.D., Drengler, S.M., Tanzer, L., Jones, K.J. J. Neurobiol. (2000) [Pubmed]
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