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Biomedical subjects

F Di Carlo

Publications and source records attributed to F Di Carlo.

18 recordsLinked to original sources
PubMed1992

Effects of a beta 2-agonist (clenbuterol) on cultured human (CG-5) breast cancer cells.

In order to gain further knowledge about the possible oestrogen-like activities of clenbuterol (a beta 2-adrenergic drug illegally used as partitioning agent in food producing animals), we treated a hormone dependent human breast cancer cell line (CG-5) with different concentrations of the drug (10(-3) M to 10(-8) M). The effects of clenbuterol and oestradiol on cell proliferation were compared. Both oestradiol and clenbuterol, at low concentrations (10(-7) M and 10(-8) M) stimulated cell proliferation, but the effects of clenbuterol were less marked and significant. Probably clenbuterol elicited cell proliferation through a different mechanism, since it did not affect the cellular oestrogen receptor concentration. Clenbuterol failed in binding to the high affinity oestrogen receptors present in the CG-5 cells. As the beta-adrenergic receptors and the susceptibility to their stimulation have been recently demonstrated in vivo and in vitro in many tumour and normal cells, it is reasonable to suppose that clenbuterol may induce cell proliferation through beta-adrenergic stimulation.

Breast Neoplasms↗
PubMed1991

Potentiation of medroxyprogesterone acetate antineoplastic activity by histidine in rat mammary tumours.

The antitumour activity of arginine, histidine and medroxyprogesterone acetate (MPA) was studied in female rats with dimethylbenzanthracene (DMBA)-induced mammary adenocarcinomas. After 15 days of treatment, regression was observed in 4 of 19 (21%), 3 of 18 (16.7%) and 22 of 59 (37.3%) tumours taken from rats given arginine, histidine or MPA, respectively. A total of 17 rats with tumours that had been non-responsive to MPA were then treated with MPA plus histidine for 15 more days; the growth of 3 lesions (17.6%) was arrested, and 5 tumours (29.4%) regressed markedly. The antineoplastic activity of MPA was found to be related to the oestrogen-(ER) and progesterone-receptor (PgR) concentrations measured in the tumours before the start of treatment, whereas that of arginine and histidine appeared to be independent of receptor status. A significant reduction in serum prolactin (PRL) levels occurred in rats that were responsive to MPA alone or to MPA plus histidine. In tumours taken from the same rats, the PRL receptor content was also significantly increased in comparison with that in non-responsive tumours. In contrast, serum PRL levels increased significantly in rats with tumours that were non-responsive to MPA, whereas no change in serum PRL or PRL receptor levels was observed in rats treated with arginine or histidine. Histidine showed the ability to increase the number of ERs and PgRs in responsive tumours; this could have been responsible for the unexpected potentiation of MPA antineoplastic activity. In contrast, the levels of ER and PgR in uteri taken from the same rats were not modified. Furthermore, the addition in vitro of histidine to cytosols obtained from tumours of control animals did not influence ER and PgR concentrations. These results suggest that the effect of histidine on ER and PgR levels is probably specific for tumour tissue and is not due to a direct activity.

Animals↗
PubMed1978

Interference of gestagens and androgens with rat uterine oestrogen receptors.

The inhibitory effect of some gestagens and calusterone on the binding of oestradiol-17beta to its specific uterine receptors has been investigated in intact rats. Progesterone, medrogestone, clogestone, medroxyprogesterone acetate and calusterone reduce the specific oestradiol-receptor interaction in vitro; this effect is dose-dependent and does not differ significantly from one drug to the other. A more relevant decrease in the amount of oestradiol-17beta bound to specific receptors has been observed with calusterone. Progesterone, clogestone, medrogestone, medroxyprogesterone acetate and calusterone given orally induce a marked decrease (between 30 and 70% depending on the dose) in the binding capacity of oestradiol-17beta to specific uterine receptors in vivo. Results from a Scatchard plot analysis suggest that the interference with the binding of oestradiol-17beta caused by both progestogens and calusterone is due to a non-competitive interaction.

Animals↗
PubMed1978

Changes in the concentration of uterine cytoplasmic oestrogen receptors induced by doxorubicin and methotrexate.

The effects of doxorubicin and methotrexate on the oestradiol-induced depletion, replenishment and subsequent increase beyond the normal value (overshoot) in the number of uterine cytoplasmic oestrogen receptors were investigated in intact rats. Injection of doxorubicin (0.5 mg/kg, i.v.) or methotrexate (1mg/kg, i.m.) 5 min after a single i.p. injection of 10 ng oestradiol-17beta (which is able to induce a 50% depletion in the number of oestrogen receptors) caused a significant increase in the oestradiol-induced depletion. Both drugs inhibited the replenishment and the overshoot phases until 48 h after treatment, although the effect was more marked with doxorubicin. Experiments in vitro showed that both methotrexate and doxorubicin affected the capacity of oestradiol-17beta to bind to specific cytoplasmic receptors, inducing an increase in binding when used at low concentrations and a decrease at higher concentrations. The effects of doxorubicin and methotrexate on the depletion, replenishment and overshoot of oestrogen receptors seemed to be partly dependent on the inhibition of protein synthesis and partly due to direct action on the binding of oestradiol-17beta to its receptors.

Animals↗
PubMed1977

[Preliminary results of treatment of hormone-dependent metastatic carcinoma of the breast with the bromocriptin-medroxyprogesterone acetate combination].

A brief account of the concept of hormone dependence in breast neoplasia is followed by the presentation of results obtained with an association of medroxyprogesterone acetate (MAP) and 2-bromo-alpha-ergocriptine (CB 154) in 14 women with metastatic cancer of the breast, hormone dependent due to the presence of the cytoplasmic receptor for 17-beta-oestradiol. All patients, in fertile or premenopausal stage, were subjected to prior surgical ovariectomy. MAP was given i.m. at a dose of 1 g/day for 30 days and then 150 mg/day. In the same time 2.5 mg CB 154 were administered every 6 hr per os. Evaluation in accordance with the criteria proposed by the Coop Breast Cancer Group showed that rapid improvement was obtained in all cases, persisting (at the time of writing) for a minimum of 6 months to a maximum of 2 yr of observation. In addition, rapid disappearance of pain was noted, particularly in subjects with secondary bone lesions. Side-effects were in all cases of slight consequence and suspension of the treatment was never necessary. The mechanism of the two drugs and the advantages of their association are discussed.

Adult↗
PubMed1977

Production of casein and the presence of estrogen receptors in human breast cancer.

The relationship between the presence of estrogen receptors and casein (evaluated on a semiquantitative basis with a specific immunofluorescence method) was statistically analyzed in 50 cases of human breast carcinomas. No significant correlation was found between these two parameters, whereas a relationship was established between the production of casein and the degree of histological differentiation. The results of this study, like those of other studies, revealed a lack of correlation between the presence of estrogen receptors and the degree of histologic differentiation.

Breast Neoplasms↗
PubMedDate not supplied

[Mechanism of action of progestins in the treatment of hormone-dependent breast cancer (author's transl)].

The in vitro interference of some gestagens with the binding of 3H-17-beta-oestradiol to cytosol specific receptors was investigated with a view to elucidating the mechanism of action of progestins in the treatment of human hormone-dependent breast cancer. A decrease (up to 85%) of oestradiol binding capacity was observed with high concentrations of progesterone, clogestone and medrogestone. These findings are in good agreement with those previously obtained by the same progestins in our laboratory on rat uterine estrogen receptors in vitro or in vivo. These results provide the support for the hypothesis that the mode of action of progestins in the therapy of mammary and perhaps uterine carcinomas is to some extent related to the inhibition of oestradiol binding to cytosol specific receptors.

Breast Neoplasms↗
PubMedDate not supplied

Opposite effects of dehydroepiandrosterone on the growth of 7,12-dimethylbenz(a)anthracene-induced rat mammary carcinomas.

The effect of dehydroepiandrosterone (DHEA) (2 mg, twice daily p.o.) on the growth of the dimethylbenz (a) anthracene (DMBA)-induced mammary carcinoma was studied in intact and ovariectomized adult female rats. DHEA treatment stimulated the tumor growth in ovariectomized animals. Conversely, the tumors of intact rats treated with DHEA progressed to a lesser extent than those of intact untreated animals (p < 0.01). Plasma levels of DHEA were higher in DHEA-fed than in untreated animals (p < .01), whereas E2 concentrations were unchanged after DHEA administration. Estrogen receptor (ER) concentrations in tumor tissue of ovariectomized animals given DHEA were no different form those found in intact rats, whereas ER were undetectable in untreated ovariectomized rats. The data indicate that DHEA stimulates the growth of DMBA-induced mammary tumors in ovariectomized rats, while it reduces the tumor progression in intact animals.

9,10-Dimethyl-1,2-benzanthracene↗
PubMedDate not supplied

Oxisuran metabolism in pigs.

The fate of oxisuran in the pig was studied with 14C-labeled drug to quantify its biotransformation and disposition. Despite interanimal differences, it was clear that the compound absorbed rapidly and biotransformed extensively to metabolites which were excreted principally in urine rather than in feces. Direct attacks upon oxisuran involved reduction to diastereo-isomeric oxisuran alcohol sulfoxides and oxidation to oxisuran sulfone. Subsequently, the oxisuran alcohol sulfoxides were reduced to a sulfide and oxidized to a sulfone. Phase II reactions appeared to be limited to sulfation of oxisuran alcohol sulfoxides and oxisuran alcohol sulfone. Pharmacokinetics were investigated for oxisuran and its metabolites.

Animals↗