PubMed Health⌕ Search

Biomedical subjects

A Boris

Publications and source records attributed to A Boris.

At least 19 recordsLinked to original sources
PubMed1988

Sebum-suppressing activity of the nonpolar arotinoid Ro 15-0778 in rodents.

Retinoids are known to modulate sebaceous gland activity in humans and animals. The nonpolar arotinoid Ro 15-0778 [(E)-1,2,3,4-tetrahydro-1,1,4,4-tetramethyl-6-(1-methyl-2-phenylethen yl) naphthalene] does not contain a polar end group and is devoid of the classical retinoid side effects of hypervitaminosis A. The favorable toxicological profile stimulated the evaluation of this arotinoid in animal models of sebum production. In castrated, testosterone-stimulated male rats, Ro 15-0778 is 50 times more potent than 13-cis-retinoic acid in inhibiting the production and subsequent secretion of sebum. The oral ED50 value of Ro 15-0778 is 30 micrograms/kg, while an oral dose of 0.5 mg/kg inhibited sebum secretion nearly 100%. In testosterone-stimulated female rats, Ro 15-0778 inhibits sebum secretion significantly with an oral ED50 of 140 micrograms/kg and an s.c. ED50 of 75 micrograms/kg. Ro 15-0778 was also evaluated for its ability to prevent testosterone induction of the immature hamster flank organ. The topical ED50 is 0.53 mg/kg and the oral ED50 is 38 mg/kg. This arotinoid is similarly active in mature male hamsters without testosterone treatment. In addition, the retinoid is active topically and orally in reducing the size of the gerbil abdominal sebaceous gland. The compound exhibits no antiandrogenic activity when tested in ventral prostrate and seminal vesicle assays in rats. Additionally, the compound does not have estrogenic activity when tested in the rat uterine weight assay. High doses of Ro 15-0778 in humans did not demonstrate significant sebum-suppressing activity.(ABSTRACT TRUNCATED AT 250 WORDS)

Androgen Antagonists↗
PubMed1986

Bone resorption, renal function and mineral status in cows treated with 1,25-dihydroxycholecalciferol and its 24-fluoro analogues.

The relative potencies of 1,25-dihydroxycholecalciferol, 24-F-1,25-dihydroxycholecalciferol, and 24,24-F2-1,25-dihydroxycholecalciferol at three doses (25, 100 or 400 micrograms) were assessed in nonlactating Jersey cows. The 24,24-F2-1,25-dihydroxycholecalciferol induced a significantly greater hypercalcemia and hyperphosphatemia than did 1,25-dihydroxycholecalciferol. The 24-F-1,25-dihydroxycholecalciferol was intermediate in its hypercalcemic and hyperphosphatemic potency. Urinary hydroxyproline excretion rate and plasma hydroxyproline concentration were not significantly increased by treatment with any of the compounds. This indicates that these compounds did not stimulate bone resorption in nonlactating, nongravid cows. Renal function was significantly impaired in cows that received a 400-micrograms dose of any compound. There was a severe reduction in glomerular filtration rate (up to 42%) and urine specific gravity. Renal function was most severely affected in cows treated with 24,24-F2-dihydroxycholecalciferol and was evident even at the 100-micrograms dosage level.

Animals↗
PubMed1981

Decrease in serum levels of 1,25-dihydroxycholecalciferol in rats and chickens fed a vitamin D-deficient diet.

Twenty-one-day-old rats placed on a vitamin D-deficient diet showed no decrease in serum, 1,25-dihydroxy vitamin D levels after 13 days on this diet. Between 13 and 20 days on this D-deficient diet there was a 50% decrease in serum 1,25-dihydroxy vitamin D. After 34 days, the level of 1,25-dihydroxy vitamin D in serum had dropped to near zero. With a vitamin D-deficient diet lacking calcium, there was an apparent stimulation of 1-hydroxylase, resulting in higher 1,25-dihydroxy vitamin D serum levels after 6--20 days on the diet. After 27 days there were no differences in 1,25-dihydroxy-vitamin D levels in animals fed a calcium-replete or calcium-deficient rachitogenic diet. When 1-day-old chickens were maintained on a rachitogenic diet for 1 week, 1,25-dihydroxy vitamin D levels were higher in animals fed the calcium-deficient diet compared with the calcium-replete diet. After 2 weeks on either rachitogenic diet, 1,25-dihydroxy vitamin D levels decreased to near zero. Measurement of 1,25-dihydroxy vitamin D levels has provided a biochemical indicator of vitamin D deficiency in chicks and rats which will complement other established biological criteria for vitamin D deficiency.

Animals↗
PubMed1980

Synthesis and biological activity of some 15-oxaestranes.

The estrogenic activity of orally administered 15-oxaestrone was evaluated by the uterotropic assay in rats and was found to be 12 times greater than that of estrone. In addition, several analogues of 15-oxaestrone were prepared and their estrogenic potency was determined.

Animals↗
PubMed1980

In vivo mobilization of bone calcium in thyroparathyroidectomized rats by 1 alpha, 25-dihydroxycholecalciferol (calcitriol) and related compounds.

Calcitriol, 0.5 microgram/rat, given subcutaneously (sc), did not mobilize 45Ca from bone in intact, pre-labeled rats, but caused significant elevation of serum radioactivity in thyroparathyroidectomized (TPTX) rats. The response to calcitriol in TPTX rats was dose-dependent with significant activity at sc doses of 40 ng/rat and above when measured at 18 hours after dosing. Parathyroid hormone, 1 alpha-hydroxycholecalciferol, 1 alpha, 24R,25-trihydroxycholecalciferol and 5,6-trans-25-hydroxycholecalciferol were also effective in TPTX rats. The latter two compounds required microgram doses to mobilize 45Ca from bone. Calcitriol, 25-hydroxycholecalciferol and 24R,25-dihydroxycholecalciferol were inactive in TPTX rats even with doses of 40 microgram/rat and measurement of serum radioactivity up to 72 hours after dosing.

Animals↗
PubMed1979

Inhibition of diphosphonate-blocked bone mineralization. Evidence that calcitonin promotes mineralization.

There is much experimental evidence which indicates that calcitonin in hibits bone mineral resorption, but there are few data available in support of the proposal that calcitonin may also promote mineralization. Ethane-1-hydroxy-1,1-diphosphonate (EHDP) administered to immature rats inhibited mineralization as evidenced by widened tibial epiphyseal plates and decreased bone ash to dry weight ratios. Concurrent dosing with salmon calcitonin (SCT) prevented or reversed the EHDP-blocked mineralization in a dose dependent manner. Administration of SCT during the period after EHDP treatment significantly improved mineralization of tibial epiphyseal plates as shown by plate width narrowing and increased uptake of radioactive calcium. These results suggest that SCT increased mineralization in EHDP-treated rats, and provide supportive evidence for the proposal that calcitonin may also promote mineralization, in addition to its well known ability to inhibit bone mineral resorption.

Age Factors↗
PubMed1978

Evidence for the promotion of bone mineralization by 1alpha,25-dihydroxycholecalciferol in the rat unrelated to the correction of deficiencies in serum calcium and phosphorus.

Concurrent administration of 1alpha,25-dihydroxycholecalciferol [1alpha,25-(OH)2-CC] to intact and thyroparathyroidectomized rats treated with ethane-1-hydroxy-1,1-diphosphonate (EHDP) prevented or reversed the EHDP-induced inhibition of bone mineralization as measured by changes in epiphyseal plate width and ash content of bone. An analog, 1alpha-droxycholecalciferol, was also effective. Recovery of bone after EHDP treatment was also significantly improved by administration of 1alpha,25-(OH)2-CC as evidenced by enhanced uptake of 45Ca by epiphyseal plates and decreased plate widths. Cholecalciferol (CC), ergocalciferol, dihydrotachysterol2, 5,6-trans-CC, 25-OH-CC, 5,6-Trans-25-OH-CC, and 1alpha24R,25-(OH)3-CC also blocked EHDP-induced epiphyseal plate widening, but required high, pharmacological dose levels. 24R,25- (OH)2-CC was inactive at doses up to 10 microgram/day. Since EHDP-treated rats are not deficient in calcium or phosphate, these data suggest that 1alpha,25-dihydroxycholecalciferol promoted bone mineralization independently of effects upon the intestinal absorption of calcium and phosphate.

Animals↗
PubMed1977

Relative activities of some metabolites and analogs of cholecalciferol in stimulation of tibia ash weight in chicks otherwise deprived of vitamin D.

Nine metabolites and analogs of cholecalciferol (CC) were tested for ability to increase tibia ash weight in chicks otherwise deprived of vitamin D. All of the compounds promoted bone mineralization in a linear log dose-response relationship. The maximal response obtained for any compound was an approximate doubling in bone ash weight compared to vehicle-treated controls. Relative potencies, based upon the calculated ash weight doubling dose, were as follows: 1 alpha, 25-(OH)2-CC = 1 alpha-OH-CC greater than CC greater than 25-OH-CC greater than 24R, 25-(OH)2-CC = 1 alpha,24R, 25-(OH)3- CC greater than 5,6-trans-25-OH-CC greater than 1 alpha, 24S, 25- (OH)3-CC greater than 5,6-trans-CC greater than 24S, 25-(OH)2-CC.

Animals↗
PubMed1977

Assessment of topical anti-inflammatory activity in rats with cantharidin-induced inflammation.

Topical application of 400 mug of cantharidin to the rat's ear caused an approximate doubling in the mean weight of uniform ear punch samples when compared to vehicle-treated controls at 72 hr, and produced a maximal response at 7 days. Dexamethasone reduced the increase in weight when applied topically, but was ineffective when given subcutaneously or orally at the same doses. Hydrocortisone, prednisolone, triamcinolone, betamethasone, flurometholone, paramethasone acetate, fluocinolone acetonide, fluocinonide, and flurandrenolide showed significant suppression of cantharidin-induced inflammation. Cholesterol, diphenhydramine, tripelennamine, chlorpheniramine, promethazine, cyproheptadine, epinephrine, phenylephrine, alpha-tocopherol, indomethacin, and bufexamac were inactive. It is suggested that the procedure employed may be useful in the screening and evaluation of topical anti-inflammatory agents.

Administration, Topical↗