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Biomedical subjects

J Meites

Publications and source records attributed to J Meites.

At least 73 records · Page 4Linked to original sources
PubMed1983

Counteraction of underfeeding-induced inhibition of mammary tumor growth in rats by prolactin and estrogen administration.

The purpose of this study was to determine whether administration of estrogen or/and haloperidol (HAL), a drug that increases prolactin (PRL) secretion, could counteract the inhibitory effects of underfeeding on growth of established carcinogen-induced mammary cancers in rats. Sprague-Dawley female rats were fed half of the complete diet consumed daily by ad libitum fed controls, beginning 1 week before daily injection of estradiol benzoate (EB) or/and HAL for 3 weeks. Body weight, mammary tumor number, and mammary tumor diameter were measured at weekly intervals, and at the end of the 3 weeks blood was collected for assay of serum PRL. Full-fed (FF) control rats showed an increase by the end of 3 weeks in average body weight, mammary tumor number, and mammary tumor size whereas half-fed (HF) rats showed a significant decrease in average body weight, tumor number, and tumor size, and serum PRL concentrations when compared with these parameters in FF rats. Administration of EB to the HF rats partially prevented loss of mammary tumor size and significantly increased serum PRL levels over those of HF or FF control rats. Injection of HAL or the combination of HAL and EB completely prevented the decrease in mammary tumor number and size in the HF rats. These results suggest that regression in number and size of established mammary tumors in HF rats during a 3-week period is due primarily to a decrease in secretion of estrogen and PRL, the two hormones essential for mammary tumor growth in rats.

Animals↗
PubMed1983

Effects of alterations in early hormonal environment on development and hormone dependency of carcinogen-induced mammary tumors in rats.

The purpose of this study was to determine the early role of estrogen and prolactin on subsequent hormone dependency of carcinogen-induced mammary tumors. Virgin 57-day-old Sprague-Dawley rats were given i.v. injections of 7,12-dimethylbenz(a)anthracene (DMBA). One day prior to and 7 days after DMBA administration, the rats were divided into separate groups and given: a daily 0.1-ml s.c. injection of vehicle (controls); haloperidol (0.5 mg/kg) to increase prolactin secretion; estradiol benzoate (1 microgram/rat) to increase estrogen levels; bromocryptine (5 mg/kg) to inhibit prolactin release; tamoxifen (TAM, 20 micrograms/rat) to inhibit estrogen action; or the combination of TAM and bromocryptine. Drug and hormone treatments were terminated after 8 days. Sixteen weeks after DMBA administration, all animals were bilaterally ovariectomized, and 4 weeks later it was determined whether the mammary tumors were hormone dependent or independent. Treatment with TAM resulted in a significant reduction in incidence of mammary tumors, but also a 3-fold increase in the percentage of these tumors that showed hormone independence after ovariectomy as compared with that of control rats. Rats treated with the combination of TAM and bromocryptine also showed a significant reduction in tumor incidence and number, but a 5-fold greater percentage of hormone-independent tumors after ovariectomy. Rats given daily injections of haloperidol or estradiol benzoate showed only small differences in mammary tumor incidence or autonomy after ovariectomy, as compared with controls given injection vehicle alone. These results suggest that rats made deficient in estrogen and prolactin at the time of DMBA administration develop fewer tumors, but the tumors that develop are not dependent on these hormones for subsequent growth.

9,10-Dimethyl-1,2-benzanthracene↗
PubMed1982

Effects of monoaminergic and cholinergic drugs on release of follicle stimulating hormone from co-incubated pituitary glands and hypothalami.

1. Male rat pituitary glands and hypothalami were incubated with agonists and antagonists of various neurotransmitters, and release of follicle stimulating hormone (FSH) measured. 2. Noradrenaline and cholinergic agonists stimulated release of FSH, responses blocked by the alpha antagonist, phentolamine, and by atropine respectively. 3. Dopamine did not affect basal, but inhibited noradrenaline-stimulated, release of FSH. The dopamine antagonist, pimozide, stimulated release of FSH. 4. Neither serotonin nor its antagonist, methysergide, affected release of FSH. 5. None of these drugs acted directly on the pituitary gland, suggesting that they act by altering secretion of the gonadotrophin releasing hormone.

Animals↗
PubMed1982

L-dopa restores amplitude of growth hormone pulses in old male rats to that observed in young male rats.

35 male Sprague-Dawley rats, 18 months old, were injected subcutaneously with the catecholamine precursor, L-dihydroxyphenylalanine (L-dopa) (100 mg/kg, twice daily), or vehicle alone, for 8 days in an attempt to increase the amplitude of growth hormone (GH) pulses in old male rats. 40% of young rats had at least one GH pulse greater than 600 ng/ml, over a 6.5 h sampling period, whereas only 22% of old vehicle-treated rats had pulses of similar amplitude. Treatment of old rats with L-dopa increased the number of animals showing elevated GH pulses to 53%. Young animals had mean GH concentrations of 136.5 +/- 14.0 ng/ml over the 6.5 h sampling period, whereas vehicle-treated old animals had mean GH levels of 95.2 +/- 7.7 ng/ml (p less than 0.05). Treatment of old animals with L-dopa increased mean plasma GH concentrations to 132.9 +/- 11.2 ng/ml (p less than 0.05) which was not significantly different from GH values in young rats. Pituitary GH concentration was less in old than in young rats (301 +/- 27.4 vs. 370 +/- 17.4 micrograms/mg protein, p less than 0.05). L-Dopa increased pituitary GH concentrations in old rats to 318 +/- 32.2 micrograms/mg protein, which was not significantly different from that in either young or old vehicle-treated animals. Hypothalamic somatostatin content in both rostral and caudal areas was lower in old than in young rats (p less than 0.01), and L-dopa had no significant effect on somatostatin content. These data indicate that L-dopa can increase the amplitude of GH pulses and elevate mean plasma GH in old male rats to levels present in young male rats, probably by increasing hypothalamic catecholamines.

Age Factors↗
PubMed1982

Effects of morphine and naloxone on inhibition by ovarian hormones of pulsatile release of LH in ovariectomized rats.

The purpose of this study was to determine the effects of morphine and naloxone on pulsatile release of LH in ovariectomized rats treated (or untreated) with ovarian steroids. Ovariectomized rats were given a subcutaneous injection of estradiol benzoate (20 micrograms) or estradiol benzoate (20 micrograms) and progesterone (10 mg) 3 days prior to experimentation. The rats were then given intravenous injections of naloxone (2 mg/kg), morphine (5 mg/kg), or 0.87% NaCl every hour for 3 h. For LH assays, 0.3 ml blood was collected via an atrial cannula 15 min after drug treatment and every 15 min thereafter for 3 h. Pulsatile LH release was suppressed by estradiol benzoate or the combination of estradiol benzoate and progesterone. Naloxone was able to counteract inhibition of pulsatile LH release by these steroids. These results suggest that the endogenous opioid peptides are involved in the negative feedback exerted by estrogen and progesterone on pulsatile LH release. Morphine had no effect on steroid inhibition of pulsatile LH release.

Animals↗
PubMed1982

Counteraction of gonadal steroid inhibition of luteinizing hormone release by naloxone.

The effect of naloxone on the negative feedback action of gonadal steroids on luteinizing hormone (LH) release was studied in castrated male and female rats. The reduction by estradiol benzoate or testosterone propionate of elevated serum LH levels in rats ovariectomized for 4 weeks was reversed by a single injection of naloxone. Injection of estradiol benzoate, together with progesterone, similarly reduced serum LH levels in ovariectomized rats, and this inhibition was partially reversed by naloxone. A single injection of testosterone propionate decreased serum LH levels in male rats castrated 48 h earlier, and naloxone completely blocked the androgen-induced inhibition of LH secretion. Chronic administration of either testosterone propionate or morphine sulfate to castrated male rats prevented the postcastration rise of serum LH. The decrease of hypothalamic LHRH in castrated rats was completely blocked by testosterone propionate or morphine sulfate administration. These results are believed to indicate that hypothalamic opiates are involved in gonadal steroid feedback inhibition of LH release.

Animals↗
PubMed1982

Influence of underfeeding during the "critical period" or thereafter on carcinogen-induced mammary tumors in rats.

Normal cycling virgin female Sprague-Dawley rats were divided into different treatment groups and subjected to half ad libitum feed intake for 2 or 4 weeks at consecutive periods of time before and/or after administration of 7,12-dimethylbenz(a)anthracene (DMBA) and then were returned to full-feed. All rats at the end of their respective under-feeding periods showed reductions in serum prolactin and cessation of estrous cycles. However, only rats underfed 1 week prior to and 1 week after DMBA administration showed significant reductions in mammary tumorigenesis or the entire 21 weeks of the experiment when compared to full-feed controls. Rat groups underfed during subsequent weeks after DMBA administration showed no alterations in mammary tumor development as compared to full-fed controls. These results demonstrate that inhibition and perhaps permanent suppression of mammary tumorigenesis occurred only in rats underfed 1 week before and 1 week after DMBA administration. The inhibitory effects produced by this under-feeding regimen on mammary tumorigenesis may be mediated by suppression of prolactin and estrogen secretion.

9,10-Dimethyl-1,2-benzanthracene↗
PubMed1981

Immunoreactive beta-endorphin in the plasma, pituitary and hypothalamus of young and old male rats.

Immunoreactive beta-endorphin (IR-beta-ENDO) was measured in the plasma, pituitary, and hypothalamus of young (3-5 mo.) and old (19-23 mo.) male Sprague-Dawley rats, using a specific radioimmunoassay. Plasma IR-beta-ENDO in old male rats (3.44 +/- 0.54 ng/ml) was more than three times higher than values observed in young male rats (1.00 +/- 0.10 ng/ml). Pituitary content and concentration of IR-beta-ENDO also were significantly greater in the old (5.85 +/- 0.51 microgram/gland and 1.17 +/- 0.10 microgram/mg protein) than in the young (3.53 +/- 0.29 microgram/gland and 0.78 +/- 0.06 microgram/mg protein) male rats. The content of IR-beta-ENDO in the hypothalamus of old and young rats was nearly the same (43.45 +/- 2.47 and 49.88 +/- 6.35 ng/hypothalamus, respectively), whereas the concentration of IR-beta-ENDO in the hypothalamus of the old male rats (3.89 +/- 0.25 ng/mg protein) was approximately 50% lower than that observed in the young male rats (7,80 +/- 0.85 ng/mg protein). These changes in plasma, pituitary, and hypothalamic IR-beta-ENDO may contribute to the increase in prolactin and decrease in gonadotropins observed in old male rats, since beta-ENDO administration is known to produce these effects on prolactin and gonadotropin secretion.

Aging↗
PubMed1981

Effects of CNS active drugs and somatostatin antiserum on growth hormone release in young and old male rats.

The capacity of several potent pharmacological agents to increase growth hormone (GH) release was tested in young (3- to 4-month-old) and old (18- to 20-month-old) male Sprague-Dawley rats. Young and old animals were injected with alpha-methyl-p-tyrosine (250 mg/kg), a catecholamine synthesis inhibitor, followed 60 min later by the alpha-adrenergic receptor agonist, clonidine hydrochloride (150 micrograms/kg). Plasma GH levels increased to greater than 276 ng/ml by 30 and 50 min in young rats, whereas values never exceeded 130 ng/ml (p less than 0.01) in old rats. Piribedil methane sulfonate (1 mg/kg), a dopamine receptor agonist, significantly increased GH in young animals 60 min after injection (p less than 0.01), but had no effect in old rats. Morphine sulfate (5mg/kg) increased plasma GH concentration in young rats to greater than 400 ng/ml at 30, 50 and 70 min after injections, whereas values in old animals never exceeded 300 ng/ml (p less than 0.01). 15 min after injection of somatostatin antiserum No. 774 (5 ml/kg), plasma GH levels increased to greater than 750 ng/ml in both young and old rats. Administration of greater volumes of somatostatin antiserum (8 ml/kg) increased GH levels more in old than in young animals 30 and 45 min after injection (p less than 0.01). These results indicate that old male rats have less capacity to increase GH in response to agents that normally enhance GH release. This may be the result of a diminished number of affinity of post-synaptic neurotransmitter receptors, or to an increased release of somatostatin. Since somatostatin antiserum in creased H equally or to a greater extent on old that in young animals, aging rats may release more somatostatin or the pituitary may be more sensitive to the inhibitory effects of this hormone.

Aging↗
PubMed1981

Evidence for hypothalamic noradrenergic involvement in naloxone-induced stimulation of luteinizing hormone release.

A single injection of the opiate antagonist, naloxone (NAL), resulted in a fourfold increase in serum luteinizing hormone (LH) concentration 20 min after injection. To determine whether noradrenergic neurons were involved, male Sprague-Dawley rats were treated with alpha-methyl-p-tyrosine (alpha-MPT), phenoxybenzamine hydrochloride (PBH), or diethyldithiocarbamate (DDC), all anti-noradrenergic drugs. Reduction of hypothalamic norepinephrine synthesis by alpha-MPT or DDC, or blockade of the alpha-receptors by PBH, resulted in complete suppression of NAL-induced LH release. These results suggest that the NAL-induced increase in LH release is mediated in part via a hypothalamic noradrenergic mechanism.

Animals↗
PubMed1981

Comparison of acute effects of dynorphin and beta-endorphin on prolactin release in the rat.

The ability of dynorphin and beta h-endorphin (beta h-EP) to stimulate prolactin (PRL) release in male rats was examined. Rats were injected intraventricularly with either 1 or 10 microgram dynorphin, 1 or 10 microgram beta h-EP, 10 microgram dynorphin together with 20 microgram naloxone (NAL), or an equivalent volume (13 microliter) of saline. Dynorphin caused a dose-dependent release of PRL which was significant 10 min after injection but not at later sampling times. beta h-EP also increased serum PRL levels and maintained elevated PRL levels for at least 60 min. NAL, a specific opiate antagonist, completely blocked dynorphin-induced PRL release. These results indicate that dynorphin is a potent stimulator of PRL release, but its stimulatory activity is transient relative to the activity exhibited by beta h-EP. Furthermore, dynorphin's action is specific since NAL completely blocked dynorphin induced PRL release.

Animals↗