Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0847097 (acidity)
 15,165 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Highly purified growth hormone (GH) has been isolated from Atlantic salmon (Salmo salar) pituitaries by extraction with acid acetone, acidic precipitation, and reversed-phase high-performance liquid chromatography (HPLC). The yield was 2.5 mg/g wet tissue. The Atlantic salmon GH (sGH) emerged as a single symmetrical peak after HPLC on a reverse phase C18 column. SDS-gel electrophoresis revealed only one band with an estimated molecular weight of 23,000. Atlantic sGH showed a uniform molecular weight, but two-dimensional (2D) gel electrophoresis of the purified sGH revealed charge heterogeneity with pI's ranging from 6.5 to 8.2. Treatment of the purified sGH with alkaline phosphatase concentrated these different forms into a single more alkaline position (pI 8.2) indicating removal of acidic groups. These results were documented using both silver- and immunostaining of the 2D SDS gels. The purified sGH was phosphorylated in vitro by a calmodulin-dependent protein kinase. Phosphorylation of sGH may be a post-translational modification resulting in several molecular forms with variable acidity. Analysis of the amino acid composition of Atlantic sGH revealed homology with GHs isolated from other teleost species and the amino-terminal sequence showed only three different amino acids within the first 25 residues compared to GH isolated from chum salmon (Oncorhynchus keta) and coho salmon (Oncorhynchus kisutch) pituitaries. Atlantic sGH had a methionine as the amino-terminal residue. Antibodies against chum sGH cross-reacted with Atlantic sGH. Antibodies against either Atlantic or chinook (Oncorhynchus tschawytscha) salmon prolactin or human GH did not cross-react with Atlantic sGH. Atlantic sGH was shown to have a slight growth-promoting activity in the rat tibia assay.
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PMID:Purification and characterization of Atlantic salmon growth hormone and evidence for charge heterogeneity. 228 75

The potency and duration of action of a single dose of etintidine, ranitidine and cimetidine were compared in placebo-controlled studies. In addition, the effect of a single night-time dose of etintidine (600 mg) on gastric acid secretion and basal hormone levels was assessed before, during and after a 28-day treatment. Nocturnal gastric acidity (23.00-07.00) was inhibited from 41.04 +/- 5.0 mmol/l to 12.9 +/- 2.8 mmol/l by 300 mg etintidine, to 6.50 +/- 2.5 mmol/l by 600 mg etintidine and to 8.58 +/- 2.5 mmol/l by 800 mg cimetidine nocte. Etintidine and cimetidine did not reduce H+-concentrations during the following day. Pentagastrin-stimulated acid output was virtually not affected after 600 mg etintidine and 800 mg cimetidine as well. By contrast, stimulated acid secretion was still suppressed by about 50% following 300 mg ranitidine. Basal levels of testosterone, prolactin etc. remained unchanged by 28-day etintidine (600 mg dose at night) treatment. Clinical studies are needed to examine the place of the single dose of etintidine (600 mg) at night for the short-term treatment of duodenal ulcer.
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PMID:[Single evening administration of etintidine in the human: effect on acid secretion and behavior of important hormones]. 286 53

Hormonal contraceptives, most of which contain norethindrone and norethynodrel combined with estrogen, maintain the body in a state of "artificial pregnancy" and can cause hormonal, vascular, metabolic, and neurolgic side effects similar to the effects seen in pregnancy. Many of these involve the skin. Herpes gestationis is a herpetiform dermatitis with vesicular and bullous eruptions which is triggered by high levels of progesterone and prolactin. Melasma, a dark brown hyperpigmentation, is frequently seen in women taking oral contraceptives. Progesterone activity changes the biochemistry and pH of the skin and sebacious glands, thereby contributing to eruptions of acne vulgaris. Contraceptive pills have been found to increase the incidence of genital candidiasis. Withdrawal from contraceptive pills is often associated with alopecia. Estrogenic substances increase the sensitivity of the skin to light and induce telangiectasia. Oral contraceptives, as well as many other drugs, have been associated with erythema nodosum. Creams, foams, jellies, diaphragms, pessaries and Nonoxynol-9 cause a phenomenon similar to contact dermatitis but with deeper ulcerations due to the acidity of the iritant chemicals.
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PMID:Pharmaceutical effect of contraceptive pills on the skin. 297 37

Differently charged isomers of human pituitary prolactin were subjected to stability studies under various conditions. The study was guided by analytical electrophoresis and radioimmunoassay. In alkaline medium (pH 10) it was found that each isohormone was converted into faster-migrating components, probably due to deamidation. A quantitative study of this alteration was made by measuring the rate constant for this conversion assuming first-order kinetics. The result indicated that the rate constant decreased with increased acidity of the examined prolactin components. Furthermore, this alteration was also found to be paralleled by a decreased immunoactivity of the components. At neutral pH the conversion reaction was studied both in 0.9% NaCl and in human serum. For the least acidic isohormone the rate constant in serum was calculated to be about four times higher than that in the saline solution which in turn was comparatively low. It was concluded that the alteration observed at pH 10 might be attributed to non-enzymic deamidation. The conversion of prolactin that occurred in human serum indicated that this reaction could be caused by enzymes. A study of the immunoactivity of human prolactin as a function of time at various storage conditions is also included in this work. The stability of the hormone was found to be strictly concentration dependent and also affected by buffer ionic strength. In the presence of ethylene glycol (50%, v/v) at -20 degrees C and at a protein concentration in the range of 0.1-2 mg/ml the hormone was found to be both immunologically and electrophoretically stable for several years.
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PMID:Stability studies on human pituitary prolactin. 409 22

In each of 7 healthy volunteers, the new furan H2-antagonist ranitidine (0.125, 0.25, 0.5, and 1.0 mg . kg-1 . hr-1) or the imidazole derivative cimetidine or normal saline were intravenously infused in the midhour of a 3-hr pentagastrin period (1.5 micrograms . kg-1 . hr-1 i.v.). With increasing doses of ranitidine, gastric acid secretion dropped dose dependently: 62, 78, 89, and 94%, respectively (P < 0.05 for all doses). A cimetidine dose of 0.82 mg . kg-1 . hr-1 (2.8 mumol . kg-1 . hr-1), equivalent to the highest ranitidine dose, led to a similar reduction of acid output (54%) as an eightfold smaller ranitidine dose. Apparently in human gastric mucosa, recognition of H2-receptors is not exclusively determined by the imidazole ring. Strong inhibitory efficacy of ranitidine was also reflected by the low calculated mean ID50 of 54 micrograms (0.15 mumol) . kg-1 . hr-1 and the IC50 of 36 ng/ml (0.1 microM). Acid inhibition by ranitidine involved both reduction in volume and acidity. The lowering effect on pepsin output was less pronounced though significant. Secretion of free N-acetylneuraminic acid and N-acetylneuraminic acid bound to glycoproteins did not change after H2-blocker administration indicating an unimpaired mucus secretion. In these short-term experiments, there were no obvious side effects or alterations in routine laboratory parameters including serum gastrin and prolactin attributable to either drug.
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PMID:Furan H2-antagonist ranitidine inhibits pentagastrin-stimulated gastric secretion stronger than cimetidine. 610 79

Gastric acid secretion was measured in six healthy volunteers following the intravenous administration (over 30 min.) of oxmetidine 200 mg, 400 mg and 800 mg in a randomized double blind trial for 12 hours. Gastric aspirates were fractionated into hourly aliquots and pH, volume, gastric acidity and gastric acid output were determined. Total gastric acid output over 12 hours was significantly reduced from 24.4 mmol/12 h (median) after placebo to 13.5 mmol/12 h, 11.8 mmol/12 h and 7.7 mmol/12 h after oxmetidine 200 mg, 400 mg and 800 mg respectively. An inhibition of at least 90% was achieved with all doses of oxmetidine and this lasted dose-dependently for 4 to 6 hours. A rise in pH to greater than 5 occurred during the 2nd or 3rd hour after dosing which lasted for 2-5 hours depending on the dose administered. Mean hourly pH was dose-dependently significantly higher for 4-6 hours following oxmetidine treatment than after placebo. A significant reduction in gastric acidity after oxmetidine infusion was also observed while the reduction in volume output calculated for 12 hours was not statistically significant. No significant rises in serum gastrin levels were observed with the oxmetidine doses used. Three out of the six subjects tested showed an increase in serum prolactin levels in response to the highest dose of oxmetidine but this was not statistically significant. The results of the present study have shown that the administration of 400 mg oxmetidine did not cause a longer pH elevation greater than 5 than 200 mg, while with 800 mg side effects were observed in one of the six subjects studied.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of three single doses of oxmetidine administered intravenously on the volume and acidity of gastric secretion, serum prolactin and gastrin concentration in healthy volunteers. 614 51

The potency and duration of a single dose of ranitidine and famotidine were compared in placebo-controlled studies. In addition, the effect of a single night-time dose of famotidine (40 mg) on gastric acid secretion and basal hormone levels was assessed before, during and after a 28-day treatment. Basal acid secretion was depressed by about 73% and 76% 12 hours after 300 mg ranitidine and 40 mg famotidine respectively. Pentagastrin-stimulated acid output was reduced by about 26% and 29%. 20 hours after both drugs, basal secretion was still inhibited by about 60%, whereas no effect on stimulated acid secretion could be detected. Nocturnal gastric acidity (23.00-07.00) was inhibited from 35.8 +/- 4.6 mmol/l to 1.8 +/- 0.5 mmol/l (94% inhibition) by 40 mg bedtime famotidine , and to 1.7 +/- 0.5 mmol/l (95% inhibition) by 300 mg ranitidine. Both drugs significantly reduced H+ concentrations during the following day. On day 29, i.e. 12 hours after the last famotidine dose, basal and stimulated acid secretion was reduced by some 50% and 26% respectively. On day 35, gastric acid output had returned to pretreatment values. Basal levels of prolactin, testosterone etc. were unchanged by 28-day famotidine treatment. Rantidine and famotidine may therefore be used as a single night-time dose in the acute treatment of peptic ulcer disease.
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PMID:[Human acid secretion during daily administration of H2-blockers]. 633 Aug 86

A method has been described for the isolation of three differently charged isohormones of rat prolactin from a discard fraction obtained after extraction of gonadotropins, thyrotropin and growth hormone from homogenized frozen pituitaries. The procedure involved extraction at pH 9.8, ammonium sulphate fractionation, molecular sieve chromatography on Sephadex G-100, and column electrophoresis in agarose suspension. The purification was monitored by radioimmunoassays and the recovered components were all found to possess a specific immunoactivity exceeding that of the standard preparation (RP-1) supplied by the NIAMDD, Bethesda, U.S.A. Increased acidity among these isohormones was found to be paralleled by significantly decreased immunopotency. Each component showed biological activity in radioreceptor assay. A high degree of purity of the isolated components was shown by analytical electrophoresis in polyacrylamide gel. Sodium dodecyl sulphate electrophoresis in the same medium showed no size heterogeneity and yielded a value of approximately 25 000 for the molecular weight of the isohormones. In addition a large form of prolactin, suggested to represent a dimer, was isolated by a further extraction step (pH 10.5) followed by molecular sieve chromatography on Sephadex G-100 and electrophoresis in agarose suspension. The large form was associated with both biopotency and immunopotency. The electrophoresis resolved the prolactin activity into three or four immunoactive components. This pleomorphism of the large prolactin was confirmed by analytical polyacrylamide gel electrophoresis. Amino acid analyses revealed a close similarity between the three monomers and the major dimeric form of the hormone.
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PMID:Isolation of rat pituitary prolactin isohormones differing in charge, size, and specific immunological activity. 712 24

The biological activity and immunoreactivity of serum prolactin (PRL) has been shown to fluctuate throughout the estrous cycle of the rat. Since the 24-kDa nonphosphorylated and phosphorylated isoforms from several species have also been shown to differ in their biological and immunoreactivities, we have investigated the possibility that the 24-kDa monomer isoform profile varied throughout the estrous cycle of the rat. The PRL isoform profile was assessed in homogenates of pituitaries and in short-term incubation media. Comparisons between homogenates, which always contained isoforms 1, 2, 3, and 3' (numbered according to increasing acidity), and media showed nonproportional release of the isoforms at all stages. Of great interest were the release of isoform 1 (a nonphosphorylated form) only at estrus and the lack of release of isoform 3' (a phosphorylated form) only in the afternoon of proestrus. This lack of release of 3' was accompanied by a marked increase in the release of isoform 2 (the unmodified polypeptide). These results suggest a unique function for isoform 1 during estrus and a role for increased isoform 2 and absent isoform 3' during the proestrus surge of PRL. Moreover, they suggest that fluctuations in the biological activity and immunoreactivity of serum PRL during the estrous cycle could be due, at least in part, to fluctuations in the isoform profile.
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PMID:Secretion of specific nonphosphorylated and phosphorylated rat prolactin isoforms at different stages of the estrous cycle. 826 62

The effect of centrally administered prolactin on gastric acid secretion and experimentally-induced gastric and duodenal ulcers was studied. The acute gastric ulcer models used were pylorus ligation, indomethacin-induced and ethanol-induced gastric ulcers. Chronic gastric ulcers were induced using acetic acid and duodenal ulcers by cysteamine hydrochloride. In pylorus ligated rats, prolactin (1 microg/kg icv) produced 45% increase in gastric content volume, significant increase in free acidity (P < 0.001), total acidity (P < 0.001) and ulcer index (P < 0.001). It did not show any significant effect on ethanol-induced and indomethacin-induced gastric ulcers. Prolactin increased the ulcer index (P < 0.001) and ulcer score (P < 0.05) in acetic acid-induced chronic gastric ulcers. It also increased ulcer area (P < 0.05) in cysteamine-induced duodenal ulcers. Therefore, the proulcerogenic activity of prolactin was due to its gastric hypersecretory effect.
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PMID:Effect of centrally administered prolactin on gastric and duodenal ulcers in rats. 1146 28


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