Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In experiments on cats ammonium acetate (AA) injected intravenously (2--4 mM/kg body weight) depressed the process of primary afferent depolarization (PAD) which were thought to be responsible for presynaptic inhibition of spinal reflexes. PAD depression is reversible and proceeds in parallel to depression of postsynaptic inhibition of monosynaptic reflexes. The ammonium depression of PAD is not connected with the block of the negative postsynaptic potential recorded from the dorsal surface of the spinal cord or with the block of the reflex electrical discharges from the ventral roots. A conclusion was drawn that one of the possible mechanisms for convulsive action of AA consists in depression of presynaptic inhibition. It is supposed that the depression of PAD by AA results from the block of the chloride ion pump existing in primary afferent terminals. The block of the pump leads to abolition of the EMF for the outwardly directed transmembrane chloride current producing PAD.
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PMID:[Block of presynaptic inhibition of spinal cord reflexes by ammonium acetate]. 91 55

Several reports have indicated the mutagenicity of the cycasin aglycone, methyl azoxymethanol (MAM). Van Den Berg and Ball (1972) have demonstrated the inhibitory effects of MAM acetate (MAMac), a more stable form of the aglycone, on DNA synthesis and cell proliferation in HeLa cells. The purpose of this study was to observe the effects of MAMac on blastogenesis in the human short-term leucocyte culture system. A depression in blastogenesis by MAMac was observed cytologically derived from two individuals. The same effect was observed utilizing [3H] thymidine as an indicator of blastogenesis in a series of cultures from 11 male individuals exposed to varying doses of MAMac, ranging from 5 through 800 mug/ml.
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PMID:PHA response and methylazoxymethanol acetate. 95 33

Concentrations of serum follicle stimulating hormone (FSH), luteinizing hormone (LH), and progesterone (P) in pseudopregnant rats treated with medroxyprogesterone acetate (MPA) were measured to determine whether the increase in LH concentration seen is instrumental in the induction of the decrease in luteal progesterone secretion, which is associated with an increase in luteal 20alpha-hydroxyprogesterone secretion. Rats were treated with 1 or 10 mg MPA on the 3rd day of pseudopregnancy. FSH, LH, and P were determined on Days 2-20. Control animals had a 13.5 day mean for pseudopregnancy. Administration of 1 mg MPA sc resulted in a diestrous period of 21.4 days. Leukocytic vaginal smears were seen for 2 months when 10 mg MPA was given. FSH concentration was unaffected by the injection. P was similar for all 3 groups, with a slight depression seen in the high dose group from Day 4 to 8 of pseudopregnancy. In controls, LH decreased from Days 2 to 5 and then increased after Day 11. In animals treated at the low dose, this increase was delayed to Day 20 and it was absent in animals treated with 10 mg MPA. It is suggested that the increase in LH at the end of pseudopregnancy is initiated by the decrease in progesterone concentration.
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PMID:Serum follicle-stimulating hormone, luteinizing hormone and progesterone concentrations in pseudopregnant rats treated with medroxyprogesterone acetate. 97 5

Four weanling swine fed for 4 weeks a commercial ration adequate in selenium and vitamin E, but supplemented with 0.5% silver acetate, developed lesions typical of selenium-vitamin E deficiency. Clinically, the pigs fed this high level of silver had anorexia, diarrhea, and growth depression; 3 of 4 pigs died. At necropsy, hepatic lesions of hepatosis dietetica were present in 4 of 4 silver-fed pigs, and 1 of 4 pigs had cardiac and skeletal muscle lesions characteristic of selenium-vitamin E deficiency. Development of lesions and mortality was prevented in 2 pigs fed the silver diet supplemented with alpha-tocopherol (100 IU/kg of diet), but not in 2 pigs fed the ration supplemented with selenium as selenite (1 ppm). Four pigs fed a lower dose level of silver (0.2% silver acetate) for 6 weeks failed to develop clinical or pathologic features of selenium-vitamin E deficiency. However, hepatic selenium content was significantly increased in pigs fed the silver-supplemented ration.
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PMID:Induction of lesions of selenium-vitamin E deficiency in pigs fed silver. 99 68

The inverse relationship between blood lead concentration and aminolevulinic acid dehydrase (ALAD) is well known. Recently, it has been suggested that a similar relationship exists between carboxyhemoglobin (COHb) and ALAD activity. This study was undertaken to examine more closely the possible effect of carbon monoxide on ALAD. Blood from 19 human volunteers was analyzed for both carboxyhemoglobin and ALAD activity. Smokers had significantly lower concentrations of ALAD than nonsmokers and a rise in carboxyhemoglobin concentration was assocaited with a fall in ALAD activity. The in vitro bubbling of carbon monoxide into human blood did not significantly effect ALAD activity. Four groups of rats (10 per group) wre exposed to carbon monoxide or dietary lead acetate according to the following design: (I) Control--no Pb or CO; (II) 500 ppm Pb acetate in diet; (III) 250 ppm CO four hours/day X 5 days/week X 4 weeks; (IV) Both Pb and CO. Analysis of the rat data showed a significant depression of ALAD by lead. The activity of ALAD in the rats exposed to CO was significantly increased suggesting the possibility of an adaptive phenomenon.
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PMID:Experiments on the effect of carbon monoxide on aminolevulinic acid dehydrase (ALAD). 103 10

The anti-inflammatory activity and the other pharmacological properties of MS-1112, a new steroid compound, were examined and compared with other glucocorticoid analogues such as hydrocortisone acetate (Hydr), betamethasone 17-valerate (Val) and dexamethasone (Dexa). Systemically administered MS-1112 and glucocorticoids had a significant effect in inhibiting rat paw edema induced by various phlogistic stimulations and increasing vascular permeabilities and granuloma formation by cotton pellet or granuloma pouch. The order of those inhibiting activity was, in general, Dexa greater than MS-1112 greater than Val greater than Hydr. Concomitantly, Xthymolysis and adrenal weight suppression and reduced rate of body weight gain after multiple systemical administration were also observed. Locally administered MS-1112 caused an inhibiting activity, without systemic side-effects. This activity was approximately 3 to 5 times more potent than that of Dexa in rat carrageenin paw edema and cotton pellet granuloma. MS-1112 was less active than Dexa in glycogen liver deposition activity and in the depression of plasma level of corticosterone but more active than Val and Hydr. In the dose administered, MS-1112 had neither androgenic and anabolic nor estrogenic and anti-estrogenic activity. From this data, it concluded that MS-1112 is a very potent agent applicable regarding permeability and retention of steroids in a local site.
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PMID:[Pharmacological study of 9 alpha-fluoro-11 beta, 17, 21-trihydroxy-16 beta-methylpregna-1, 4-diene-3,20-dione-17-benzoate (betamethasone-17-benzoate, MS-1112), a local anti-inflammatory agent. (1). Its anti-inflammatory and other pharmacological properties]. 116 96

The potent skin tumor promoter (12-O-tetradecanoyl phorbol-13-acetate (TPA) stimulates epidermal macromolecular synthesis as well as proliferation, but little is known of specific functional aberrations produced by TPA. This report presents results of a study on the effects of TPA on epidermal histidase (L-histidine ammonia lyase), an enzyme found in normal epidermis but not in dermis or in mouse squamous cell carcinomas. Histidase activity was assayed on postmitochondrial supernatants obtained from hairless mouse epidermis after removal by keratotome. Topical TPA treatment at doses active in tumor promotion (1.7 to 17.0 nmoles/application) produced dose-dependent decreases in epidermal histidase specific activity at 19 hr posttreatment. The onset of the decrease occurred at 12 hr with recovery to control level specific activity by 5 days, showing kinetics similar to those obtained for stimulation of DNA synthesis. This decrease in histidase could not be attributed to a general inhibition of soluble protein synthesis or to the appearance of an inhibitor of histidase activity. The strong promoter TPA produced a greater histidase decrease than did the moderate promoter and mitogen 12,13-didecanoyl phorbol at equimolar dose, while phorbol, a nonpromoter and nonmitogen, produced no effects on histidase. The relationship of this histidase depression to tumor promotion and not initiation is further indicated by the finding that (a) Tween 60, a structurally unrelated tumor promotor, also produced a decrease in histidase; and (b) the tumor initiator urethan and an initiating dose of 9,10-dimethybenz(a)anthracene showed no effects on histadase activity.
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PMID:Decrease of epidermal histidase activity by tumor-promoting phorbol esters. 118 5

Five experiments were conducted involving both juvenile and adult Bobwhite quail (Colinus virginianus) to study the toxicity of lead acetate, lead shot, powdered lead and antimony. Performance of juvenile birds receiving up to 1,500 p.p.m. of lead as lead acetate was not significantly influenced during the six-week experimental period. Feeding 3,000 p.p.m. lead as lead acetate was not significantly influenced during the six-week experimental period. Feeding 3,000 p.p.m. lead as lead acetate was associated with a significant depression of body weight and an increase in mortality. Feeding growing quail up to 2,000 p.p.m. lead from either lead acetate or powdered lead, 3 or 6% antimony (as % of shot dosage or 5 lead shot per week caused no significant effects upon either body weight or mortality. No significant trends were noted in body weight, feed intake, semen quality or organ weight of adult quail that received up to 1,500 p.p.m. lead from lead acetate. Dosing adult Bobwhite quail cocks with 10 or more lead shot per week caused a significant increase in nortality, and more than 90% of those dosed with 30 shot per week died by the end of four weeks.
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PMID:Lead toxicity of bobwhite quail. 119 3

A marked increase in preglomerular resistance mediated through the renin-angiotensin system has been proposed as the mechanism for the sustained decrease in glomerular filtration rate seen following release of 24-hour ureteral obstruction. The importance of the renin-angiotensin system in mediating this response was evaluated by determining whole kidney and single nephron function following release of 24-hour ureteral obstruction in rats with normal renal renin content and in rats depleted of renal renin by desoxycorticosterone acetate acetate (DOCA) and saline treatment. The DOCA and saline treatment was effective in reducing renal renin content to less than 10% of the normal values. However, when compared to nonobstructed kidneys, both whole kidney filtration rate and single nephron filtration rate were similarly and significantly reduced in both groups following release of 24-hour ureteral obstruction. Single nephron stopflow techniques were used to determine the net hydrostatic force for filtration. The net hydrostatic force for filtration in control nonobstructed nephrons averaged 37.8 +/- 1.1 mm. Hg, but was significantly decreased to 22.5 +/- 2.2 mm. Hg in the normal renin obstructed kidney and to 18.8 +/- 1.0 mm. Hg in the renin-depleted obstructed kidney. It is concluded that the marked depression in glomerular filtration rate seen following release of 24-hour ureteral obstruction is due to increased afferent arteriole resistance and that the renin-angiotensin system is apparently not important in mediating the response.
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PMID:Influence of renin depletion on renal function after release of 24-hour ureteral obstruction. 124 84

The effects of methylazoxymethanol (MAM) acetate on colony survival, cell proliferation and DNA synthesis of murine lymphoma L5178Y cells are studied. Decreased sensitivity and immediate depression of cell proliferation and DNA synthesis were found in L5178Y cells in contrast to the reports on HeLa cells. Pre-labelling with 5-bromodeoxyuridine (BUdR) did not enhance significantly the carcinogen-induced cell lethality. Post-treatment with caffeine greatly enhanced cell lethality and depression of cell proliferation. These effects of caffeine were diminished when the cells had passed through two generations following the MAM acetate treatment. Experiments with synchronized cells showed that the action of caffeine was located primarily in S phase following the MAM acetate-treatment. These results strongly suggest that in L5178Y cells, MAM acetate induces damage, which is repaired by a mechanism analogous to post-replication repair of UV light-induced damage.
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PMID:Evidence for caffeine-sensitive damage in methylazoxymethanol acetate-treated L5178Y cells. 124 56


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