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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Studies were conducted to determine the effects of high levels of dietary silver nitrate and copper sulfate on the response of chicks to toxic levels of dietary selenium. Adding 5 ppm or more selenium to a basal stock diet significantly reduced growth rate, and 40 ppm or high significantly increased mortality during the 2-week experiments. Deitary silver or copper (1,000 ppm) counteracted the growth depression and prevented mortality at the higher levels of selenium. Hepatic selenium reached a maxiumum in chicks fed the basal diet with 10 ppm dietary selenium. Hepatic selenium of chicks fed silver was less than that of the control chicks when diets containing 10 ppm or less selenium were fed. Adding copper to the diet resulted in considerable accumulation of selenium in the liver, which was evident even at the lower levels of added selenium. Rseults of an experiment to determine the effects of deitray silver and copper on the distribution of 75-Se administered either orally or in tramusculary showed that silver interfered with absorption of selenium. The results of these experiments suggest that silver modifies selenium toxity both by interfering with selenium absorption and by causing the accumulation of a nondeleterious selenium compound in the tissues. Copper modifies selenium toxicity primarily by causing the accumulation of a nondeleterious compound in the tissues.
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PMID:Modification of a selenium toxicity in chicks by dietary silver and copper. 114 4

Copper IUDs, oral contraceptives, "morning-after' pills and injectables are discussed in general in this review. Small IUDs are less effective, but better tolerated. An exception is the Dalkon shield, which is no longer manufactured because several women died from latent infections when they became pregnant. The Copper T IUD is tolerated much better than the Copper 7, and has only a 3% failure rate. Copper Ts must be replaced every 2 years, however, and are difficult to remove. A beneficial effect of IUDs is cure of uterine adhesions; a subjective side effect if discomfort reported by husbands. Strict contraindications or oral contraceptives are history of cholostatic jaundice of pregnancy, thromboembolism, essential hypertension, tension, diabetes, gynecologic cancer and pregnancy. Relative contraindications are hyperthyroidism, hyperlipidemia, and depression. Depressions occuring soon after starting pills may be due to unconscious rejection; those appearing later may be due to the progestagen itself. The subjective sequelae of pills are more likely in maternal women, women raised to feel guilty for using contraception, women susceptible to believing sensational media reports about pills, and women dominated by their husband's views. Pills are beneficial for essential dysmenorrhea, menstrual irregularity, premenstrual syndrome, depression, frigidity due to fear of pregnancy, uterine hypotrophy, ovarian cyst, certain ovarian dystrophies such as Stein Levinthan syndrome, menopausal symptoms, acne and hirsutism. The morning after pill, 5 mg ethinyl estradiol for 3 consecutive days, is indicated only in exceptional cases such as rape. Injectables are more suitable for those who desire long-term contraception and whose who want no more children. A lower cancer rate has been reported for users of depot progestagens than for women notu sing contraception.
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PMID:[Subjective and objective aspects of modern methods of contraception]. 114 75

Subcutaneous injection of copper sulphate into the rat produced a significant depression in the relative and absolute uptake of oestradiol by the uterus. With progesterone, an enhancement in the absolute count uptake in the uterus, muscle, liver and kidney occurred. The absolute uptake of oestradiol in muscle, liver and kidney were also enhanced.
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PMID:Systemic copper and sex steroids uptake by rat tissues. 123 79

Zinc nutritional status was examined in 10 adult patients with biopsy-proven celiac disease; five of these patients were clinically well on gluten-free diets at the time of study. Plasma zinc and taste acuity were used as indices of zinc nutrition. Depression of plasma zinc and lowered taste discrimination were observed among the untreated patients, and some patients who were otherwise in clinical remission also had impaired zinc nutrition. With confirmation of plasma copper depression in patients with celiac sprue, these observations indicate that trace metal deficiency is another common nutritional complication of adult celiac disease.
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PMID:Zinc nutrition in celiac sprue. 126 87

Tissue and organ deposition and blood parameters were evaluated as indices of mineral and trace element absorption in rats. The absorption of elements was quantified in relation to nitrogen retention, i.e., considering the weight gain and new tissue synthesis. A rapeseed meal diet was supplied with three levels of calcium, two levels of zinc, and two levels of copper in a factorial design. In general, an increase in dietary mineral content increased the relative absorption, which in turn, increased the tissue deposition progressively. Striated muscle, however, did not respond to either an increased calcium or zinc supply. Furthermore, an increased calcium absorption caused a depression of the fractional phosphorus and magnesium content of femur bones. The copper content of the kidneys and the heart muscle was directly proportional to the amount of absorbed zinc and iron, respectively. The iron content of tissue was, in general, inversely proportional to zinc absorption and showed a tendency to be directly proportional to copper absorption. The zinc level in tissues was, in a similar way, inversely correlated to measured calcium absorption. In conclusion, interactions between elements do not only affect the intestinal element absorption, but also the distribution of already absorbed elements in tissues and organs.
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PMID:Tissues and organs as indicators of intestinal absorption of minerals and trace elements, evaluated in rats. 128 Sep 83

1. The M-like current IK(M,ng) in differentiated NG108-15 mouse neuroblastoma x rat glioma hybrid cells has been studied using tight-seal, whole-cell patch-clamp recording. 2. When calculated from steady-state current-voltage curves, the conductance underlying IK(M,ng) showed a Boltzmann dependence on voltage with half-activation voltage Vo = -44 mV (in 3 mM [K+]) and slope factor (a) = 8.1 mV/e-fold increase in conductance. In 12 mM [K+] Vo = -38 mV and a = 6.9 mV. The deactivation reciprocal time constant accelerated with hyperpolarization with slope factor 17 mV/e-fold voltage change. 3. The reversal potential for deactivation tail currents varied with external [K+] as if PNa/PK were 0.005. 4. Steady-state current was increased on removing external Ca2+. In the presence of external Ca2+, reactivation of IK(M, ng) after a hyperpolarizing step was delayed. This delay was preceded by an inward Ca2+ current, and coincided with an increase in intracellular [Ca2+] as measured with Indo-1 fluorescence. Elevation of intracellular [Ca2+] with caffeine also reduced IK(M, ng). 5. IK(M, ng) was inhibited by external divalent cations in decreasing order of potency (mM IC50 in parentheses): Zn2+ (0.011) greater than Cu2+ (0.018) greater than Cd2+ (0.070) greater than Ni2+ (0.44) greater than Ba2+ (0.47) greater than Fe2+ (0.69) greater than Mn2+ (0.86) greater than Co2+ (0.92) greater than Ca2+ (5.6) greater than Mg2+ (16) greater than Sr2+ (33). This was not secondary to inhibition of ICa since: (i) inhibition persisted in Ca(2+)-free solution; (ii) La3+ did not inhibit IK(M, ng) at concentrations which inhibited ICa; and (iii) organic Ca2+ channel blockers were ineffective. Inhibition comprised both depression of the maximum conductance and a positive shift of the activation curve. Addition of Ca2+ (10 microM free [Ca2+]) or Ba2+ (1 mM total [Ba2+]) to the pipette solution did not significantly change IK(M, ng). 6. IK(M, ng) was reduced by 9-amino-1,2,3,4-tetrahydroacridine (IC50 8 microM) and quinine (30 microM) but was insensitive to tetraethylammonium (IC50 greater than 30 mM), 4-aminopyridine (greater than 10 mM), apamin (greater than 3 microM) or dendrotoxin (greater than 100 nM). 7. IK(M, ng) was inhibited by bradykinin (1-10 microM) or angiotensin II (1-10 microM), but not by the following other receptor agonists: acetylcholine (10 mM), muscarine (10 microM), noradrenaline (100 microM), adrenaline (100 microM), dopamine (100 microM), histamine (100 microM), 5-hydroxytryptamine (10 microM), Met-enkephalin (1 microM), glycine (100 microM), gamma-aminobutyric acid (100 microM) or baclofen (500 microM).(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Kinetic and pharmacological properties of the M-current in rodent neuroblastoma x glioma hybrid cells. 140 9

Agonist challenged aortic prostacyclin production was examined in copper-adequate, -marginal and -deficient rats fed AIN-based diets providing 6.7, 1.7 and 0.8 micrograms Cu/g, respectively. Aortic rings were incubated in Krebs-Henseleit salts, 10 mmol/L HEPES buffer, pH 7.4, 95%:5% O2:CO2, 37 degrees C, and equilibrated for 1 h. Equilibrated rings were challenged with buffer (basal), 273.0 nmol/L thrombin and angiotensin II at 84.6 pmol/L and 846.0 pmol/L. Prostacyclin production, determined at 10 minutes by RIA as 6-keto prostaglandin F1 alpha, in basal and 84.6 pmol/L angiotensin II ring incubations was significantly reduced by 28 to 48% in copper-deficient rats. With thrombin or 846.0 pmol/L angiotensin II prostacyclin production was significantly reduced by 18 to 55% in copper-marginal and copper-deficient rats. Copper-dependent superoxide dismutase activity was significantly depressed by 30 and 57% in aortae of copper-marginal and copper-deficient rats. Lipid peroxidation, estimated by the thiobarbituric acid test, was significantly increased by 85% in copper-deficient rats, with a nonsignificant 40% increase in aortae from copper-marginal rats. The results suggest that the decreases in aortic prostacyclin production in aortae from both copper-deficient and copper-marginal rats are associated, in a dose-dependent manner, with copper-dependent superoxide dismutase depression and increases in aortic lipid peroxidation.
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PMID:Copper-marginal and copper-deficient diets decrease aortic prostacyclin production and copper-dependent superoxide dismutase activity, and increase aortic lipid peroxidation in rats. 143 51

Making use of a model pair Aedes aegypti--Plasmodium gallinaceum, the authors assess the susceptibility of mosquito female survivors to malaria agent after treatment of larvae with various bioactive substances. Eight binary combinations of 6 preparations have been tried: dimilin and uvemon, insect development regulators; fundosol and copper sulfate, fungicides; phytobacteriomicin (PBM), a larvicidal antibiotic; bactoculicide, a bacterial agent. Combinations of PBM with compounds differing by their mechanisms of action were found to inhibit the specific effect of PBM on the vector, PBM specific effect consisting in depression of mosquito susceptibility to P. gallinaceum. PBM combinations with some agents may alter other parameters of the vector potential: combinations of copper sulfate or uvemon with low concentrations of PBM potentiated the larvicidal effect, and PBM mixtures with fungicides reduces the activity of female attacks.
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PMID:[The susceptibility of mosquitoes for Plasmodium gallinaceum in the joint use of biologically active substances]. 143 76

The copper-deficient rat-trypanosome system was used to study copper deficiency in Sprague Dawley rats infected with Trypanosoma lewisi. Throughout the observational period, animals on the deficient diet had lower plasma and liver copper concentrations compared with complete and pair-fed animals. In all dietary groups, the food intake and body weight changes of rats inoculated with T lewisi showed significant increases over the noninoculated controls. The rate of these indices were significantly less in the copper-deficient animals compared with the animals fed complete diets. Copper-deficient and pair-fed control rats showed greater numbers of parasites than controls throughout the infection. The duration of the trypanosomal infection was longer in copper-deficient rats compared with other groups. In all of the dietary groups, severe depression in the primary and secondary antibody responses (IgM and IgG) to in vivo immunization with sheep erythrocytes was observed in infected animals over noninfected controls. The results of the present study indicate that during copper deficiency, there are significant changes in food consumption and body weight and enhanced susceptibility to infection as measured by an increased parasitemia and depression in the antibody responses.
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PMID:Interaction of nutrition and infection: effect of copper deficiency on resistance to Trypanosoma lewisi. 150 61

Lipid peroxidation may contribute to the nephrotoxicity of cephaloridine, a beta-lactam antibiotic. Copper and Se may protect against free radical damage, and dietary Se deficiency potentiates cephaloridine nephrotoxicity. The objectives of this study were to further investigate potentiation of cephaloridine toxicity by Se deficiency and to determine whether Cu deficiency increases cephaloridine-induced injury. Weanling male Sprague-Dawley rats were fed adequate, Cu-deficient, Se-deficient, and Se and Cu-deficient diets for 4 wk and subsequently injected i.p. with cephaloridine (1200 mg/kg body wt) or saline. Nephrotoxic response to cephaloridine occurred, with increased plasma urea, kidney weight, excretion of urinary enzymes, and kidney lesions. Cephaloridine also increased plasma sorbitol dehydrogenase activity. Selenium deficiency depressed kidney glutathione peroxidase activity (78%) and potentiated cephaloridine nephrotoxicity. Copper deficiency did not increase cephaloridine nephrotoxicity; the small depression (13%) in kidney Cu,Zn-superoxide dismutase activity may not have been sufficient to impair antioxidant status. However, the marked depression in kidney glutathione peroxidase activity during Se deficiency may have impaired antioxidant status and enhanced cephaloridine-induced injury. In contrast to results in the kidney, neither Se deficiency nor Cu deficiency potentiated cephaloridine hepatotoxicity, as assessed by plasma SDH activity.
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PMID:Cephaloridine nephrotoxicity is potentiated by selenium deficiency but not copper deficiency in rats. 158 39


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