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)

Previous work showed that dietary lead (Pb) increases the relative concentration of arachidonic acid (20:4) as a percentage of total fatty acids, and decreases the relative proportion of linoleic acid (18:2) to arachidonic acid (18:2/20:4) in chick liver, serum, and erythrocyte membranes. The present investigation was undertaken to examine the time-course and magnitude of the fatty acid alterations with increasing dietary Pb levels. We also examined the effects of Pb on the fatty acid composition and lipid peroxide content of hepatic subcellular organelles. In Exp. 1, chicks were fed diets containing 0, 62.5, 125, 250, 500, or 1000 ppm added Pb (as Pb acetate trihydrate) from 1 to 21 d of age. After 21 d, no growth effects were observed; however, Pb lowered the 18:2/20:4 ratio and increased 20:4 concentration in total liver and serum lipids, and in total hepatic phospholipids in a dose-dependent manner. Hepatic mitochondrial membrane fatty acids were not altered, nor was there any increase in hepatic lipid peroxidation. In Exp.2, chicks were fed diets containing 0, 500, 1000, or 2000 ppm added Pb from 1 to 21 or 22 d of age. Pb depressed growth in a dose-dependent manner. In addition, Pb lowered the 18:2/20:4 ratio and increased 20:4 concentration in total liver lipids and in hepatic mitochondrial and microsomal membranes in a dose-dependent manner. Total hepatic lipid peroxidation was increased over control values by 1000 ppm Pb, and hepatic microsomal lipid peroxidation was increased by dietary Pb levels of 1000 and 2000 ppm. In Exp. 3, body weight, hepatic microsomal lipid peroxidation, and fatty acid composition were determined in 4-, 9-, 14-, 18-, and 23-d-old chicks fed 0 or 1500 ppm added Pb. Body weights of Pb-treated chicks were significantly lower than those of control chicks by day 18. Microsomal 20:4 concentration and peroxidation increased, and the 18:2/20:4 ratio decreased with age in both groups, but the changes were of greater magnitude in the Pb-treated chicks. The results suggest that some of the manifestations of Pb toxicity may be a reflection of increased concentration of 20:4 in specific membranes. Further, since the Pb-induced alterations in fatty acid composition were noted in the absence of any growth depression, we propose that fatty acid composition is more sensitive than growth rate to the presence of lead in the diet.
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PMID:Lead-induced tissue fatty acid alterations and lipid peroxidation. 170 34

Two experiments were conducted with day-old broiler chicks reared to 18 or 19 d of age. The objectives were: (1) to examine the effects of the antioxidant ethoxyquin (EQ) on peroxidation in feeds containing fish oil (FO) or lead (Pb), and (2) to determine whether systemic effects of Pb, which are attributed to tissue peroxidation, can be reversed by dietary EQ. Experiment 1 was a 2 x 2 factorial arrangement with the factors being 4% dietary cottonseed oil (CSO) vs FO and dietary Pb as lead acetate trihydrate (0 vs 1000 ppm). Feed was mixed 1 d prior to initiation of the experiment and stored at 4 degrees C until it was placed in the feeders. Experiment 2 was a 2 x 2 x 2 factorial arrangement with the factors being 3.5% dietary oil (CSO vs FO), dietary Pb (0 vs 1000 ppm), and EQ (0 vs 75 ppm). Feed was mixed 1 d prior to initiation of the experiment and held at room temperature thereafter. Growth depression by FO and Pb was less pronounced in Experiment 1 than in Experiment 2. In Experiment 2, FO and Pb increased the concentration of feed peroxide, and the increases were prevented by EQ. The growth depression by FO was completely reversed by EQ. EQ reversal of Pb-induced growth depression, although substantial, was not complete. The FO diet without Pb had a peroxide content (12.4 meq/kg feed) similar to the CSO + Pb diet (12.3 meq/kg feed); however, growth was not similar (407 vs 213 g body weight at 19 d, respectively). The results suggest that the toxic effects of Pb are mediated by peroxidative alterations both in the feed and in tissues. The ability of EQ to reverse significantly Pb effects on growth suggests a systemic action of this antioxidant.
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PMID:Interactions of dietary lead with fish oil and antioxidant in chicks. 172 12

Cardiopulmonary bypass is known to cause neutrophil activation, and activated neutrophils appear to be of importance in myocardial reperfusion injury. This study examined the effect of a preischemic infusion of activated neutrophils on the recovery of myocardial function after 40 minutes of hypothermic global ischemia. Studies were carried out in three groups of Langendorff-perfused rabbit hearts: control, control (unactivated) neutrophil infusion, and phorbol myristate acetate-activated neutrophil infusion. The activated neutrophil group showed significant deterioration in function during the activated neutrophil infusion. All three groups demonstrated significant depression of function initially after reperfusion, but the two control groups subsequently recovered to baseline levels. The activated neutrophil group, however, showed a persistent significant depression in ventricular force, rate of ventricular tension development, and rate of ventricular relaxation as well as a significant increase in coronary vascular resistance. It is concluded that activated neutrophils depress myocardial function and contribute to impaired recovery of function after global hypothermic ischemia.
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PMID:Activated neutrophils impair rabbit heart recovery after hypothermic global ischemia. 173 63

A volatile anesthetic-gated current was characterized in patch-clamped cultured postnatal rat hippocampal neurons. In this preparation, the major volatile anesthetics, isoflurane, halothane, and enflurane, open an anion-selective conductance. This volatile anesthetic-gated current exhibits anion selectivity with a chloride-to-acetate permeability ratio of 15, shows outward rectification well described by the constant field equation, and is activated in a dose-dependent fashion with half-maximal response to isoflurane at 0.8 mM (0.032 atm). The current persists in the absence of external Ca2+ and is not blocked by strychnine, a glycine antagonist. However, the gamma-aminobutyric acidA (GABAA) antagonists, bicuculline and picrotoxinin, and the nonspecific anion channel blocker, 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid (DIDS), completely block the response. These observations suggest that volatile anesthetics, like several other general anesthetics such as barbiturates, steroids, and etomidate, have a GABA-mimetic effect on vertebrate central neurons in culture. It is not clear whether this GABAA-gating property is a prerequisite for all general anesthetics. However, under normal physiological conditions of low intracellular Cl-, it is likely that drugs with both direct GABA agonist and GABA modulatory properties will produce overall depression of the central nervous system by increasing the normal inhibitory synaptic influence and by directly hyperpolarizing neurons.
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PMID:Volatile anesthetics gate a chloride current in postnatal rat hippocampal neurons. 174 Feb 40

Our previous studies have shown that a phagocytic challenge with IgG-coated erythrocytes (EIgG) depressed macrophage triggered H2O2 production in vitro, and in vivo there was a decrease in the survival rate following bacteremia. The phagocytosis of an equal number of IgG-coated erythrocyte ghosts had none of these effects, indicating that the contents of the erythrocytes are important for these effects. The present study evaluated the role of the scavengers of reactive oxygen intermediates within erythrocytes in the depression of H2O2 production triggered with phorbol myristate acetate following a phagocytic challenge with EIgG. Elicited rat peritoneal macrophages (PM) were challenged with EIgG prepared from normal E or E with inactivated catalase, depleted glutathione, hemoglobin converted to methemoglobin, or fixed with formaldehyde. The depression of triggered H2O2 production was similar when equal numbers of normal EIgG and EIgG with inactivated scavengers were phagocytized. When the phagocytic challenge with normal EIgG was carried out in the presence of cytochalasin B, no depression of triggered H2O2 production was observed. Cytochalasin B partially blocked the phagocytosis of EIgG, so that with larger doses of EIgG there was sufficient ingestion of EIgG to depress H2O2 production in untreated PM. These results indicate that the scavengers of reactive oxygen intermediates present in erythrocytes are neither required nor sufficient to depress H2O2 production by macrophages.
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PMID:Scavengers of reactive oxygen intermediates do not mediate the depression of macrophage hydrogen peroxide production caused by erythrocyte phagocytosis. 175 28

The purpose of this study was to determine if exogenous insulin-like growth factor-I (IGF-I) would improve growth rate or body composition of young broiler chickens. Broiler cockerels were given a daily intramuscular (im) injection of sodium acetate buffer (buffer control), 100 or 200 micrograms recombinant-derived human IGF-I (rhIGF-I) per kg body weight from 11 to 24 days of age. Exogenous IGF-I did not affect the average daily gain, average daily feed consumption, or the gain-to-feed ratio of broiler chickens. Although daily injection of 200 micrograms/kg of rhIGF-I reduced (P less than 0.05) body ash content, there was no significant effect of IGF-I treatment on either body fat or protein content. Plasma GH levels were depressed (P less than 0.05) by chronic treatment with rhIGF-I. In contrast, plasma levels of T3 and T4 were not affected by rhIGF-I treatment. The half-life of rhIGF-I in plasma was determined at 25 days of age in naive control or chronically-injected chickens after a single intravenous dose of 50 micrograms rhIGF-I/kg. We found a single compartment, first-order disappearance pattern of rhIGF-I from chicken plasma. The half-life (t1/2) of rhIGF-I in plasma was similar (t1/2 = 32.5 min) for naive controls (injected once) or chronically-treated chickens which had received a daily injection of rhIGF-I (100 or 200 micrograms/kg) for 14 d. These data indicate that daily injection of IGF-I cannot be used to enhance growth performance or body composition of broiler chickens when given during the early growth period. The depression of plasma GH levels in rhIGF-I-injected chickens supports a negative-feedback role of IGF-I on pituitary GH secretion.
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PMID:Response of young broiler chickens to chronic injection of recombinant-derived human insulin-like growth factor-I. 178 8

Leuprorelin (leuprolide, D-Leu6-(des-Gly10-NH2)-LH-RH ethylamide) acetate is a super-active agonist of luteinizing hormone-releasing hormone (LH-RH). We developed once-a-month injectable microcapsules of this agonist by our novel in-water drying method. This depot formulation can release the drug at an apparent zero-order rate over one month with bioerosion of copoly (lactic/glycolic acid) utilized as a wall material of the polycore microcapsules. A dramatic prolonged depression of pituitary-gonadal axis, chemical castration, was achieved by the once-a-month injection in experimental animals; it expects a reliable efficacy for treating hormone-dependent prostatic, breast cancers and endometriosis. Studies on the dosage design of this new delivery system of leuprorelin are summarized.
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PMID:[Once-a-month injectable microcapsules of leuprorelin acetate]. 179 29

The aim of this study was to evaluate the anti-ischemic efficacy of 2 different doses of benazepril (B), a new ACE-inhibitor, 10 and 20 mg, given per os. Fifteen male patients gave informed, written consent; they were aged 40-67 years, with stable effort angina pectoris and were randomly given, in double-blind condition, a tablet containing B 10 mg, B 20 mg or placebo (PL), once a day, according to a 3 x 3 latin square design. Bicycle exercise tests were performed on the same day, 2 and 10 hours after the last drug intake. B 10 mg and B 20 mg, in patients with stable effort angina, compared to placebo, increased ischemic threshold and decreased ischemic ST depression at maximal work, after 2 hours but not after 10 hours. In conclusion B 10 mg and B 20 mg showed anti-ischemic activity 2 hours after drug intake.
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PMID:[Effects of benazepril, a new ACE inhibitor, in effort angina pectoris]. 179 89

1. Bradykinin (cumulative concentrations of 0.007-0.09 micrograms ml-1) produced a dose-related, but statistically insignificant depression of the isometric contraction of the isolated, spontaneously beating atria of the guinea-pig. The same concentrations of bradykinin did not change the atrial rate, but a tendency to a slight decrease was observed. 2. Enalapril (4.06 or 13.54 mumol l-1), produced a dose-related potentiation of the effect of the highest concentration of bradykinin on the isometric contraction. 3. Captopril (equimolar concentrations) also potentiated the effect of the highest concentration of bradykinin on the isometric contraction. This effect of captopril was not dose-related. 4. Both enalapril and captopril did not change the effect of bradykinin on the heart rate. 5. Bradykinin induced dose-related hypotensive responses in anaesthetized cats (0.03-1.0 microgram/kg b.w., i.v.) with a tendency towards bradycardia. 6. Enalapril (0.3 and 1.0 mg/kg b.w., i.v.) significantly potentiated bradykinin-induced hypotension and bradycardia. However, the potentiating effect of enalapril was not dose-dependent. 7. Captopril (0.1, 0.3 and 1.0 mg/kg b.w., i.v.) significantly potentiated bradykinin-induced hypotension and bradycardia. Also, the potentiating effect of captopril was not dose-dependent. 8. The failure of ACE inhibitors to potentiate the cardiodepressant and hypotensive effects of bradykinin in a dose-dependent manner is explained with some other mechanism(s) independent of ACE inhibition.
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PMID:The potentiation of cardiodepressant and hypotensive effects of bradykinin by enalapril and captopril both in vitro and in vivo. 181 Aug 15

We reviewed the records of 42 patients with Wilson's disease participating in a zinc acetate treatment protocol and interviewed 17 of them. Five of the patients studied were asymptomatic. A significant number of symptomatic patients (64.8%) reported psychiatric symptoms at the time of initial presentation. These symptoms were severe enough to warrant psychiatric intervention in almost half of all symptomatic patients before the diagnosis of Wilson's disease was made. Personality changes, particularly irritability and aggression, were most commonly described (45.9%), followed by depression (27%). Cognitive changes, anxiety, psychosis, and catatonia, while less frequent, also occurred. These data underscore the need to include Wilson's disease in the differential diagnosis of psychiatric disorders.
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PMID:The psychiatric presentations of Wilson's disease. 149 90


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