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)

Male rats were fed vitamin E-adequate, Torula yeast-based diets for 30 days to assess the influence of dietary selenium (0, 0.1, or 1.0 ppm) on the toxicity of dietary cadmium (0, 30, or 60 ppm). At all selenium levels, increased cadmium intake depressed feed consumption, reduced feed efficiency and lowered body weight gain. In liver, concentrations of cadmium and zinc increased, and iron concentration decreased with increased intake of cadmium. Dietary selenium did not affect concentrations of cadmium, zinc, iron or copper in liver. Blood hemoglobin level declined and relative heart weight (g/100 g body wt) increased with increased intake of cadmium. Increased selenium intake partially alleviated the cadmium-induced depression in blood hemoglobin levels in rats fed diets that contained 30 ppm cadmium, and partially ameliorated the cadmium-induced increase in heart size in rats fed either 30 or 60 ppm cadmium. Hepatic and renal glutathione peroxidase (GSH-Px) activity increased with increased selenium intake. Increased cadmium intake did not affect renal GSH-Px activity. Hepatic GSH-Px activity in rats fed diets that contained 0.1 ppm selenium decreased with increased cadmium intake; however, hepatic GSH-Px activity was not affected by dietary cadmium in rats fed diets that contained 1.0 ppm selenium. Interactions between nontoxic levels of dietary selenium and relatively high levels of dietary cadmium apparently resulted in an antagonism of selenium metabolism by cadmium in some systems, and partial amelioration of cadmium toxicity by selenium in other systems
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PMID:Some metabolic interrelationships between toxic levels of cadmium and nontoxic levels of selenium fed to rats. 707 26

Three experiments were conducted with 9-d-old crossbred chicks to determine the effect of supplemental L-cysteine.HCl.H2O on tolerance to excess dietary Cd. Cd levels of 30 or 60 mg/kg added to a fully fortified corn-soybean meal diet depressed both body weight gain and gain:feed ratio and increased kidney Cd concentration. Supplemental cysteine (i.e., .59% L-cysteine.HCl.H2O) did not alleviate the depression of weight gain or gain:feed ratio due to Cd feeding but did decrease kidney Cd accumulation. Eimeria acervulina infection (i.e., duodenal coccidiosis) depressed rate and efficiency of weight gain and resulted in increased Cd concentrations in kidney tissue. Cystein supplementation increased kidney cadmium concentration even further in E. acervulina-infected birds.
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PMID:Tolerance of the chick to excess dietary cadmium as influenced by dietary cysteine and by experimental infection with Eimeria acervulina. 709 21

Pregnant rats were injected subcutaneously on day 10 of pregnancy with 0.0, 0.25, 0.50, 1.0 or 3.0 mg cadmium/kg and sacrificed at term (day 21). There were no fetal or maternal deaths following the cadmium exposure with the exception of the e.0 mg/kg level where a 54% fetal mortality rate was observed. At doses of 1.0 mg/kg or less, non-specific parameters of fetal toxicity including body weight, crown-rump length, and liver weight were not significantly different from control values. The same was true of term placental weight as well as maternal weight gain over the 48-h treatment period. Following gel-filtration of hepatic cytosols from control fetuses, over 70% of the endogenous cytosolic zinc was associated with a peak previously described as metallothionein. It was found that cadmium exposure at sub-lethal doses caused a depression in both total cytosolic zinc and metallothionein-bound zinc levels in the fetus, whereas both these parameters increased in the maternal liver. In vitro cadmium saturation prior to gel filtration revealed that the cadmium-binding capacity of the metallothionein peak was significantly reduced at all dosage levels in the fetus but increased in maternal liver. These findings suggest that maternal administration of cadmium can depress fetal metallothionein levels and cytosolic zinc levels at doses which do not produce overt fetal toxicity. This reduction in fetal metallothionein is in sharp contrast with the well established finding of induction of metallothionein seen in the adult following exposure to cadmium.
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PMID:Depression of metallothionein in fetal rat liver following maternal cadmium exposure. 725 78

The effects of manganese chloride were studied in two human cell lines HeLa and human embryonic diploid fibroblasts in V79 Chinese hamster lung cells, and L-A mouse fibroblasts. Manganese produces a dose-dependent depression of proliferation along with a decrease of the mitotic rate. Effects on viability are accompanied by increased release of the intracellular enzyme lactic dehydrogenase. Lactic acid is stimulated indicating enhanced glycolytic activity. The colony forming ability and the rate of DNA synthesis are inhibited in a dose- and time-related fashion. Comparing these results with those of previous studies of the cytotoxicity of lead, mercury, and cadmium in the same test systems, similar effects are observed, though with different intensities and slight differences between the cell lines. As regards depression of viability, the following rank order of toxicity can be established: Pb2+ < Mn2+ < Hg2+ < Cd2+; as regards reduction of proliferation lead is less and cadmium more effective than manganese, while mercury effects vary depending on the cells tested. Concerning colony formation and DNA synthesis the toxicity of manganese is again higher than that of lead and manganese, especially the influence on DNA synthesis, show immediate recovery after cessation of exposure indicates that the genetic material is not directly involved and that the effects on proliferation colony formation, and DNA synthesis are the consequences of several elaborate processes at the cellular level.
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PMID:[Cytotoxicity of manganese for mammalian cells in vitro--comparisons with lead, mercury and cadmium]. 746 17

Uranyl nitrate (UO2(NO3)2) has been shown to be capable of increasing transmitter release from the motor nerve accompanied by the potentiation of nerve evoked muscle contraction. In this paper, we have demonstrated that UO2(2+) induced an initial twitch depression followed by a later twitch potentiation in low (0.35 mM) Ca2+ medium. Although UO2(2+) has been identified as a K(+)-channel blocker, we have found it only partially blocked the fast K(+)-current (IK(f) as recorded in the perineurial sheath of the mouse triangularis sterni preparation. Increasing the concentration of UO2(2+) to a high concentration of 0.4 mM did not further inhibit IK(f) but markedly prolonged the duration of the outward current of the nerve terminals. From the time course of its appearance together with the specific inhibition by 4-aminopyridine, dendrotoxin and beta-bungarotoxin, which has been shown to be capable of blocking the K(+)-current of the motor nerve terminal, it was proposed that UO2(2+) prolonged the duration of the nerve terminal spikes by an enhancement of an IK(s)-like current, which was further characterized by its susceptibility to be enhanced by low K+, low Ca2+ and Cd2+ but attenuated by high K+ and high Ca2+. These cation effects not only supported UO2(2+)-induced IK(s) current but also excluded the possibility of an enhancement of Ca(2+)-activated K(+)-current induced by UO2(2+) plus TEA. The significance of this enhancement of IK(s) induced by UO2(2+) has been elucidated by the finding that dendrotoxin inhibited but tetraethylammonium potentiated not only UO2(2+)-induced IK(s) but also UO2(2+)-induced twitch depression.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Enhancement of a slow potassium current component by uranyl nitrate and its relation to the antagonism on beta-bungarotoxin in the mouse motor nerve terminal. 761 42

1. Voltage-activated ionic currents of three identified neurons of Lymnaea stagnalis L. were compared in control snails and in animals having been exposed to a cadmium- or lead-enriched environment for 2 weeks. We determined the presence, amplitude, and changes, if any, in the current-voltage characteristics of calcium and potassium currents in each of the three neurons from each of the three groups of animals. Finally, we have compared the effects of acute administration of Cd2+ or Pb2+ on neurons from control and chronically exposed animals. 2. Chronic exposure to cadmium resulted in a near doubling of the high voltage-activated calcium current. 3. No differences were found in the effects of acute application of Cd2+ or Pb2+ on neurons of pretreated and control animals. Cadmium was a potent blocker of the Ca current in either case, while lead caused only a 20% inhibition of the Ca current in neurons of both control and lead-exposed animals. 4. Potassium currents were affected in both Cd(2+)- and Pb(2+)-exposed animals. While the sustained outward current was not influenced noticeably, the fast K current was affected in different ways in different neurons. Some did not show this current in the controls but expressed it in neurons from the exposed animals. Other neurons showed the current in the controls and its depression in exposed animals. Acute application of cadmium did not modulate the K current, but lead enhanced the peak amplitude of the transient K current in neurons of both exposed and control snails.
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PMID:Effects of chronic exposure to cadmium- or lead-enriched environments on ionic currents of identified neurons in Lymnaea stagnalis L. 764 Dec 35

When male guinea pigs were given a single dose of Cd (2.0 mg Cd2+/kg, ip) 72 hr prior to sacrifice, the hepatic reduced glutathione (GSH) level did not change although glutathione S-transferase (GST) activities toward the substrates 1-chloro-2,4-dinitrobenzene (CDNB), 1,2-dichloro-4-nitrobenzene (DCNB), ethacrynic acid (EAA), and 1,2-epoxy-3-(p-nitrophenoxy) propane (ENPP) increased significantly as compared to controls. Cd did not change the renal GSH level and GST activities toward CDNB and EAA. However, significant increase was observed in the GST activity for DCNB whereas GST activity for ENPP was significantly inhibited by Cd. When the animals were given a single dose of Ni (14.8 mg Ni2+/kg, sc) 16 hr prior to sacrifice, significant increases were observed in hepatic GSH level and GST activities toward CDNB, DCNB, EAA and ENPP. Ni, however, depressed the renal GSH level and GST activities toward CDNB, DCNB and ENPP significantly. The renal GST activity toward EAA remained unaltered. For the combined treatment, guinea pigs received the single dose of Ni 56 hr after the single dose of Cd and then they were killed 16 hr later. In these animals, no significant alteration was observed in the hepatic GSH level. The augmentation of elevation was observed in hepatic GST activities toward CDNB and DCNB. Combined metal treatment did not potentiate the elevation of hepatic GST activities toward EAA and ENPP to any greater degree. The depression of renal GSH level was significantly ameliorated by the combined treatment. Combination treatment potentiated the depression of renal GST activity for ENPP but not for CDNB.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Differential combined effect of cadmium and nickel on hepatic and renal glutathione S-transferases of the guinea pig. 769 89

Spreading depression (S.D.) can be reproducibly evoked in the retinas of 3- to 6-day-old chickens by K+ ions, N-methyl-D-aspartate (NMDA), kainate (KA), and quisqualate (QA). Specific NMDA antagonists inhibit S.D. evoked by all the above agents. The very selective non-NMDA receptor antagonist 2,3-dihydroxy-6-nitro-7-sulfamoylbenzo(f)quinoxaline (NBQX) blocks QA- and KA-evoked S.D. but not NMDA- or K(+)-evoked S.D. These findings indicate that NMDA receptor activation is the vital event in the triggering of S.D. in this tissue, and that QA and KA trigger S.D. indirectly via excitation of NMDA receptors. Tetrodotoxin, cadmium chloride, conotoxin, baclofen and adenosine agonists are all ineffective in blocking K(+)-, NMDA-, QA- or KA-evoked S.D. L-trans-Pyrrolidine-2,4-dicarboxylic acid, a glutamate uptake blocker, does inhibit QA-evoked S.D. It is therefore argued that a presynaptic release of vesicular, glutamate 'neurotransmitter stores' is not the mechanism of action of QA and KA. A mechanism involving a reversal of the glutamate uptake carrier is suggested.
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PMID:The triggering of spreading depression in the chicken retina: a pharmacological study. 809 63

The interactions between different heavy metal compounds which affect their cytotoxicity towards rabbit alveolar macrophages were investigated. The cells were exposed in vitro to combinations of As3+, Cd2+, Hg2+, Ni2+, or V5+ with different concentrations of another heavy metal compound. Toxicity was determined as the depression of zymosan-induced release of superoxide anion radicals. Significant antagonisms occurred in the combinations Cd2+/Zn2+, Hg2+/As3+, and Hg2+/Se4+, while significant synergisms were exhibited by the combinations Cd2+/Cu2+, Cd2+/Sn2+, Hg2+/Cu2+, Ni2+/Cd2+, Ni2+/Cu2+, Ni2+/Sn2+ and V5+/Cu2+. In the combinations As3+/Zn2+, Hg2+/Cd2+ and Hg2+/Zn2+, both kinds of interactions were observed depending on the concentrations of the heavy metal compounds. An interpretation of the measured heavy metal interactions with reference to the toxicity of heavy metal-containing dusts is attempted.
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PMID:Cytotoxicity of dust constituents towards alveolar macrophages: interactions of heavy metal compounds. 813 19

Left ventricular function during exercise and recovery was investigated in patients with angina pectoris, ST segment depression during exercise and angiographically normal coronary arteries (syndrome X) using a continuous left ventricular function monitor with cadmium telluride detector (CdTe-VEST). Fourteen patients with syndrome X and 14 patients with atypical chest pain without ST segment depression during exercise and normal coronary arteries (control group) performed supine ergometric exercise after administration of 740-925 MBq of technetium-99m labelled red blood cells, and left ventricular function was monitored every 20 s using CdTe-VEST. Left ventricular ejection fraction (EF) response was impaired (< or = 5% increase from rest to peak exercise) in 11 or 14 patients with syndrome X but in none of the control patients. Resting EF was similar in the two groups (62.1% +/- 6.7% in patients with syndrome X, 61.9% +/- 6.2% in controls); however, EF increase from rest to peak exercise was lower in syndrome X (-3.1 +/- 9.5% vs 14.7% +/- 7.4%, P < 0.001). After cessation of exercise, all patients showed rapid EF increase over baseline and this EF overshoot was lower (19.3% +/- 8.3% vs 26.4% +/- 7.3%, P < 0.001) with the time to EF overshoot longer (114 +/- 43 s vs 74 +/- 43 s, P < 0.05) in patients with syndrome X. Thus, in patients with syndrome X, left ventricular dysfunction was frequently observed during exercise in spite of normal epicardial coronary arteries.
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PMID:Left ventricular dysfunction during exercise in patients with angina pectoris and angiographically normal coronary arteries (syndrome X) 816 44


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