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

Single nuclear gene inheritance was shown to be responsible for increased resistance to: eight diverse inhibitors of mitochondrial function (antimycin, carbonylcyanide-m-chlorophenylhydrazone, chloramphenicol, oligomycin, tetracycline, triethyltin bromide, triphenylmethylphosphonium bromide and triton-X-165); and an inhibitor of cytoplasmic protein synthesis (cycloheximide). Continuous monitoring of oxygen uptake during respiratory adaptation showed that anerobic pretreatment of resistant cells sensitized respiratory adaptation to chloramphenicol and antimycin. However, since a depression of mitochondrial function by catabolite repression did not result in sensitization to antimycin, alteration of the mitochondrial membrane does not appear to be responsible for resistance to mitochondrial inhibition. Alteration of cellular binding sites was not responsible for resistance since in vitro mitochondrial protein synthesis was sensitive to chloramphenicol and in vitro mitochondrial respiration was sensitive to oligomycin, carbonylcyanide-m-chlorophenylhydrazone, and antimycin. Autoradiography of an ethylacetate-ethanol extract of [14C]chloramphenicol-treated resistant cells indicated that resistance was not due to enzymatic modification of inhibitors. The maintenance of an antimycin-resistant respiration by protoplasts of resistant cells ruled out the involvement of the cell wall in cellular resistance. The reduced transport of [14C]chloramphenicol by resistant cells (1% of normal cells) indicated that a single nuclear gene mutation can alter the permeability of the plasma membrane to many diverse inhibitors.
 ...
PMID:Reduced plasma membrane permeability in a multiple cross-resistant strain of Saccharomyces cerevisiae. 109 46

The acute effects of ethanol (ETOH) on cardiac function in 32 normal subjects has been studied utilizing systolic time intervals. Seven (group I) 13 (group II), and 12 subjects (group III), reported an average daily consumption of less than 1 oz, 1-2 oz, and more than 2 oz of ETOH, respectively. Progressively higher control values from group I to group III in PEP, PEPI, ICT and PET/LVET were observed (PEP-I vs PEPI-III: P smaller than 0.05; PEP/LVET-I vs PEP/LVET-II and PEP/LVET-III: P smaller than 0.05). There was progressively less change in these variables following acute ETOH (P smaller than 0.02-0.05 in group I; P equals NS in group III, group II intermediate). This indicates some degree of chronic myocardial impairment in group II and especially in group III, which tends to be proportionate to the degree of chronic ETOH exposure. These data are not necessarily disparate with previous reports of little or even a salutary hemodynamic effect of ETOH in normal subjects. Thus, the relative stability of LVET post ETOH, coupled with the observed increase in heart rate, is consistent with previous reports of ETOH-induced rate-dependent increments in cardiac output with unchanging stroke volumes, in spite of the presence of acute myocardial depression. The observations reported herein demonstrate the probable incremental influence of ETOH consumption in a chain of events which may culminate in alcoholic cardiomyopathy.
 ...
PMID:The basis for differences in ethanol-induced myocardial depression in normal subjects. 113 3

The objective of this study was to investigate the mechanism by which ethanol inhibits intestinal absorption of sugars. In vitro experiments on hamster jejunum have shown that the presence of ethanol in the mucosal solution caused an inhibition of the net transport of water and glucose. There was also a decrease in the intracellular water content and an increase in the intracellular sodium and potassium concentration of the gut tissue. In contrast, the intracellular glucose concentration decreased in the presence of ethanol. These ethanol-induced changes were directly related to the ethanol concentration of the mucosal solution. In the presence of 450 mM (2%) ethanol in the mucosal solution, there was also a significant inhibition of transmural potential difference, estimated glucose metabolism, and both unidirectional fluxes of sodium. The net flux of sodium to the serosal side however did not decrease significantly. These effects of ethanol cannot be fully explained by its osmotic action, and it is suggested that the ethanol-induced reduction in glucose transport could be mainly the result of an interference with the carrier-mediated coupled entrance of glucose and sodium across the brush border. A depression of cellular metabolism could also have played a role in this process.
 ...
PMID:Effect of ethanol on sodium-dependent glucose transport in the small intestine of the hamster. 113 33

1. Hypoxic and hypercapnic ventilatory drives were measured in eight healthy male subjects before and after ingestion of ethanol, in a dose of 17 mmol/kg body weight. 2. A significant decrease in hypoxic ventilatory drive was observed at 20 min after ethanol (P less than 0.05). A significant depression in hypercapnic drive was observed at 70 min after indigestion of ethanol (P less than 0.05). The mean peak blood ethanol (24mmol/1) occurred at 20 min, at which time the lowest mean hypoxic drive was recorded. 3. Ethanol in moderate doses produced a depression of both hypoxic and hypercapnic ventilatory drives in normal subjects. This suggests that ethanol may play a role in the precipitation of acute respiratory failure in certain patients in whom the ventilatory drive is already impaired, as in chronic airways obstruction.
 ...
PMID:Effect of ethanol on the ventilatory responses to oxygen and carbon dioxide in man. 114 93

Fifteen male mice from each of 4 inbred strains (C57BL/6J, BALB/cJ, CBA/J, and DBA/2J) were tested to determine their voluntary self-selection of a 10% solution of 1,2 propanediol (1,2 PD), A 3-carbon alcohol of low toxicity. As with ethanol, the C57BL/6J strain consumed significantly greater amounts that the 3 other low ethanol-selecting strains. A second experiment determined that the 3 low selecting strains suffered significantly greater depression of the central nervous system from 1,2 PD than the high selecting C57BL strain. It was also found that ethanol is a much more potent depressant that 1,2 PD. These results are discussed in terms of the possible role of neural sensitivity in regulating consumption levels of the 2 alcohols.
 ...
PMID:Voluntary selection of and tolerance to 1,2 propanediol (propylene glycol) by high and low ethanol-selecting mouse strains. 115 Sep 48

Varying concentrations of ethyl alcohol were injected either into the left main coronary artery or intravenously in anesthetized intact dogs. Effects of alcohol on intracardiac conduction (by His bundle electrogram) were examined at spontaneous and paced (atrial) heart rates. Alcohol by the intracoronary route prolonged atrioventricular node and intraventricular conduction times by approximately 5 to 15%. These changes preceded a depression of left ventricular systolic pressure and of the rate of rise of left ventricular pressure and an elevation of left ventricular end-diastolic pressure. Intracoronary injections of contrast medium (sodium diatriozoate) or iso-osmolar solutions of sucrose and injections of similar amounts of alcohol in the ascending or descending aorta did not affect intracardiac conduction. Increasing atrial pacing rates resulted in prolongation of atrioventricular nodal conduction intervals, but did not influence intraventricular conduction time. At each pacing rate, alcohol depressed both atrioventricular nodal and intraventricular conduction. The data suggest that alcohol has a direct depressant effect on intracardiac conduction.
 ...
PMID:Altered intracardiac conduction after acute administration of ethanol in the dog. 115 36

Volunteers inhaled a constant concentration of 50 ppm trichloroethylene (Tri) for 6 hrs per day on 5 consecutive days. Simultaneous ethanol (EtOH) ingestion (blood level 0.6%) inhibits the metabolization of Tri to trichloroethanol (TCE) and trichloroacetic acid (TCA) by 40% on the average. Oxidation of Tri to TCA does not occur as long as EtOH is present. During this time period the blood Tri-concentration increases 2 1/2-fold, that in the expired air rising 4-fold, as compared to Tri inhalation without EtOH. TCE glucuronidation is not subject to inhibition. On concurrent inhalation of Tri, the EtOH and acetaldehyde levels are slightly increased over the control values without Tri. The mechanisms underlying the alternate inhibition of mixed-function oxygenases and aldehyde dehydrogenase on simultaneous intake of Tri and EtOH are discussed. The intolerance reaction occurring on combined exposure to Tri and EtOH can be interpreted as an accumulation of Tri in the CNS resulting from the complete depression of Tri oxidation.
 ...
PMID:Metabolism of trichloroethylene in man. III. Interaction of trichloroethylene and ethanol. 117 50

The constant failure to produce a liver cirrhosis that can be ascribed to alcohol in the rat promoted the present study in guinea-pigs. The animals were given 40 per cent of calories as ethanol during 8 months. However, no alcoholic hepatitis or cirrhosis developed. Triglycerides and cholesterol increased in the liver and in serum. The persistance of liver triglyceride increase in spite of a rather low fat content of the diet is in contrast to experiences in the rat. A slight depression of coagulation factors II, VII, X and XI was observed in the ethanol-fed animals.
 ...
PMID:Effects on lipids, coagulation factors and liver histology of long-term ethanol administration to guinea-pigs. 117 46

With the use of ethanol in hyperalimentation regimens and for the inhibition of premature labor, there is increased opportunity for exposure of the fetus to this potentially toxic substance. We reviewed the literature regarding the effects of ethanol on the fetus and neonate, and illustrate its potential toxicity by the report of a case of neonatal depression secondary to acute maternal ethanol ingestion.
 ...
PMID:Acute transplacental ethanol intoxication. 119 Jan 80

The mechanism of the hypothermia produced in mice by the naturally occurring cannabinoids, delta9-tetrahydrocannabinol, cannabinol, and cannabidiol, was investigated by evaluating the direct effect of these drugs on the oxygen consumption of tissue homogenates and isolated mitochondria. The tissues studied were brain, liver, skeletal muscle, and heart; the mitochondrial preparations were limited to brain and skeletal muscle. The in-vitro studies included a description of the influence of various cannabinoid vehicles containing Tween 80, ethanol, Pluronic F68, and albumin on the oxygen consumption of tissue preparations. Of these vehicles, only albumin was without effect on all tissues. The other vehicles produced diverse responses, including some that were qualitatively different; the data illustrate that the influence of each vehicle on oxygen consumption must be defined for each tissue employed. In spite of the different vehicle effects, delta9-tetrahydrocannabinol generally reduced oxygen consumption of all tissue preparations; however, the vehicles were capable of modifying the dose-effect relationship. The results of all three drugs prepared in Pluronic F68 on brain and skeletal muscle indicated that the cannabinoids generally cause a dose-related depression of oxygen consumption. The findings demonstrate that the cannabinoids can directly decrease oxidative metabolism of tissue and isolated mitochondria and that a marked response occurs in the concentration range of 1 X 10(-5) to 1 X 10(-4) M. Because these concentrations can exist in tissues following the in-vivo administration of delta9-tetrahydrocannabinol, the results suggest that the depressant effect of the cannabinoids on metabolic rate may contribute to the mechanism of the hypothermia produced by the drugs.
 ...
PMID:The influence of delta9-tetrahydrocannabinol, cannabinol and cannabidiol on tissue oxygen consumption. 119 14


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>