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)

Subcellular fractions in hearts from rats with severe acute uremia (24 hours after total nephrectomy) and moderate chronic uremia (2 weeks after five sixths nephrectomy) were studied and compared with preparations from acute and chronic sham-operated rats, respectively. Calcium- and magnesium-sensitive actomyosin adenosine triphosphatase (ATPase) activities were normal in both groups. Acute uremia was associated with a significant depression of sarcolemmal Na+,K+ ATPase activity. Calcium transport by fragmented sarcoplasmic reticulum was also depressed in the presence and absence of oxalate in acute uremia. Mitochondrial calcium transport and adenosine triphosphate (ATP) and creatine phosphate (CP) concentrations were normal in these animals. Chronic uremic animals showed no abnormal subcellular mechanisms. These data suggest a direct effect of acute uremia on some membrane functions in myocardial cells. The discrepancies observed between acute and chronic uremic groups may be due to a different degree of uremic state. The observation of depressed calcium transport by fragmented sarcoplasmic reticulum (FSR) in acute uremic hearts which were previously shown to have increased contractile reserve suggests that studies of calcium transport in FSR may not always truly reflect the contractile capacity of the heart.
 ...
PMID:Studies of subcellular control factors in hearts of uremic rats. 13 36

Gram-negative endotoxin (Escherichia coli, 4 mg/kg) was found to produce a sustained fall in systemic arterial pressure, left ventricular pressure, and cardiac output that could be blocked by the histamine antagonist diphenhydramine. Histamine infusion was found to produce a parallel depression of systemic arterial pressure. Further, endotoxemia was found to produce a significant depression of myocardial contractility (dP/dt max) that could also be blocked by diphenhydramine. Cardiac myofibrillar adenosine triphosphatase (ATPase) activity from endotoxin-shocked hearts was found to be depressed, ATPase activity from subendocardial myofibrils being more depressed than that from subepicardial myofibrils. Myofibrillar ATPase activity was significantly protected by pretreating the animals with diphenhydramine. It is concluded that the initial hemodynamic phase of endotoxin shock is histamine-mediated and that this hemodynamic depression can be blocked with diphenhydramine. Further, it appears that endotoxin is capable of depressing myocardial contractility by depressing contractile protein function (myofibrillar ATPase activity)--the subendocardial surface more so than the subepicardial surface--and this depression of myocardial contractility can be blocked with diphenhydramine.
 ...
PMID:Diphenhydramine protection of the failing myocardium during gram-negative endotoxemia. 15 4

Effects of vanadate on ouabain binding and inhibition of sodium and potassium adenosine triphosphatase (Na+ + K+)-ATPase) were investigated under various ionic conditions. 1. Vanadate facilitated ouabain binding to (Na+ + K+)-ATPase in the presence of Mg2+ and this facilitation was partially reversed by catechol. 2. Vanadate antagonized the ability of high concentrations of NaCl to inhibit ouabain binding in the presence of magnesium. 3. Ouabain binding to the vanadate-enzyme complex, formed from magnesium and vanadate, was more sensitive to depression by potassium than that to the phosphoenzyme formed from magnesium and inorganic phosphate. 4. Preincubation of (Na+ + K+)-ATPase with vanadate in the presence of magnesium initially formed a potassium-insensitive complex as shown by a rapid initial rate of ouabain binding. However, within 5 min potassium overcame the vanadate potentiation of ouabain binding regardless of the order in which it was added to the reaction mixture. 5. Under conditions of enzyme turnover, vanadate failed to antagonize the inhibitory power of ouabain despite the presence of a high concentration of potassium. This suggests a possible relationship between the sensitivity of the sodium pump in various tissues to the cardiac glycosides and intracellular vanadate concentrations.
 ...
PMID:Effects of vanadate on ouabain binding and inhibition of (Na+ + K+)-ATPase. 22 60

To study the extent, duration, and localization of metabolic changes in vein-to-vein grafts in rats, the sequential changes in enzymatic activity of veno-venous grafts in rats were evaluated by histochemical demonstration of the activity of two oxidoreductases (lactate dehydrogenase and succinate dehydrogenase) and two hydrolytic enzymes (adenosine triphosphatase and alkaline phosphatase). All the enzymes studies showed a decrease in staining 1 day after transplantation, the change being most pronounced for AFOS in the subendothelial layer. The recovery of staining intensity was noted after 3 days, the enzyme activity reaching the pregrafting level at 1 week. Different from the previous observations on vein-to-artery grafts, these vein-to-vein grafts showed less depression of enzyme activity during the first days after transplantation, neither did they display a continuing strong activity later on, probably due to lack of a thickening intimal layer.
 ...
PMID:Enzyme histochemical studies on veno-venous grafts in rats. 252 65

The effect of a single dose of 5 mg/kg body weight of aflatoxin B1 on rat liver mitochondrial enzymes, succinate dehydrogenase (SDH) and Mg++ adenosine triphosphatase (Mg++-ATPase) and on certain lipids were studies at various intervals of time from 3 to 24 hours. A significant decrease in the specific activity of SDH was observed after 6, 12, 18 and 24 hr treatment. The Mg++-ATPase activity remained unaffected up to 12 hr but appreciably decreased after, 18 and 24 hr of the treatment. The level of phospholipids and cholesterol were not altered after 3, 6 and 12 hr treatment, thereafter (18 and 24 hr) an increase was observed in both the lipids following the aflatoxin treatment. Medroxyprogesterone acetate (MPA) did not cause any alteration in the specific activities of these enzymes as well as levels of cholesterol and phospholipids. The treatment with MPA caused significant increase in contents of cytochromes P-450, b5 and activities of Arylhydrocarbon hydroxylase (AHH), UDP-glucuronyl transferase (UDP-GT) and NADPH-cytochrome C-reductase of hepatic microsomes. It was observed that pretreatment with medroxyprogesterone acetate (MPA) could significantly minimuze the depression caused in mitochondrial SDH and Mg++-ATPase activities by aflatoxin B1.
 ...
PMID:Modification of aflatoxin B1-induced changes in certain mitochondrial enzymes and lipids by medroxyprogesterone acetate. 294 74

Effects of bepridil [1-[3-isobutoxy-2]benzylphenyl-amino)propyl pyrrolidine) on oxidative phosphorylation, oligomycin-sensitive adenosine triphosphatase, swelling, Ca++ uptake and Na+-induced Ca++ release processes of mitochondria isolated from rabbit heart were investigated. Bepridil, in concentrations greater than 5 microM, produced uncoupling of oxidative phosphorylation and stimulated oligomycin-sensitive adenosine triphosphatase activity. At low concentrations it prevented inorganic phosphate-induced swelling and associated depression of oxidative phosphorylation. Its effectiveness in preventing swelling and depression of oxidative phosphorylation was found to be dependent on inorganic phosphate concentration. A concentration of 1 microM of bepridil was effective in producing 50% less depression of phosphorylating respiration in the presence of 10 mM inorganic phosphate. Concentrations of bepridil above 25 microM inhibited the rate of Ca++ uptake. A 50% inhibition of Ca++ uptake was observed at 93 microM bepridil. The rate of Na+-induced Ca++ release was also inhibited by bepridil. A 50% inhibition of the rate of Na+-induced Ca++ release occurred at 11 microM of bepridil. When the Na+-dependent Ca++ release process was about 80% inhibited by 25 microM bepridil, the uptake process still remained at the same level as the untreated control. Results suggest that in addition to reported effects on sarcolemma and sarcoplasmic reticulum, mitochondria are also affected by bepridil.
 ...
PMID:Action of bepridil, a new calcium channel blocker on oxidative phosphorylation, oligomycin-sensitive adenosine triphosphatase activity, swelling, Ca++ uptake and Na+-induced Ca++ release processes of rabbit heart mitochondria in vitro. 315 32

1. Kidneys were kept anoxic at 4 degrees , 20 degrees and 38 degrees . Mitochondria were then isolated and their oxidative phosphorylation and respiration were determined. 2. Under all conditions the rate of phosphate esterification was affected to a greater extent, or earlier, than oxygen consumption. 3. Glutamate and succinate were used as substrates. The depression of P/O ratio was greater for glutamate at 4 degrees , and for succinate at 20 degrees . 4. Anoxia abolished the inhibiting effect of fluoride on respiration. 5. Phosphate esterification, after anoxia, was higher in the presence of fluoride than its absence, whereas in control preparations they were the same. 6. The decrease in P/O ratio did not appear to be due to activation of adenosine triphosphatase, as activities of both Mg(2+)-and dinitrophenol-activated adenosine triphosphatases were decreased after anoxia.
 ...
PMID:The effect of temperature and anoxia of kidney on the subsequent oxidative phosphorylation of mitochondria. 422 26

Glucose, insulin, potassium (GIK: 300 g glucose + 50 U insulin + 80 mEq KC1/L) was administered to anesthetized dogs as a 30-ml bolus followed by 1.5 ml/kg/h for 2 h. Five populations were studied: control (C, n = 6); 60 min hypothermic arrest both without (I, n = 6) and with pretreatment (I + GIK, n = 6); 60 min hypothermic arrest followed by reperfusion without (R, n = 6) and with pretreatment (R + GIK, n = 6). Glycogen content declined during the ischemic and reperfusion periods whether or not GIK pretreatment was utilized. Glycogen values did not differ significantly among the four groups. GIK pretreatment significantly protected sarcoplasmic reticulum (SR) calcium uptake rates. SR Ca2+ + Mg2+ adenosine triphosphatase (ATPase) activity was unaffected in the I group, depressed in the R group, but protected by GIK pretreatment. Myofibrillar pCa-ATPase activity was significantly depressed in the I group and unaffected by GIK pretreatment. In the R + GIK group, myofibrillar pCa-ATPase activity was identical to controls at all calcium concentrations except for Vmax. In vitro, generation of the superoxide anion by a xanthine-xanthine oxidase system at pH 7.0 significantly depressed both SR calcium uptake and ATPase activity, and this depression was partially reversible by glucose. Generation of the hydroxyl free radical and pH 6.4 significantly depressed calcium uptake but not ATPase activity, and this depression was reversible with glucose + superoxide dismutase. GIK pretreatment exerts a protective effect on the excitation-contraction coupling system during hypothermic global ischemia and reperfusion. Glycogen augmentation after short-term GIK infusion was not significantly different. It is hypothesized that an additional mechanism by which GIK may protect subcellular function is by serving as a scavenger of free radicals generated during the ischemic/reperfusion process.
 ...
PMID:Glucose, insulin, potassium protection during the course of hypothermic global ischemia and reperfusion: a new proposed mechanism by the scavenging of free radicals. 618 57

Cell lines resistant to ethidium bromide have been developed from cultured mammalian BHK21/C13 cells and these same cells transformed by Rous sarcoma virus (C13/B4). Cells resistant to 2 micrograms ethidium bromide per milliliter have been cloned. One clone of the control and one of the virus-transformed cell lines has been employed for characterization. The resistant cells, in the presence of 2 micrograms ethidium bromide/ml, grow at approximately the same rate as the untreated parental cells. The control cells possess a "normal" karyotype (44 chromosomes), while the corresponding ethidium bromide mutant has a reduced chromosome number of 41 and a number of translocations. The mitochondria displayed morphological alterations compared to the parental lines during the transition phase prior to the isolation of the ethidium bromide-resistant cells. The mitochondria of the ethidium bromide-resistant mutants appear somewhat enlarged with a normal morphology. The effect of ethidium bromide on selected respiratory enzymes in normal and virus-transformed ethidium bromide-resistant baby hamster kidney cells was determined. Ethidium bromide-resistant cells exhibited a depressed level of cytochrome aa3. This depression could not be reversed by growth in ethidium bromide-free media. Ethidium bromide-resistant cells possessed the same cytochrome b, c, and c1 levels per cell as their corresponding parental lines. Purified mitochondria isolated from virus-transformed ethidium bromide-resistant cells exhibited a depression in cytochrome oxidase-specific activity, while the ethidium bromide-resistant control cells did not. All cell lines studied showed a depression in NADH-ferricyanide and NADH-cytochrome c reductase-specific activities relative to their parental BHK21/C13 cells. No increase was observed in virus-transformed ethidium bromide-resistant cells. Ethidium bromide-resistant control cells exhibited a two-fold increase in oligomycin-insensitive adenosine triphosphatase activity relative to their parental cells. All of the cell lines studied possessed equivalent oligomycin-sensitive adenosine triphosphatase-specific activity except for the virus-transformed, dye-resistant mutant, whose activity was increased.
 ...
PMID:Control and virus-transformed baby hamster kidney cells resistant to ethidium bromide. I. Characterization and the respiratory enzymes. 625 Oct 98

The influence of adrenochrome (1-100 microgram/ml or 5.6 x 10(-6)-5.4 x 10(-4) M) on microsomal calcium binding, calcium uptake and Ca++-stimulated Mg++-dependent adenosine triphosphatase (ATPase) activities was studied in vitro. Adrenochrome decreased microsomal calcium binding, calcium uptake and Ca++-stimulated Mg++-dependent ATPase activities. The inhibitory effect of adrenochrome on microsomal calcium uptake activity of the isolated membrane was independent of pH (6.0-8.0), calcium concentrations (10-200 muM), protein concentration (0.02-0.10 mg/ml), temperature (25-37 degrees C) and incubation time (2-30 min). Kinetic study of calcium uptake activity in different concentrations of ATP showed that the inhibition was of a mixed type. Perfusion of hearts with adrenochrome resulted in marked depression in contractile force and the microsomal fraction obtained from these hearts showed depressed calcium binding, calcium uptake and Ca++-stimulated Mg++-dependent ATPase activities. The depression in microsomal The influence of adrenochrome (1-100 microgram/ml or 5.6 x 10(-6)-an irreversible nature. It is proposed that cardiodepressant action of adrenochrome may partly be explained on the basis of its inhibitory effect on the calcium transporting ability of the sarcoplasmic reticulum.
 ...
PMID:Effects of adrenochrome on calcium accumulating and adenosine triphosphatase activities of the rat heart microsomes. 644 3


1 2 3 Next >>