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)

Young adult rats absorbed 50 p.p.m. Cd2+ added to drinking water. After 6 weeks, 3, 6 and 9 months of treatment, the ultrastructural condition of liver, kidney and muscle was observed by electron microscopy. The choice of these tissues was determined by their differences in the capacity to accumulate Cd2+: the liver is able to concentrate a considerable amount of metal, but redistributes it throughout the entire organism, while the kidney collects it in view of its elimination. Muscle contains the least Cd2+. A general regression in mitochondria cristae accompanied by a vesiculation and a fragmentation of endoplasmic reticulum appeared simultaneously in the three tissues, at as early as 6 weeks of treatment, and extended progressively with its continuation supporting evidence of a general attack of the intracellular membrane systems. Cd2+ stimulation of membrane-degrading enzymes such as phospholipases and proteases was suggested. A concomitant diminution in glycogen stores was noted. Active synthesis of neutral lipids, especially cholesterol esters, took place in liver mitochondria of treated rats in collaboration with rough endoplasmic reticulum, and progressively generated a multiplication of electron-transparent inclusions in cytoplasm. Isolated mitochondria from liver, kidney and muscle of Cd2+-treated rats maintained partial energy coupling, but displayed a rapid early fall in cytochrome oxidase followed by a partial restoration after 6 months of treatment, and a progressively slackening of succinate dehydrogenase. Isolated vesicles of liver mitochondria inner membrane of treated rats behaved as intact mitochondria, indicating changes inside the membrane itself. Addition in vitro of the metal ion to mitochondria and also to inner membrane vesicles isolated from control rats revealed that Cd2+ was able to stop completely succinate dehydrogenase, but was totally ineffective on cytochrome oxidase. Membrane fixation of Cd2+ on the flavoprotein or SH associated with succinate dehydrogenase is proposed. Considering the close parallelism of the extensive depression of microsomal NADPH cytochrome c reductase and the rapid fall in mitochondrial cytochrome oxidase, it is suggested that an indirect inhibition process occurs, through Cd2+-induced diminution of a constituent common to all cytochromes in the cell.
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PMID:Mitochondria alterations in Cd2+-treated rats: general regression of inner membrane cristae and electron transport impairment. 293 99

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.
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PMID:Modification of aflatoxin B1-induced changes in certain mitochondrial enzymes and lipids by medroxyprogesterone acetate. 294 74

The duration of the presumed metabolic depression of syngeneic vena cava to aorta transplants was determined in rats and the site and type of energy metabolism in the vein grafts assessed. The aerobic metabolic activity was measured from the histochemical reactivity of the enzymes, succinate dehydrogenase and cytochrome oxidase, and the anaerobic activity by staining with lactate dehydrogenase. The activity of the hexose-monophosphate shunt was assessed by the histochemical demonstration of glucose-6-phosphate dehydrogenase. Sixteen hours after grafting a pronounced metabolic depression was noted. Recovery occurred 24 hours after transplantation. The most intense staining was from lactate dehydrogenase in the vein grafts and in the non-transplanted veins. At the end of the observation period of four months the grafts were definitely more strongly stained than the non-transplanted veins, with most of the activity in the thickened intima. This layer had a metabolic profile resembling that of the media of the adjacent aorta.
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PMID:Histochemical examination of energy metabolism in aortic vein grafts in rats. 302 37

Biochemical investigations were performed on cardiac muscle samples from seven dogs with cardiomyopathy and on cardiac muscle from a varied selection of normal dogs. Biochemical examination of cardiac muscle from clinical cases of cardiomyopathy revealed that the concentrations of three enzymes were significantly altered. These were, catalase, succinic dehydrogenase and malate dehydrogenase. Depressed enzyme concentrations were recorded from both ventricles but were significant only on the left for catalase, on the right for malate dehydrogenase and in both ventricles for succinic dehydrogenase although the depression in this case was also greater on the right.
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PMID:Biochemical investigations of cardiomyopathy in the dog. 362 75

1. Some properties of succinate dehydrogenase [succinate-(acceptor) oxidoreductase, EC 1.3.99.1] in membrane preparations from Micrococcus lysodeikticus (N.C.T.C. 2665) were investigated. 2. In the spectrophotometric assay system adopted the reaction velocity was shown to be proportional to the amount of membrane added. Dichlorophenol-indophenol, reduced photochemically in the presence of phenazine methosulphate, or enzymically by the membrane-bound enzyme, was shown to undergo reoxidation in the dark. 3. The membrane-bound enzyme was found to be inactivated at temperatures above 10 degrees C. 4. The specific activity of membrane-bound succinate dehydrogenase was found to increase between two- and three-fold in diluted membrane preparations equilibrated at 0 degrees C for 6h. Membranes treated with sodium deoxycholate showed no enzyme activation on dilution but displayed maximal activity, all activity being sedimentable at 103000g. The increase in specific activity observed on dilution could be partially inhibited by fixation with glutaraldehyde, or by the presence of bovine serum albumin. 5. The addition of Mg(2+) or Ca(2+) ions to membrane suspensions caused an overall depression of enzyme activity. 6. The results suggest the presence of an ;inhibitor' that affects the expression of membrane bound succinate dehydrogenase activity.
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PMID:Factors influencing the activity of succinate dehydrogenase in membrane preparations from Micrococcus lysodeikticus. 549 52

Using histochemical techniques, the reactivities of selected enzymes and other metabolic components were examined in the myocardium, coronary arteries, and coronary arterioles of normal, two-week-sympathectomized, and sham-operated canine hearts. There were no differences in the histochemistry of coronary arteries in any of the hearts, but important differences were noted in the myocardium and especially in the arterioles. The reactivities of the enzyme glucose-6-phosphate dehydrogenase and the nucleic acids were increased in arterioles of the sympathectomized heart, possibly indicating an increased protein synthesis. The reactivities of succinate dehydrogenase, NAD-isocitrate dehydrogenase, and cytochrome oxidase were reduced in myocardium and arterioles of sympathectomized hearts as well as in arterioles of sham-operated hearts; the changes were greater in the sympathectomized arterioles where there was also observed an increase in reactivity of lactate dehydrogenase. These findings suggest a depression in aerobic metabolic capacity and, in the case of the sympathectomized arteriole, imply a possible shift in adaptation from aerobic to anaerobic metabolism.
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PMID:The myocardium and its vasculature: a histochemical comparison of the normal and chronically sympathectomized dog heart. 615 74

Human mammary tumours were grown in diffusion chambers in the heterologous host--Charle's Foster rat. The effect of oophorectomy-induced alterations of the hormonal environment of the host in breast tumour cells grown in the diffusion chamber were studied with respect to their growth patterns and enzymatic characteristics. The tumour cells not only survived but actively proliferated as indicated by the increase in cell count and formation of cell sheets as well as by the presence of mitotic figures. Cytochemical studies of certain enzymatic activities, i.e. succinic dehydrogenase, alkaline phosphatase, acid phosphatase and beta-glucuronidase indicate--except for a slight depression of the overall activity--that the distribution patterns are more or less maintained following diffusion chamber culture. The alteration of the hormonal environment by oophorectomy influences the cell growth and the enzymatic activity of the human tumour cells inside the diffusion chambers. The results clearly indicate that D.C. culture technique provides a useful method for assessment of growth and hormonal responsiveness of human tumours.
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PMID:Studies on growth and enzymatic characteristics of human mammary tumours grown in heterologous host. 668 51

Dose-dependent increases in alkaline phosphatase and acid phosphatase activities, decreases in myeloperoxidase activity of neutrophils and depression of lymphocyte glycerophosphate dehydrogenase and succinate dehydrogenase activities were discovered in rat nephropathy induced by mercuric chloride at doses of 0.1-1.0 mg/kg. These changes manifest the intensity of the oxidation-reduction process, the reduction of Kreb's cycle and alpha-glycerophosphatic shunt, the damage by peroxidation and the increase in catabolic processes. The morphometric data of nephron structure reflected the functional cell stress and they were compared with leucocyte enzyme status changes.
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PMID:Some aspects of testing drugs for nephrotoxicity in rats. 677 35

A previous study of endotoxemia in dogs demonstrated that exogenous prostacyclin (PGI2), normally a product of vascular endothelium, restored the cardiac index to normal and improved survival. To account for these results, a study was undertaken to test whether PGI2 would alter isolated rat or dog cardiac mitochondrial function following incubation with plasma from endotoxemic animals. A group of five animals served as anesthetized controls. A second group of seven mongrel dogs was given 1.75 mg Escherichia coli endotoxin/kg and was observed for 5 hours without treatment. Anesthesia did not alter cardiopulmonary function; however, 30 minutes after endotoxin administration, the cardiac index decreased from 148 +/- 25 (mean +/- SD) to 111 +/- 12 ml/kg . min (P less than 0.05) and further decreased to 89 +/- 20 ml/kg . min after 4 hours. Dog plasma obtained 2 to 5 hours after endotoxin infusion, incubated with rat or dog myocardial mitochondria, decreased succinate dehydrogenase (SDH) activity (P less than 0.05) and depressed mitochondrial respiration in the presence of the substrate succinate and adenosine diphosphate (ADP) from 180 to 87 Natoms oxygen/mg protein . min (P less than 0.05). There was no change in oxygen consumption when substrate alone was present, nor did plasma alter the amount of ADP phosphorylation as a function of oxygen consumption. A third group of seven animals, 30 minutes after administration of 1.75 mg endotoxin/kg, was treated with 100 ng/kg . min PGI2 for 3 hours. PGI2 infusion in this group prevented the decrease in cardiac index. Plasma obtained during and after PGI2 infusion did not decrease mitochondrial SDH activity, which remained higher than that in controls (P less than 0.001); mitochondrial respiration was also not altered. A correlation was observed between cardiac index and SDH activity (r = 0.58, P less than 0.001) and between cardiac index and mitochondrial respiration (r = 0.61, P less than 0.001). In PGI2-treated dogs cardiac mitochondria were functionally and structurally normal in contrast to the depression and disruption produced by endotoxemia, as observed by enzymatic assay as well as electron microscopy. These results suggest that endotoxemia depresses cardiac mitochondrial respiration, an event related to the decrease in cardiac index. In contrast, cardiac function and mitochondrial respiration are maintained with PGI2 treatment.
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PMID:Myocardial protection with prostacyclin after lethal endotoxemia. 704 19

The effect of antimycin A and funiculosin, two inhibitors which block electron transfer in the b-c1 complex, on electron flow and electrochemical potential difference of H+ ions in mitochondria at static head (state 4) is investigated. In addition, the respiratory control ratio is determined as the ratio between uncoupler stimulated and static-head electron flow. Malonate, a competitive inhibitor or succinic dehydrogenase, is used for comparison. All three inhibitors cause an extensive depression of static-head electron flow but only a limited decrease in the electrochemical potential difference of H+ ions. With the antimycin-type of inhibitors, the respiratory control ratio slightly increases up to about 50% inhibition of electron flow and then steeply declines. With malonate, a strong decrease of the respiratory control ratio is observed in a concentration range where the electron flow is inhibited less than 10%. It is shown than the data do not comply with the generally accepted hypothesis of a leak conductance being regulated by the electrochemical potential difference of H+ ions. They can be interpreted in terms of not tightly coupled redox-driven H+-pumps. A non-vanishing electron flow at static head then arises predominantly from molecular slipping in the pumps, and the (constant) leak conductance yields only a minor contribution.
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PMID:Effect of funiculosin and antimycin A on the redox-driven H+-pumps in mitochondria: on the nature of "leaks'. 727 16


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