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)

Certain former operations in capacitor manufacturing resulted in extensive direct contact of the workers with electrical grade polychlorinated biphenyls (PCBs). A study group of 194 such individuals, all exposed to Aroclor 1016 and many previously exposed to Aroclors 1242 and/or 1254, was examined before (1976) and after (1979) discontinuance of PCB use in the operations (1977). At the two examinations, the approximate geometric mean serum levels (in ppb) and 5 to 95% ranges were for lower PCBs (LPCB), 363 (57-2270) and 68 (12-392); and for higher PCBs (HPCB), 30 (6-142) and 19 (4-108), respectively. The statistical associations among 42 measured clinical chemical and hematological parameters, five different measures of PCB exposure, and seven confounding variables observed in the two examinations were determined by three regression procedures. Similar regressions were performed with DDE, which was present at background levels. The principal statistical findings were a depression in serum bilirubin and elevations in serum GGTP and lymphocyte levels at the time of the first examination, and only an elevation in monocytes at the second. Appraisal of the results suggested an induction of microsomal enzymes which appeared to be subsiding after the cessation of direct exposure to PCBs. The statistical association between serum levels of PCBs and lipids reported by others was confirmed, but shown to be explained by the partitioning behavior of PCB in the body, rather than to changes in liver function. No evidence for health impairment related to PCBs was found, despite the high serum levels of PCBs in the study population.
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PMID:Effects of PCB exposure on biochemical and hematological findings in capacitor workers. 286 33

Hepatocytes from rainbow trout reared on a diet containing cyclopropenoid fatty acids were analyzed for alterations in protein composition and synthesis by double label experiments. Both cytosolic and microsomal hepatocyte fractions were investigated. In the cytosolic fraction, the synthesis of proteins in the range of 68,000 to 74,000 daltons were significantly decreased. The identity of these proteins remains uncertain. A pronounced depression in both the mass and apparent synthesis of a 200,000 to 240,000 dalton microsomal protein was also observed. Immunoblotting with antibodies raised against goose acetyl-CoA carboxylase and avidin-peroxidase staining suggest that this protein is acetyl-CoA carboxylase. Moreover, synthesis of this protein as well as mass of the protein in cyclopropenoid fatty acid-fed fish were less than 20% of that found in control fish.
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PMID:Alterations in the synthesis of proteins in hepatocytes of rainbow trout fed cyclopropenoid fatty acids. 287 26

The most widely used H2-receptor antagonist, cimetidine, is known to interact with cytochrome P-450 drug-metabolizing enzymes and, therefore, interacts with other drugs which may be administered concurrently. In this study, effects of three H2-receptor antagonists, famotidine, ranitidine, and L-643,441, on drug interaction were studied using cimetidine as a positive control. Cimetidine and L-643,441, but not famotidine or ranitidine, prolonged antipyrine elimination and hexobarbital-induced sleeping time. The effect of cimetidine and famotidine on the anticoagulant effect on warfarin in rats was also investigated. Pretreatment of rats with cimetidine produced a significant depression of plasma prothrombin complex activity, whereas concomitant administration of famotidine did not alter the plasma prothrombin complex activity. Whereas cimetidine is known to impair the elimination of a number of drugs metabolized by microsomal mixed function oxidase enzyme systems, the results of the present study suggest that famotidine and ranitidine have little effect on these enzyme systems.
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PMID:Comparative effects of H2-receptor antagonists on drug interaction in rats. 287 21

The effects of normobaric hyperoxia on both microsomal membrane fluidity and mechanism of phospholipid synthesis in rabbit liver and kidney have been studied. Hyperoxia induces in both organs an impairment of de novo synthesis of glycerolipids which could be due to an inactivation of acyltransferase activities involved in the initial formation of phosphatidic acid. The ability to replace phospholipid fatty acids by reacylation mechanism decreases slightly in the hyperoxic kidney, while it does not change in the hyperoxic liver. Concerning the effect of high arterial pO2 on microsomal membrane fluidity, the hyperoxic liver shows a more fluid environment within the membrane core of microsomes; however, no difference was shown in that of microsomal membrane core of hyperoxic kidney. An insight into the lipid composition of microsomes indicates that liver microsomal membranes have lower cholesterol content and higher unsaturation degree of phospholipid fatty acids, whereas hyperoxic kidney microsomes become more saturated and did not show any difference in their cholesterol content. In both hyperoxic liver and kidney microsomes, phospholipid content decreases in agreement with the depression of phosphatidic acid biosynthesis. These results are discussed in relation to the values of microsomal membrane microviscosity obtained.
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PMID:Lipid alterations in liver and kidney induced by normobaric hyperoxia: correlations with changes in microsomal membrane fluidity. 288 41

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

Induction of xanthine oxidase in mouse liver by interferon (IFN) was studied with three different recombinant human leukocyte IFN molecules: IFLrA, IFLrD and the hybrid IFLrA/D(Bgl II). The ability of different IFN species to induce xanthine oxidase correlated with their ability to depress liver cytochrome P-450-dependent drug metabolism, supporting the hypothesis that reactive oxygen metabolites generated by xanthine oxidase might be responsible for this impairment of liver function by IFN. The antioxidant N-acetylcysteine protected in vivo against the depression of liver drug metabolism by IFLrA/D. IFLrA/D was also found to induce liver microsomal heme oxygenase, an effect that was probably secondary to the observed depression of cytochrome P-450.
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PMID:Induction of xanthine oxidase and heme oxygenase and depression of liver drug metabolism by interferon: a study with different recombinant interferons. 301 3

The subcellular distribution of the 5'-nucleotidase activity was investigated in normal and hypertrophied pig hearts; normal rat hearts were used for comparison. The left ventricular hypertrophy was induced in pigs by banding the supravalvular aorta for 4, 8 and 12 weeks. By employing different procedures for the isolation of cardiac membranes, a major catalytic site for 5'-nucleotidase was found to be located at sarcolemma in rat heart and microsomes (sarcoplasmic reticulum) in pig heart. A progressive decrease in the homogenate and microsomal 5'-nucleotidase activity occurred upon the development of myocardial hypertrophy in pigs. This reduction in microsomal 5'-nucleotidase activity was characterized by a depression in both apparent Vmax and Km values. These results indicate that a primary 5'-nucleotidase pool is present in the intracellular compartment of the pig heart and is altered during the development of hypertrophy.
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PMID:Subcellular distribution of cardiac 5'-nucleotidase: alteration of microsomal pool in hypertrophied pig heart. 301 68

We evaluated the possibility that oxyions of vanadium might react with molybdate and, in that manner, interfere with the Fiske-Subbarow colorimetric determination of inorganic phosphate. Phosphate (Pi) standard curves were prepared (0.03-0.30 mumole/ml) in the presence and absence of oxyvanadium solutions (2 X 10(-4) M) prepared from ortho- and metavanadate. Molybdate prepared in 5 N sulfuric acid was added to each standard. Upon addition of a reducing agent to develop color of the phosphomolybdate complex, a less intense color was observed at any given Pi concentration in the presence of oxyvanadium species. The slope of the regression line for the Pi standard curve in the presence of 2 X 10(-4) M oxyvanadium species was markedly depressed. The effect of oxyvanadium was similar when solutions were prepared from ortho- and metavanadate, despite differences in pH of these solutions. In addition, in the final reaction the pH was similar in the presence and absence of oxyvanadium, independent of the source of vanadate used to prepare solutions. Thus, interference by oxyvanadium did not appear to be related to changes in pH of samples containing vanadium oxyions. Interference was concentration dependent and the minimal concentration of vanadium oxyions that interfered was 5 X 10(-5) M. The effects of oxyvanadium (2 X 10(-4) M) on Mg+2-dependent and Na+-K+-ATPase activities in a renal microsomal preparation were then evaluated through the measurement of inorganic phosphate generation. Enzyme activities were determined with and without correction for interference by oxyvanadium with the method of Fiske and Subbarow. A significant artifactual depression of Mg+2 ATPase activity, but not Na+-K+-ATPase activity, was consistently observed when enzyme activities were not corrected for interference by oxyvanadium with the measurement of inorganic phosphate. These data indicate that when effects of high vanadate concentrations (5 X 10(-5) M) on ATP hydrolyzing enzymes are evaluated through changes in Pi generation, artifactual depression of enzyme activity may occur.
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PMID:High vanadate interferes with the Fiske-Subbarow determination of inorganic phosphate. 302 May 67

Imipramine administration (50 mg kg-1, i.p.) to Sprague-Dawley male rats (240-290 g) 6 or 10 h after CCl4 (1 ml kg-1, i.p.) partially prevents liver necrosis induced by the hepatotoxin. When imipramine is given 30 min before CCl4, it inhibits in part the CCl4-induced lipid peroxidation and the covalent interactions of reactive metabolites with microsomal lipids or proteins and partially prevents CCl4-induced cytochrome P-450 destruction, but not glucose 6 phosphatase activity depression. Imipramine administration prior to CCl4 does not modify levels of the hepatotoxin reaching the liver or the body temperature of CCl4 treated animals. Early preventive effects of imipramine on cytochrome P-450, might be attributed to inhibition of covalent interactions of reactive metabolites. The hypothesis that imipramine exerted late preventive effects by interfering with calcium deleterious effects or by modulation of protein and phospholipid synthesis or degradation is analyzed.
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PMID:Imipramine prevention of carbon tetrachloride-induced liver necrosis at late states of the intoxication process. 302 54

The relationship between the development of galactose-induced cataractogenesis and rat lens microsomal prostaglandin (PG) biosynthesis was studied. Within 24 hr of the introduction of 50% galactose to the rat's diet, lens PGF2 alpha production fell dramatically to 31% of control. Following the initial depression of PGF2 alpha biosynthesis, the ability to generate PGF2 alpha in lens microsomes slightly recovered reaching 58- and 53% of controls at day 2 and day 5 on the sugar diet, respectively. Determination of microsomal PGF2 alpha biosynthesis at 9- and 21 days revealed a continued decline in PG synthesis with complete cessation of PGF2 alpha synthesis by day 36 (hypermature cataracts, +5). The decreased PGF2 alpha biosynthetic capacity was a result of decreased cyclo-oxygenase activity since: PGE2 production demonstrated a similar time course for inhibition; and lens microsomes from control and galactose fed rats revealed no difference in the PGs produced from PGH2 endoperoxide. Neither galactose (1 mM) nor galactitol (1 mM), when added to control microsomal preparations inhibited PG biosynthesis, eliminating the possibility of a direct effect of the sugar, or its metabolite, on cyclo-oxygenase activity. While PG biosynthesis was rapidly inhibited by the galactose feeding no changes were observed in basal lens cyclic AMP levels measured during the first 5 days of the feedings. These results demonstrate that depressed PG biosynthesis is an early consequence of galactose feeding.
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PMID:Rat lens prostaglandin biosynthesis during galactose-induced cataractogenesis. 302 46


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