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)

The effects of chronic dietary exposure to technical pentachlorophenol (PCP-T) on humoral immune responses in mice were examined. Primary and secondary splenic antibody responses to the T-dependent antigen, sheep red blood cells (SRBC), were examined in Swiss-Webster mice using our recently developed screening technique, the Hemolytic Antibody Isotope Release (HAIR) assay. To assess direct effects of PCP-T on B cells, the splenic plaque-forming cell response and serum antibody titers to the T-independent antigen, dinitrophenyl (DNP)-Ficoll, were examined. PCP-T exposure altered both the kinetics and the magnitude of the humoral antibody responses to SRBC and DNP-Ficoll. Peak splenic antibody production and serum antibody titers were delayed and the magnitude of the antibody responses were dose-dependently suppressed by PCP-T exposure. IgM responses appeared to be more sensitive to PCP-T-induced suppression than the IgG response. Significant depression of the IgM anti-SRBC splenic HAIR response was apparent as early as 2 weeks after initiation of PCP-T exposure and persisted for at least 8 weeks after termination of PCP-T feeding. Liver weight and serum lactate dehydrogenase (LD-L) and alanine aminotransferase (ALT) levels were significantly elevated during PCP-T exposure and returned to control levels after a 4-6 week recovery period. The immunotoxic effect of PCP on humoral immunity was observed only in animals exposed to technical grade PCP known to be contaminated with significant levels of other chlorinated phenols as well as non-phenolic impurities including chlorinated dioxins, furans, and diphenyl ethers. Animals exposed to analytical grade PCP did not exhibit depressed humoral immunity.
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PMID:Immunotoxicity of technical pentachlorophenol (PCP-T): depressed humoral immune responses to T-dependent and T-independent antigen stimulation in PCP-T exposed mice. 676 29

Pulps from rat incisor have been dissected out and the respiratory activity in the tissues has been measured in a Gilson respirometer (modified Warburg technique). Local anesthetics lidocain (xylocain) and prilocain (citanest) in concentrations 2.5%, 5%, and 10% have been added to the medium. Effects on the membrane permeability i.e. on the potassium-sodium pump has been studied using incubation at 37 degrees C in 24NaCl. The influx of 24Na has been registered in a scintillation counter. The anaerobic respiratory activity has been studied determining lactate dehydrogenase activity with a spectrophotometric technique. The results show that the concentrations of local anesthetics in the medium of 5% and 10% caused a significantly lower respiratory activity of the cells in the dental pulp. This was not the case in the concentration 2.5%. The isotope studies show a decreased uptake in all concentrations indicating a depression of the potassium-sodium pump activity. The lactate dehydrogenase activity was significantly lower in all concentrations of local anesthetics.
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PMID:Effects of local anesthetics on aerobic and anaerobic metabolism of the dental pulp. 693 6

The effect of 19 antimicrobial agents on human polymorphonuclear leukocyte function was evaluated by chemiluminescence assays, yeast phagocytosis and killing, and lactate dehydrogenase release. Tetracycline and trimethoprim inhibited chemiluminescence and reduced killing at therapeutic concentrations of 2 microgram/ml. Cephalothin inhibited yeast killing at a concentration of 20 microgram/ml, but a significant depression of polymorphonuclear leukocyte chemiluminescence was encountered only at higher levels of 200 microgram/ml. The inhibition shown by these drugs was reversible. None of the other antimicrobial agents tested demonstrated inhibition of chemiluminescence, phagocytosis, or killing at usual clinical serum levels. No antimicrobial agent tested caused release of lactate dehydrogenase from polymorphonuclear leukocytes. The results suggest that therapeutic concentrations of tetracycline, trimethoprim, and cephalothin may inhibit optimal polymorphonuclear leukocyte microbicidal function.
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PMID:Effect of antimicrobial agents on human polymorphonuclear leukocyte microbicidal function. 702 50

True reference values (TRV) should ultimately be determined in blood from inactive, unstimulated rats but in practice, acceptable reference values (ARV) may be established using blood from decapitated or anesthetized animals if one is cognizant of variations associated with blood sampling procedures. Data reported here illustrate some variations in serum biochemical values following decapitation or anesthesia. Decapitation does not provide serum in which ARV for sodium, potassium or lactate dehydrogenase can be found but ARV can be determined for glucose, insulin and several other parameters. It is suggested that both TRV and ARV for serum electrolytes be determined using serum from cannulated rats. All three anesthetics raised glucose levels and ether and halothane increased alkaline phosphatase activity. Both halothane and Innovar-VetR decreased insulin:glucose ratios suggesting inhibition of insulin release from the pancreas. Innovar-VetR also produced hypoxia due to severe respiratory depression and bradycardia as well as hyperuricemia, hyperglycemia and hyperphosphatemia. Techniques most likely to provide ARV should be of the shortest possible duration, afford least respiratory and cardiovascular suppression and minimize stimulation of the sympathetic nervous system.
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PMID:Variation of rat serum biochemical values following decapitation or anesthesia with ether, halothane or Innovar-VetR: rapid Innovar-VetR-induced hyperuricemia and hyperglycemia. 704 81

Short-term exposure of mice to low O3 doses, as defined by the product of concentration and exposure time (ct), was observed to induce alterations in two enzyme systems: first, that leading to changes in hepatic reduced ascorbic acid (RAA) content, and second to changes in plasma creatine phosphokinase (CPK) activity. RAA alterations were noticed immediately, 30 min and 120 min after termination of the exposure period, whereas CPK showed alterations immediately and 15 min after termination of the exposure. Later determinations, i.e., 24 hr after O3 exposure for RAA and 30 min after 03 exposure for CPK, revealed no significant differences when compared to control animals. Although differences in sensitivity existed, the dose response curves for both systems were more or less similar, showing a short decrease for the initial very low O3 doses, followed by a profound rise and a gradual decrease to control levels for subsequent ct doses. Exceptions were the 30 min curve for RAA and the immediate curve for CPK in so far as that both showed an additional depression. Neither plasma histamine nor plasma lactic acid dehydrogenase (LDH3) were observed to be altered by the range of O3 doses employed. These findings were explained on the basis of adaptation of the organism to a potentially noxious O3 stimulus by enhanced metabolic processes: a weak stimulus leading to only a small adjustment, and stronger stimuli to elevated enzyme activity as well. With increasing doses of O3 this elevation in enzyme activity was found to be gradually diminished, possibly due to a steadily growing demand, leaving the overshoot becoming continually smaller until a balanced state is achieved.
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PMID:Distinct enzymatic responses in mice exposed to a range of low doses of ozone. 723 52

Furazolidone (FZ) at a dose of 700 ppm was fed to turkey poults beginning at 2 weeks of age. In trial 1, plasma collected by venipuncture was assayed for glutamic oxalacetic transaminase (GOT), lactate dehydrogenase (LDH), and total protein at 19, 23, 26, and 30 days of age. Significant (P less than or equal to .05) differences were noted only in levels of plasma LDH, which were elevated in FZ-fed poults at all stages studied. In Trial 2, plasma collected by venipuncture was assayed for creatine phosphokinase (CPK), GOT, glutamic pyruvic transaminase (GPT), and LDH daily from 15 through 19 days of age and for protein at 19 days of age. Significant elevations (P less than or equal to .05) were noted in levels of plasma a) CPK at 15 days, b) GOT at 18 days, and c) LDH at 17 and 19 days. A significant (P less than or equal to .01) depression in plasma protein was observed at 19 days. Plasma GPT was either absent or present in very low concentrations. These data suggest that FZ exerts its primary effect on the myocardium. THe initial myocardial changes occur prior to their detection by known electrocardiographic (ECG) technics.
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PMID:Effect of furazolidone on plasma enzyme and protein levels in turkey poults. 732 76

Effects of daily dosing with bitterweed (Hymenoxys odorata) on voluntary feed consumption and concentrations of serum constituents were determined in 2 experiments, using 12 lambs each. Feed intake decreased linearly as the bitterweed dose increased. Serum total protein and albumin decreased and urea nitrogen, creatinine, and total bilirubin increased with the increasing bitterweed dose. Serum lactic dehydrogenase, aspartate transaminase, and creatine kinase activities increased at the highest bitterweed dose (0.264% of live body weight/day, air-dry basis). Depression in voluntary feed intake was more sensitive to the bitterweed dose than were serum constituents. This dose-related decrease in ad libitum feed intake provides a useful and less expensive short-term assay for assessing treatments for reducing bitterweed toxicosis, compared with the customary LD50 tests.
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PMID:Effects of bitterweed (Hymenoxys odorata) on voluntary feed intake and serum constituents of sheep. 732 32

Succinylcholine chloride administered to horses anesthetized with halothane in oxygen and mechanically ventilated, caused slight but statistically insignificant (P less than 0.01) increases in creatine phosphokinase, lactic dehydrogenase, and aspartate aminotransferase activity. The increases in these enzymes have been explained on the basis of muscle damage resulting from succinylcholine chloride induced muscle fasciculations and by hypoperfusion of tissues due to depression of the cardiovascular system caused by general anesthesia. These changes were not clinically apparent based upon the absence of myoglobinuria and ease of recovery. There was no significant effect of treatment observed on other biochemical variables. The findings in the present study agree with previous observations on serum creatine phosphokinase, lactic dehydrogenase, and aspartate aminotransferase activity.
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PMID:Biochemical effects of succinylcholine chloride in mechanically ventilated horses anesthetized with halothane in oxygen. 740 95

Thirteen biochemical parameters (viz. glucose, calcium, inorganic phosphorous, urea nitrogen, uric acid, cholesterol, albumin, total protein, total bilirubin, alkaline phosphatase, lactate dehydrogenase, aspartate aminotransferase, and alanine aminotransferase) were determined in serum and partly in liver of rats 1-28 days after i.p. aflatoxin B1 (AFB) (3 mg/kg). Histological examinations of the liver were also made in parallel to the biochemical studies. In the serum, enzyme activities and total bilirubin level increased and peaked on the 2nd day, while other activities of aspartate aminotransferase and alanine aminotransferase in the liver significantly decreased and reached a minimum on the 2nd day after AFB administration. The depression of the liver enzyme activities persisted over 7 days. The liver protein content also reduced transiently during 1-1.5 days. However, all biochemical parameters returned to normal levels 2 weeks after treatment, and remained so throughout the rest of experimental period. Histological changes in the liver were very similar to those reported by other.
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PMID:Sequential biochemical and histological changes in rats treated with aflatoxin B1. 742 38

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


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