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 phenol, guaiacol and m-cresol on erythrocytes, hepatocytes, dipalmitoyl phosphatidylcholine (DPPC)-liposomes and surface tension were studied at various concentrations. Phenol at 10 mM caused a slight inhibition of hypotonic hemolysis in rat erythrocytes. Guaiacol at 4 and 10 mM and m-cresol at 0.6 to 10 mM caused a significant inhibition of hypotonic hemolysis. In the enzyme leakage from isolated rat hepatocytes, phenol at 0.001 to 0.4 mM and 2 to 10 mM, guaiacol at 2 to 10 mM and m-cresol at 0.001 to 4 mM caused an inhibition in GOT leakage. The leakage of GPT from hepatocytes was inhibited by phenol at 0.4 to 10 mM, guaiacol at 2 to 10 mM, and m-cresol at 0.001 to 4 mM. m-Cresol at 10 mM caused increases in GOT and GPT leakage. The inhibition of phenol and m-cresol on the LDH leakage in hepatocytes were observed at a concentration of 0.001 mM and 0.1 to 1 mM, respectively. Guaiacol or m-cresol at 10 mM caused an increase in LDH leakage. Phase-transition temperature of DPPC-liposomes was depressed by phenol and m-cresol at 1 to 10 mM and by guaiacol at 5 and 10 mM. Guaiacol at 1 and 10 mM and m-cresol at 10 mM caused a depression of surface tension, but phenol caused no change in surface tension. The order of effects on erythrocyte, hepatocyte and DPPC-liposome membranes was m-cresol greater than phenol greater than or equal to guaiacol. In the present study, phenol and its related compound showed a positive correlation between their effects on various membranes and germicidal effects as evaluated by the phenol coefficient, but the effects were not related to a depression of surface tension.
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PMID:[Effects of phenol and related compounds on erythrocytes and hepatocytes from rats and dipalmitoyl phosphatidylcholine-liposomes]. 360 69

The effect of essential oils, eugenol, thymol and menthol, on erythrocytes, hepatocytes, dipalmitoyl phosphatidylcholine (DPPC)-liposomes and surface tension were studied at various concentrations. Maximal inhibition of eugenol, thymol and menthol on the hypotonic hemolysis in rat erythrocytes were observed at a concentration of 2 mM, 1 mM and 1 mM, respectively. Eugenol at 4 mM and thymol at 2 mM caused an acceleration of hypotonic hemolysis. In isolated rat hepatocytes, thymol caused an increase in GOT leakage, but eugenol at 4 mM and menthol at 0.1 and 0.4 mM inhibited the GOT leakage. The leakage of GPT from hepatocytes was inhibited by eugenol at 0.1 mM and 0.4 to 4 mM and menthol at 0.1 to 0.6 mM. The inhibition of eugenol and menthol on the LDH leakage in hepatocytes were observed at a concentration of 0.001 to 4 mM and 0.1, 0.4 and 0.6 mM, respectively. Thymol caused no change in GPT and LDH leakage. Eugenol, thymol and menthol indicated a depression of surface tension at a concentration of 0.1 mM. The rank by order of surface activity was eugenol greater than thymol. Eugenol, thymol and menthol depressed the phase-transition temperature of DPPC-liposomes. The depression of phase-transition temperature by thymol was greater than that by eugenol and menthol. These results suggest the periapical tissue damage produced by essential oils may be related to membrane lysis and surface activity and that their tissue penetration may be related to membrane affinity and lipid solubility.
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PMID:Effects of essential oils on erythrocytes and hepatocytes from rats and dipalmitoyl phosphatidylcholine-liposomes. 362 86

Phagocytic activity as a function of the reticuloendothelial system (RES) has been studied in CCl4-induced liver injury by using the carbon clearance test. Liver damage in mice was induced by administration of 20% CCl4 in olive oil (p.o.). After a single administration of CCl4, significant increases in liver/body weight ratio, serum GOT and GPT levels, alpha, beta and gamma-globulins and BSP retention, and decreases in serum albumin, an activity of the hepaplastintest and the correct phagocytic activity, alpha value, were found. After 15 administrations of CCl4 (3 times a week), mild increases in serum GPT level and BSP retention and decreases in the activity of the hepaplastintest and both phagocytic indices, K and alpha values, were observed. However, zymosan treatment 3 days before sacrifice induced an increase in K value depressed by multiple administrations of CCl4. The depression of carbon uptake by Kupffer cells can be seen by light microscopy after multiple administrations of CCl4 compared with that of saline and olive oil. These findings indicate that the RES phagocytosis is suppressed more strongly in chronic liver injury by 15 CCl4 administrations than in acute injury by a single one, although the biochemical parameters indicating liver injury are shown to have an opposite tendency. A clear correlation between the alteration of RES activity and the degree of liver injury was not noted.
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PMID:Function of reticuloendothelial system on CCl4 induced liver injury in mice. 409 93

New antitumor anthracycline antibiotic, aclacinomycin A was given to dd-mice and Wistar rats for acute toxicity study. The LD50 values were 29 approximately 39 mg/kg (i.v., i.p. and s.c.) and 62 approximately 69 mg/kg (p.o.) in mice, and 18 approximately 28 mg/kg (i.v., i.p. and s.c.) and 58 approximately 59 mg/kg (p.o.) in rats, respectively, which were calculated by mortality rate during a 14 day observation period. Depression of spontaneous activity, anorexia, diarrhea and slight alopecia were observed. Autopsy findings in animals killed by drug included atrophy of the thymus and spleen, and hyperemia and hemorrhage in the stomach and intestines. But no remarkable change was found in animals which survived through the observation period. Mongrel dogs were given the drug intravenously at 3, 5, 7.5, 10 and 15 mg/kg, respectively. All dogs (3/3) in the three higher dose groups and 1/3 dog in 5 mg/kg dose group died within day 0 approximately 5. Others survived more than 27 days. Depression of spontaneous activity and anorexia were found from 30 minutes to 2 hours after administration, followed by vomiting and diarrhea. Increase of GOT, GPT and LDH and decrease of WBC count were detected in dogs which died. Hyperemia and hemorrhage of the lungs, stomach and intestine were found among the groups given higher doses, whereas no significant changes were recognized among the two lower dose groups.
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PMID:[Acute toxicity of aclacinomycin A in mice, rats and dogs (author's transl)]. 692 57

KW2083 7-N-(p-hydroxyphenyl) mitomycin C is a mitomycin C derivative, but not its masked compound. KW2083 differs from mitomycin C in various points. A phase I study of KW2083 by single intravenous injection was performed in 21 patients with advanced solid tumor. The dose limiting factor of this drug is marrow depression, and 70mg/m2 causing marked thrombocytopenia was determined as maximum tolerated dose. The thrombocyte count and the WBC count reached to nadir the minimum 2 to 3 weeks after and 1 to 2 weeks after the administration and recovered in 1 to 2 weeks and in 2 to 3 weeks respectively. As gastrointestinal symptoms, nausea or vomiting (38.1%), and anorexia (28.6%) occurred soon after the administration, and stomatitis and diarrhea were also observed in one case each. In addition, petechia, hemorrhagic tendency and fever were found in one case each. Patients receiving 70mg/m2 showed slight alopecia and transient slight in GOT and GPT elevation.
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PMID:[Phase I study of KW2083 7-N-(p-hydroxyphenyl) mitomycin C]. 718 79

The oral administration of CCl4 (2.5 ml/kg) to male rats inducted increase in the activity of serum GPT, accumulation of hepatic triglyceride, acceleration of depression in the activities of microsomal enzymes, disaggregation of hepatic polyribosomes, and decrease in the ability of in vitro protein synthesis 0.5 hr after the intubation. When, however, a small dose of CCl4 (0.25 ml/kg) were given, the defects in hepatic polyribosomes and mixed-function oxygenase system were most marked among the above toxic changes.
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PMID:Microsomal injury in the liver of rats treated with carbon tetrachloride. 727 27

The response of hepatic and haemotopoetic functions to treatment with praziquantel was studied using healthy and schistosome-infected mice. Female CF1 mice harbouring an 18 week old infection with Schistosoma mansoni and healthy uninfected mice of the same age were orally treated with 1 x 250 mg praziquantel/kg. The respective uninfected controls received the vehicle only. Blood samples were taken one, five, 14 and 28 days after treatment. Parameters studied were: activity of GOT, GPT and AP, concentration of glucose, blood clotting time, haemoglobin content, erythrocyte and leucocyte counts, PCV and body weight. The data were analyzed to reveal the effect of the three independent variables involved: infection, treatment and time after treatment. Infection of mice with S. mansoni for 18 weeks resulted in a depression of body weight, in a decrease of plasma GOT activity and of PCV and in increases of plasma GPT and AP activities, leucocyte counts and clotting time. Plasma glucose concentrations remained unaffected. The effects of treament with praziquantel were confined to the infected group. Changes attributable to the variable time were also more pronounced or even restricted to the infected treated group. Treatment of infected mice with praziquantel resulted in a temporary elevation of plasma GOT and GPT activities on Day 1 after treatment. Values had returned to normal on Day 5. Treatment further resulted in a slight but prolonged elevation of AP activities, a high leucocyte count on Day 5 after treatment and a normalization of the underweight and anaemic state of the infected mice. The nature of the effects observed after treatment with praziquantel is discussed in the light of corresponding data on the effect of treatment with hycanthone and SQ 18.506 in schistosome infected mice and Mastomys. It is concluded that the changes observed can be regarded as secondary, reflecting host responses to damaged parasites and healing processes.
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PMID:Effect of praziquantel on clinical-chemical parameters in healthy and schistosome-infected mice. 743 2

Activity of some enzymes (GOT, GPT, OCT, AP, GGTP, HE) was studied in a group of 74 workers, exposed to professional chronic combined pesticide effects. Enzyme changes were followed up depending on exposure. There was a statistically significant increase in GOT, GPT and OCT activities and decrease in HE. Paralleling this, an insignificant depression of AP and GGTP in comparison with the control group was observed. The relationship between these enzyme changes and liver function are discussed. Implication of toxic factor in the development of these changes is suggested.
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PMID:[Enzymatic changes in chronic pesticide exposure]. 744 53

99mTc-DTPA-galactosyl human serum albumin (99mTc-GSA) is a new liver imaging agent which binds to heptic binding protein. This study evaluated the sensitivity of 99mTc-GSA kinetics and imaging anatomy to congestive hepatic injury in rats. Regional hepatic congestion was induced by clamping the left hepatic vein for 5, 10, 20, 40, or 90 min. After recanalization, 99mTc-GSA was intravenously administered to rats. A dynamic imaging study was performed, followed by static liver imaging performed for 5 min. A hepatic accumulation index, t90, was obtained on the basis of the dynamic data. A significant difference in t90 was observed between the experimental groups and the controls (p < 0.01). A significant difference in s-GPT also was observed between the experimental groups and the controls (p < 0.01). Excellent correlations were seen between t90 and ligation time (r = 0.967, p < 0.001), and t90 and s-GPT (r = 0.907, p < 0.001). Marked depression in hepatic 99mTc-GSA uptake was observed in rats with 40 or 90 min of hepatic vein occlusion. In conclusion, 99mTc-GSA is useful for evaluating hepatic injury in rats induced by hepatic vein occlusion.
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PMID:[Usefulness of 99mTc-GSA liver scintigraphy in evaluating hepatic injury in rats induced by temporary hepatic vein occlusion]. 802 58

An inverse relation is known to link blood potassium with renal synthesis and the release of ammonia. Given the liability of hyperammonemia for precipitating hepatic encephalopathy (HE), 28 patients affected by stage I HE were equally divided into two groups and maintained up to their death at the highest (5.4-5.5 mEq/l) or the lowest (3.5-3.6 mEq/l) normokalemia levels. When compared with the lowest normokalemia group, the highest one showed an early, albeit transient, improvement in the mental state (as assessed by both EEG and psychiatric investigations) and to a lesser extent in hepatic functions (as assessed by the variations in serum bilirubin, GPT, GGT and plasma prothrombin time). In the highest normokalemia group the survival was also prolonged. The cause of this improvement may be related to the induced decrease in blood pH, the consequent depression of renal ammoniagenesis and the rise in the arterial and urine NH+4/NH3 ratios. These factors reduce the entry of ammonia into the cells and enhance the urinary excretion of this metabolite, respectively.
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PMID:The importance of the highest normokalemia in the treatment of early hepatic encephalopathy. 816 17


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