Rat serum and liver homogenate enzymes splitting N-acetyl-L-tyrosine ethyl ester

1968 ◽  
Vol 33 (10) ◽  
pp. 3366-3371
Author(s):  
M. Petáková ◽  
E. Simonianová ◽  
O. Jozová ◽  
M. Rybák ◽  
J. Hladovec
Keyword(s):  
Ethyl Ester ◽  
Liver Homogenate ◽  
Rat Serum

Rat serum hydrolases cleaving N-acetyl-L-tyrosine ethyl ester

1974 ◽  
Vol 39 (7) ◽  
pp. 1925-1932
Author(s):  
E. Simonianová ◽  
M. Petáková
Keyword(s):  
Ethyl Ester ◽  
Rat Serum

Inhibition of passive anaphylaxis induced in the rat hind paw and peritoneal cavity by N-(2-oxo-3,5,7-cycloheptatrien-l-yl)-aminooxoacetic acid ethyl ester (AY-25,674)

1978 ◽  
Vol 56 (6) ◽  
pp. 1005-1010 ◽  
Author(s):  
R. R. Martel ◽  
J. Klicius ◽  
J. Pinski
Keyword(s):  
Mast Cells ◽  
Ethyl Ester ◽  
Peritoneal Cavity ◽  
Immunoglobulin E ◽  
Acid Ethyl Ester ◽  
Disodium Cromoglycate ◽  
Activity Profile ◽  
Rat Serum ◽  
Short Time ◽  
Orally Active

Passive anaphylaxis induced in the rat hind paw and peritoneal cavity with rat serum containing immunoglobulin E antibody was inhibited by N-(2-oxo-3,5,7-cycloheptatrien-1-yl)-aminooxoacetic acid ethyl ester (AY-25,674). In contrast with disodium cromoglycate (DSCG), AY-25,674 was orally active. Otherwise, the activity profile of AY-25,674 was similar to that of DSCG. Peak activity occurred a short time after administration, large doses produced tachyphylaxis, and anaphylactic histamine release from mast cells was inhibited. AY-25,674 did not inhibit increased vascular permeability produced by nonreaginic antibody, compound 48/80, serotonin, or histamine. It is concluded that AY-25,674 produces its antiallergic effects by inhibiting mediator release from mast cells by a mechanism similar to that of DSCG.

scholarly journals The study of lipotropic action of extract from fruit prunus domestica «Prunofit» byanimal models of alcoholic liver diseases

2020 ◽  
pp. 86-91
Author(s):  
V. M. Kravchenko ◽  
Z. V. Shovkova ◽  
I. V. Senyuk ◽  
O. V. Shovkova
Keyword(s):  
Fatty Acids ◽  
Liver Damage ◽  
Unsaturated Fatty Acids ◽  
Folk Medicine ◽  
Liver Homogenate ◽  
Total Lipids ◽  
Prunus Domestica ◽  
Rat Serum ◽  
Reference Drug ◽  
Irritable Bowel

Searchingof drugs that normalize the function of the digestive glands are important because disruption of digestion underlie the pathogenesis of many diseases such as gastroesophageal reflux disease, hepatitis, gastric ulcer, irritable bowel syndrome, cancer etc. The use of herbal objects containing fibres is a promising direction for solving of the mentioned problem. We were attracted by fruits of Prunus domestica which are rich in fibres (homo- and heteropolsaccharides) and are used in folk medicine as a laxative and hepatoprotective agent. The aim of this experimental study was to investigate the lipotropic properties of «Prunofit» extract. The study of lipotropic properties of the «Prunofit» was carried out in the conditions of subacute toxic liver damage caused by the introduction of ethanol.The content of total lipids (TL), total cholesterol (TCh), triacylglycerols (TGs), unsaturated fatty acids (UFA) and total phospholipids (TPL) were determined in liver and blood serum. Obtained results of the lipotropic properties study of the «Prunofit» extract at a dose of 200 mg/kg against the background of alcoholic liver damage showed a decrease in the intensity of lipolysis, fatty hepatosis, and manifestations of hyperlipidemia. It has occurred due to a decrease in the content of total lipids, cholesterol, triglycerides and free fatty acids in the homogenate rat liver by 27.9%, 7.2%, 27.5% and 38%, respectively, and rat serum by 28%, 42.2%, 8.15%, 47.1%, respectively, compared with the control pathology. Against the background of model pathology, «Prunofit» extract tended to increase the content of total phospholipids in the liver homogenate by 37.34% and in serum by 30.2% compared with the control pathology. According to its ability to inhibit fatty liver infiltration, the «Prunofit» extract was at the level of the reference drug «Methionine» at a dose of 155 mg/kg.

Hydrolysis of esters and amides of 20R- and 20S-dihydroprednisolonic acid in rat serum and liver homogenate

1989 ◽  
Vol 12 (2) ◽  
pp. 68-72
Author(s):  
Kue Jeong Yeon ◽  
Si Myung Byun ◽  
Henry J. Lee ◽  
Sean Hyang Lee ◽  
Hyun Pyo Kim
Keyword(s):  
Liver Homogenate ◽  
Rat Serum ◽  
Hydrolysis Of Esters ◽  
Hydrolysis Of

FUNCTIONAL HETEROGENEITY OF THE THYROID AND POSSIBLE PRESENCE OF IODOTYROSINE-LIKE COMPOUNDS IN NORMAL SERUM

1965 ◽  
Vol 48 (2) ◽  
pp. 199-208 ◽  
Author(s):  
J. D. Wiener
Keyword(s):  
Human Subjects ◽  
Thyroid Tissue ◽  
Normal Serum ◽  
Schematic Model ◽  
Functional Heterogeneity ◽  
Rat Serum ◽  
Iodine Metabolism ◽  
Normal Rat ◽  
Isotope Equilibrium ◽  
Equilibrium Experiment

ABSTRACT After the administration of 131I to normal animals or human subjects, labelled thyroxine and triiodothyronine, but at most traces of labelled iodotyrosines can be detected in the serum. However, several investigators using various methods claim to have found considerable amounts of one or both of these iodotyrosines when assaying the stable (non-radioactive) iodinated compounds in the serum. Considering the available evidence as convincing for the present, an attempt has been made to explain this discrepancy. A schematic model of the thyroidal iodine metabolism is proposed, based on (a) the hypothesis that the iodotyrosines are present in the circulation in a »masked« form (i. e. protected against deiodination), and (b) the known functional heterogeneity of the thyroid tissue. This heterogeneity should be of a qualitative as well as quantitative nature. As the physical decay rate of 131I is short in comparison with the turnover rate of the masked iodotyrosine pool, an isotope equilibrium experiment with rats was carried out, using the long-lived isotope 125I. The results of this experiment, viewed together with those of a similar investigation published by others, seem to lend support to the proposed mechanism. The presence of non-negligible amounts of a diiodotyrosine-like compound in normal rat serum seems fairly well established.

TSH DETERMINATION IN RAT SERUM BY A HOMOLOGOUS RADIOIMMUNOASSAY

1974 ◽  
Vol 77 (1_Suppl) ◽  
pp. S127
Author(s):  
J. Golstein ◽  
L. Vanhaelst ◽  
M. Bonnyns ◽  
G. Rothenbuchner
Keyword(s):  
Rat Serum

Regulation of insulin-like growth factor-binding protein-1 in rat serum

Diabetes ◽  
1994 ◽  
Vol 43 (2) ◽  
pp. 232-239 ◽  
Author(s):  
M. S. Lewitt ◽  
H. Saunders ◽  
J. L. Phyual ◽  
R. C. Baxter
Keyword(s):  
Growth Factor ◽  
Binding Protein ◽  
Insulin Like Growth Factor ◽  
Rat Serum ◽  
Factor Binding

In Vitro Diabetogenic Effect of Cadmium on Liver

2017 ◽  
Vol 8 (01) ◽  
Author(s):  
Agung Biworo ◽  
Dwi Rezki Amalia ◽  
Gratianus Billy Himawan ◽  
Lisda Rizky Amalia ◽  
Valentina Halim ◽  
...  
Keyword(s):  
Glucose Metabolism ◽  
Liver Homogenate ◽  
Liver Cells ◽  
Male Rats ◽  
Glycogen Level ◽  
Liver Sample ◽  
Km Value ◽  
Cd Exposure ◽  
Menten Constant

The objectives of this study were to determine the effect of cadmium (Cd) on glucose metabolism disruption in liver cells homogenate in vitro. The glucose metabolism disruption was analyzed by measuring the level of liver glucose, glycogen and methylglyoxal (MG), and the activity of glucokinase activity. In this experiment, a liver sample was taken from male rats (Rattus novergicus). Samples then homogenized and divided into four groups with; C served as control which contains liver homogenate only; T1 which contains liver homogenate + 0.03 mg/l of cadmium sulphate (CdSO4); T2 which contains liver homogenate + 0.3 mg/l of CdSO4; and T3 which contains liver homogenate + 3 mg/l of CdSO4. After treatment, liver glucose, glycogen, and MG levels, and glucokinase activity were estimated. The activity of liver glucokinase was estimated by measuring the Michaelis-Menten constant (Km) value. The results revealed that Cd exposure could significantly increase glucose and MG levels, the Km value of glucokinase, and decreased the glycogen level in liver cells (P>0.05). These results indicated that Cd exposure induced the disruption of glucose metabolism in the liver.

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