Effect of Whole-Body Irradiation on the Half-Life of Antipyrine and on the Microsomal Enzyme System of Rats

Enzyme ◽  
1983 ◽  
Vol 30 (3) ◽  
pp. 205-208
Author(s):  
Christian Thiriot ◽  
Francois Gaboriaud ◽  
Pierre Bernard
Keyword(s):  
Half Life ◽  
Enzyme System ◽  
Whole Body ◽  
Microsomal Enzyme

scholarly journals Reconstituted Liver Microsomal Enzyme System That Hydroxylates Drugs, Other Foreign Compounds, and Endogenous Substrates

1973 ◽  
Vol 248 (2) ◽  
pp. 456-460
Author(s):  
Anthony Y.H. Lu ◽  
Wayne Levin ◽  
Susan B. West ◽  
Martin Jacobson ◽  
Dene Ryan ◽  
...  
Keyword(s):  
Enzyme System ◽  
Microsomal Enzyme ◽  
Endogenous Substrates

A rifampicin-induced hepatic microsomal enzyme system for the generation of cyclosporine metabolites

1995 ◽  
Vol 32 (3) ◽  
pp. 141-148 ◽  
Author(s):  
M.B. Tamolang ◽  
W.T. Liu ◽  
H. Pang ◽  
Ying Ren ◽  
P.Y. Wong
Keyword(s):  
Enzyme System ◽  
Microsomal Enzyme ◽  
Hepatic Microsomal Enzyme

Rate of loss of radioiron from mouse and man

1960 ◽  
Vol 198 (4) ◽  
pp. 784-786 ◽  
Author(s):  
John D. Bonnet ◽  
Alan L. Orvis ◽  
Albert B. Hagedorn ◽  
Charles A. Owen
Keyword(s):  
Life Span ◽  
Half Life ◽  
Whole Body ◽  
Entire Body ◽  
Rapid Loss ◽  
Male And Female ◽  
Female Mice ◽  
Steady Rate ◽  
Normal Man ◽  
The Difference

Forty-two male and female mice, 8 weeks old, were given radioiron (Fe59) in doses of 0.006–0.1 µc, containing 0.013–0.17 µg of iron, by intraperitoneal or intravenous routes. Assays of the radioactivity of the whole body revealed an initial rapid loss of Fe59 (15–20%) lasting about 6 days. Thereafter the Fe59 left the mice at a steady rate of 0.39%/day (half-life 180 days). One 34-year-old normal man was given 10.6 µc of Fe59, containing 8.2 µg of iron, intravenously. Based on counts from the entire body, the biologic rate of loss of the Fe59 was about 0.14%/day (half-life 500 days), and there was little or no initial loss such as occurred in the mouse. The Fe59 in the circulating erythrocytes was essentially unchanged for the first 3 months. It then fell to a new level of about 90% of the previous one; the mid-point of the fall was about 120 days after the administration of the radioiron. The difference in the rates of loss of radioiron from mice and man seems to be related primarily to the life span of the circulating red cells.

scholarly journals Characteristics of the rat liver microsomal enzyme system converting cholecalciferol into 25-hydroxycholecalciferol. Evidence for the participation of cytochrome p-450

1979 ◽  
Vol 184 (3) ◽  
pp. 491-499 ◽  
Author(s):  
T C Madhok ◽  
H F DeLuca
Keyword(s):  
Vitamin D ◽  
White Light ◽  
Microsomal Fraction ◽  
Enzyme System ◽  
Initial Reaction ◽  
Microsomal Enzyme ◽  
Reaction Velocity ◽  
Calcium And Phosphorus ◽  
Cytochrome P 450 ◽  
25 Hydroxycholecalciferol

Properties of the rat hepatic cholecalciferol 25-hydroxylase have been studied. An assay system has been developed in which 25-hydroxycholecalciferol production is linear for at least 2h in both homogenates and microsomal fraction. Furthermore, the initial reaction velocity is linearly related to the amount of liver tissue or microsomal fraction. This enzyme system also metabolizes an analogue of cholecalciferol, namely dihydrotachysterol 3, into 25-hydroxydihydrotachysterol 3. The 25-hydroxylase is in the microsomal fraction and not in mitochondria. It has a Km of 44 nM for cholecalciferol and 360 nM for dihydrotachysterol 3. Its activity is not altered by dietary concentrations of calcium and phosphorus. Vitamin D-deficient rats have higher activities of the hepatic 25-hydroxylase than those receiving 25 ng of cholecalciferol daily. The 25-hydroxylase is inhibited by metyrapone. An atmosphere of CO/O2 (9:1, v/v) inhibits the reaction by 87%. This inhibition is partially reversed by white light. Additionally, cholecalciferol and 25-hydroxycholecalciferol competitively inhibit aminopyrine demethylase. These results support the idea that the cholecalciferol 25-hydroxylase is a cytochrome P-450-dependent mono-oxygenase.

Sedation and analgesia in the critically ill

2010 ◽  
pp. 3153-3157
Author(s):  
Gilbert Park ◽  
Maire P. Shelly
Keyword(s):  
Pain Relief ◽  
Critically Ill ◽  
Tracheal Tube ◽  
Critically Ill Patients ◽  
Hepatic Failure ◽  
Half Life ◽  
Enzyme System ◽  
Onset Of Action ◽  
Fast Onset ◽  
Sedation And Analgesia

Nearly all critically ill patients need analgesia, anxiolysis, hypnosis, or measures to help them tolerate their tracheal tube. Although making the patient unconscious may appear the easiest way to achieve this, it is fraught with hazards. Pain relief and tube tolerance—these are the first priority, and usually involves giving opioids. Morphine, which has both analgesic and sedative effects, is the opioid against which others are judged. Remifentanil is a relatively new agent that has properties useful in critically ill patients: fast onset of action, a predictable short half-life (10–21 min), and it is broken down by a nonspecific enzyme system present in plasma such that accumulation does not occur, and the drug wears off rapidly, even after prolonged infusions and in renal or hepatic failure....

scholarly journals Effects of Cimetidine and Phenobarbitone on Paracetamol Induced Hepatotoxic Rats

1970 ◽  
pp. 13-15
Author(s):  
Layla Afroza Banu ◽  
Hosne Ara Begum ◽  
SAR Choudhury
Keyword(s):  
Enzyme System ◽  
Treated Group ◽  
Protective Role ◽  
Significant Rise ◽  
Alanine Transaminase ◽  
Aspartate Transaminase ◽  
Simultaneous Administration ◽  
Microsomal Enzyme ◽  
Hepatic Microsomal Enzyme ◽  
Long Evans

The effects of cimetidine and phenobarbitone on paracetamol induced hepatotoxicity were studied in Long Evans Norwegian strain rats of either sexes. Orally administration of paracetamol 150 mg/ kg body weight for 21 days. On 22nd days after treatment there was significant increase of serum Alanine transaminase (AST), Aspartate transaminase (AST) and Alkaline phosphatase (Alk. phos) level. Orally administration of phenobarbitone 20 mg/kg b.w. along with paracetamol produced highly significant rise of serum ALT, AST and Alk. phos, levels as compared to the paracetamol treated group. But simultaneous administration of paracetamol and cimetidine produced significant decrease of serum ALT, AST and Alk. phos.level. When phenobarbitone is used concurrently with paracetamol, induced hepatic microsomal enzyme system which in turn aggravates the paracetamol induced hepatotoxicity but when cimetidine was administered simultaneously with paracetamol inhibited hepatic microsomal enzyme system and exhibits a protective role on paracetamol induced hepatotoxicity.The experiment was designed to demonstrate the effect of paracetamol on hepatotoxicity and its prevention by simultaneous administration of cimetidine. Further experiment was also designed to demonstrate the induction of hepatic microsomal enzyme system (HMES) by phenobarbitone on paracetamol induced hepatotoxicity. DOI: 10.3329/bjpp.v23i1.5725Bangladesh J Physiol Pharmacol 2007; 23(1&2) : 13-15

Human biokinetics of injected bismuth-207

2001 ◽  
Vol 20 (12) ◽  
pp. 601-609 ◽  
Author(s):  
D Newton ◽  
R J Talbot ◽  
N D Priest
Keyword(s):  
Half Life ◽  
Male Volunteer ◽  
Healthy Male Volunteer ◽  
Metabolic Model ◽  
The Body ◽  
Whole Body ◽  
Radiological Protection ◽  
Bismuth Compounds ◽  
Terminal Half Life ◽  
Radioactivity Measurements

A healthy male volunteer received an intravenous injection of 207Bi as citrate. Levels of the tracer in blood and in excretion samples, and its retention and distribution within the body, were investigated by appropriate radioactivity measurements. Levels in blood fell very rapidly, with only 1% of the injection remaining at 7 h and only ca. 0.1% at 18 days. There was rapid initial excretion, with 55% lost during the first 47 h, principally in urine; however, longer-term losses were much slower and 0.6% remained in the body at 924 days, when the contemporary rate of loss implied a half-life of 1.9 years. Integration of the retention pattern suggested that steady exposure to bismuth compounds could lead ultimately to a body content of 24 times the daily systemic uptake. The largest organ deposit was in the liver, which after 3 days contained ca. 60% of the contemporary whole body content, consistent with reports of hepatotoxicity. These findings differ markedly from the metabolic model for bismuth proposed by the International Commission on Radiological Protection, which envisages a terminal half-life in the body of only 5 days and kidney as the site of highest deposition.

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