scholarly journals Isolation of a Microsomal Enzyme System Involved in Glucosinolate Biosynthesis from Seedlings of Tropaeolum majus L

1996 ◽  
Vol 111 (3) ◽  
pp. 831-837 ◽  
Author(s):  
L. Du ◽  
B. A. Halkier
1973 ◽  
Vol 248 (2) ◽  
pp. 456-460
Author(s):  
Anthony Y.H. Lu ◽  
Wayne Levin ◽  
Susan B. West ◽  
Martin Jacobson ◽  
Dene Ryan ◽  
...  

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

1979 ◽  
Vol 184 (3) ◽  
pp. 491-499 ◽  
Author(s):  
T C Madhok ◽  
H F DeLuca

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.


Author(s):  
Layla Afroza Banu ◽  
Hosne Ara Begum ◽  
SAR Choudhury

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


1972 ◽  
Vol 153 (1) ◽  
pp. 294-297 ◽  
Author(s):  
Anthony Y.H. Lu ◽  
Martin Jacobson ◽  
Wayne Levin ◽  
Susan B. West ◽  
Ronald Kuntzman

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