The effect of amflutizole, a xanthine oxidase inhibitor, on ischemia-evoked purine release and free radical formation in the rat cerebral cortex

1994 ◽  
Vol 33 (10) ◽  
pp. 1197-1201 ◽  
Author(s):  
M.H. O'Regan ◽  
M. Smith-Barbour ◽  
L.M. Perkins ◽  
X. Caoa ◽  
J.W. Phillis
1997 ◽  
Vol 41 ◽  
pp. 30-30 ◽  
Author(s):  
Carol B. Andersen ◽  
David J. Hoffman ◽  
Congwu Du ◽  
Jane E. McGowan ◽  
S. Tsuyoshi Ohnishi ◽  
...  

2004 ◽  
Vol 38 (3) ◽  
pp. 283-293 ◽  
Author(s):  
Susanna Waters ◽  
Anita Fae ◽  
Jagdish Gondalia ◽  
Jan Holm ◽  
Lars Karlström ◽  
...  

1984 ◽  
Vol 62 (12) ◽  
pp. 2943-2949 ◽  
Author(s):  
Ya'acov Y. Leshem

In senescence physiology, experimental data indicate causative relationships among cytokinin, lipoxygenation, anti-oxidation, and lipid-associated free radical scavenging. During both normal and induced senescence, there is a rise in lipoxygenase (LOX) which catalyzes the oxidation of polyunsaturated fatty acids containing the cis, cis-1,4-pentadiene configuration. These include linoleic and linolenic acids, which are of common occurrence in plants and inter alia may be situated in membranal phospholipids. Lipoxygenation causes the production of free radicals such as the superoxide, fatty acid, and peroxy species. Cytokinin (CK) lowers LOX and superoxide dismutase activities significantly in senescing foliage and is mimicked by the endogenous lipid antioxidant, α-tocopherol (vitamin E), in its chlorophyll-retaining and LOX-lowering effects. Further experimentation indicated that CK interaction with free radicals may occur in two ways, (i) CK may act as a direct free radical scavenger by virtue of the fact that the hydrogens of the α-carbon atom in the amine bond can be extracted, resulting in the formation of an amide: [Formula: see text][Formula: see text] (this mechanism may also, in part, explain polyamine effects), (ii) CK may serve as an incipient preventative of free radical formation by inhibiting oxidation of plant purine compounds, which at certain stages of breakdown release superoxide and hydroxyl free radicals. This effect is probably associated with a lowering of substrate affinity for xanthine oxidase. This assumption is further borne out by similar senescence-retarding effects of selective xanthine oxidase inhibitors such as allopurinol. These observations collectively indicate that prevention of free radical formation and (or) their direct scavenging should be included in the multifactorial antisencscence mode of action of cytokinin.


1991 ◽  
Vol 69 (7) ◽  
pp. 944-950 ◽  
Author(s):  
Shabbir M. Moochhala ◽  
Kenneth W. Renton

It has been suggested that the loss of cytochrome P-450, which is mediated by interferon and its inducers, can result from the generation of free radical species by the enzyme xanthine oxidase. Cytochrome P-450, aminopyrine N-demethylase, and ethoxyresorufin deethylase were depressed by 35, 36, and 38%, respectively, in the livers of hamsters 24 h following the administration of a synthetic interferon (IFN-α-Con1) which contains the most frequent amino acid sequences of the human subtypes. Interferon increased the activities of the D and O forms of xanthine oxidase by 65 and 74%, respectively, in the same animals. The induction of the D form of xanthine oxidase, which is the precursor of the O form, preceded the loss in cytochrome P-450. The protein synthesis inhibitor, actinomycin D, prevented the interferon-induced loss of drug biotransformation and the increase in xanthine oxidase. The free radical scavenger, α-tocopherol, and the xanthine oxidase inhibitor, allopurinol, also prevented the loss of cytochrome P-450 mediated by the interferon inducer poly rI.rC. In chickens in which xanthine oxidase cannot be formed, poly rI.rC had no effect on cytochrome P-450 levels. These results suggest that xanthine oxidase induction may play some role in the interferon-mediated loss of cytochrome P-450.Key words: cytochrome P-450, xanthine oxidase, drug metabolism, interferon.


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