Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:1.17.3.2 (xanthine oxidase)
 8,383 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Male C57Bl/10 mice were chronically fed hexachlorobenzene (HCB) (0.02% of the diet) alone or in combination with a single subcutaneous dose of iron (12.5 mg iron per mouse). After eight weeks the group of mice pretreated with the iron overload was highly sensitized to the porphyrogenic effect of HCB, as shown by liver porphyrin accumulation. A synergistic effect of iron was evident on other parameters too, such as HCB-induced hepatic damage, activation of type O of xanthine oxidase, and decreased activity of copper zinc superoxide dismutase and glutathione peroxidase(s). None of these parameters was affected by iron alone. Iron alone and in association with HCB markedly raised the level of lipid peroxides, the increase in the HCB group being smaller. The combined treatment resulted in a significant reduction of HCB's inductive effects on microsomal heme and cytochromes P-450 and b5 and on the activity of aryl hydrocarbon hydroxylase. The content of nonprotein sulfhydryl groups was reduced to the same extent in mice treated with HCB or HCB plus iron. The results suggest that reactive intermediates such as are formed by lipid peroxidation are not sufficient on their own to create the conditions for uroporphyrinogen decarboxylase impairment, as evident in the group of mice receiving iron overload alone. Conversely, HCB administration induced a specific condition of imbalance in the liver between formation and inactivation of reactive intermediates which was associated with hepatic porphyrin accumulation and was potentiated by concomitant administration of iron.
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PMID:Investigations on the role of free radical processes in hexachlorobenzene-induced porphyria in mice. 323 39

The effect of an antigenic challenge with sheep red blood cells (SRBC) on the activities of cytochrome P-450-dependent and -independent xenobiotic metabolizing enzymes and on lipid peroxidation in the liver was investigated. The studies were carried out using three mouse strains of C57B1/10 and three strains of C3H backgrounds which are cogenic, differing genetically at the H-2 complex. The basal levels of aryl hydrocarbon hydroxylase (AHH) and 7-ethoxycoumarin O-deethylase (7-Ec) were different among congenic strains. The activity of 7-Ec was lower in C3H background mice than in B10 background mice. Similarly, the difference due to the strain and the H-2 locus was detected in the activities of P-450-independent enzymes such as malathion and diethyl succinate carboxylesterases, glutathione S-transferase, and epoxide hydrolases in microsomal and cytosolic fractions. The degree of immune responsiveness in these mice was determined by a plaque forming cell assay. Within the same background, the H-2b mouse strain was a high responder and the H-2k a low responder to SRBC. However, treatment with SRBC had no significant depressive effect on P-450-dependent enzyme activities except in C3H/He. Activity of AHH was suppressed in C3H/He mice. Treatment with SRBC had no effect on P-450-independent enzyme activities except for malathion carboxylesterase: the activity was increased in C3H/He and C3H.JK, whereas it was decreased in B10. The basal level of lipid peroxidation was lower in C3H/He and C3H.JK. The treatment produced a significant enhancement in lipid peroxidation in C3H/He, B10 and B10.BR (P less than 0.05) with a concomitant increase in xanthine oxidase activity (P less than 0.05). Thus, the present study revealed that a specific antigenic challenge, unlike non-specific immunostimulants (e.g. poly IC, endotoxin), does not necessarily inhibit P-450-dependent xenobiotic metabolizing enzymes even though antigen challenge increased XO activity and lipid peroxidation. The possible roles of an increase in lipid peroxidation and xanthine oxidase activity in immune response to SRBC and xenobiotic metabolizing enzymes are discussed.
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PMID:Effect of induction of T-cell-dependent antibody with sheep red blood cells on P-450-dependent and -independent xenobiotic metabolizing enzymes. 348 42

The effects of beta-naphthoflavone (beta-NF, 80 mg/kg i.p. for 2 consecutive days) on P-450-dependent and -independent enzymes, lipid peroxidation and xanthine oxidase were investigated in 9 strains of young (3-month-old) male mice. Three H-2 congenic strains on each of three different genetic backgrounds were studied. The backgrounds were C57BL/10 (abbreviated as B10), C3H, and A strain mice. The reported longevities (weeks) as expressed in 10th decile of survivorship are significantly different among the H-2 congenic strains on each of these backgrounds: it ranges from 155 to 170 weeks in B10, from 138 to 150 in C3H and from 114 to 134 in A background mice. The inducibility of aryl hydrocarbon hydroxylase (AHH) with beta-NF was highest in B10, intermediate in C3H/He and non-inducible in other C3H mice and in all mice on the A strain background. Within the B10 background, inducibility of AHH varied widely among mice of different H-2 haplotypes: 549 +/- 34 (H-2k), 360 +/- 72 (H-2b) and 349 +/- 47 (H-2r) percent of the mean control values (n = 5; mean +/- S.D.), without change in activities of P-450-independent enzymes. In C3H mice the H-2k haplotype showed inducibility (213 +/- 34%), while other haplotypes, specifically H-2b and H-2j, did not. beta-NF increased the activities of xanthine oxidase in B10 and A background strains, without interbackground differences. Lipid peroxidation was significantly increased in A background strains and in an H-2 dependent manner. The relationship between Ah responsiveness and reported longevities of these nine strains is discussed.
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PMID:H-2, Ah, and aging: the immune response and the inducibility of P-450 mediated monooxygenase activities, xanthine oxidase, and lipid peroxidation in H-2 congenic mice on C57BL/10, C3H, and A strain backgrounds. 382 Nov 93