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)

Pathobiological effects of eugenol (4-allyl-2-methoxyphenol), a major constituent of betel quid (BQ), were studied on oral mucosal fibroblasts. At a concentration higher than 3 mmol/L, eugenol was cytotoxic to oral mucosal fibroblasts in a concentration- and time-dependent manner. Cell death was associated with intracellular depletion of glutathione (GSH). Most of the GSH was depleted prior to the onset of cell death. At concentrations of 3 mmol/L and 4 mmol/L, eugenol depleted about 45% and 77% of GSH after one-hour incubation. In addition, eugenol decreased cellular ATP level in a concentration- and time-dependent manner. Eugenol also inhibited lipid peroxidation. Inhibition of lipid peroxidation was partially explained by its dose-dependent inhibition of xanthine oxidase activity. The IC50 of eugenol on xanthine oxidase activity was about 0.3 mmol/L. No DNA strand break activity for eugenol was found at concentrations between 0.5 and 3 mmol/L. Taken together, frequent exposure of oral mucosa to a high concentration of eugenol during the chewing of BQ might be involved in the pathogenesis of oral submucous fibrosis and oral cancer via its cytotoxicity. In contrast, eugenol at a concentration less than 1 mmol/L might protect cells from the genetic attack of reactive oxygen species via inhibition of xanthine oxidase activity and lipid peroxidation.
 ...
PMID:Eugenol triggers different pathobiological effects on human oral mucosal fibroblasts. 800 31

The effect of eugenol on xanthine oxidase (XO) xanthine(X)-Fe+3-ADP mediated lipid peroxidation was studied in liver microsomal lipid liposomes. Eugenol inhibited the lipid peroxidation in a dose dependent manner as assessed by formation of thiobarbituric acid reactive substances. When tested for its effect on XO activity per se, (by measuring uric acid formation) eugenol inhibited the enzyme to an extent of 85% at 10 microm concentration and hence formation of O2.- also. However, the concentration of eugenol required for XO inhibition was more in presence of metal chelators such as EDTA, EGTA and DETAPAC, but not in presence of deferoxamine, ADP and citrate. The antiperoxidative effect of eugenol was about 35 times more and inhibition of XO was about 5 times higher as compared to the effect of allopurinol. Eugenol did not scavenge O2.- generated by phenazine methosulfate and NAD but inhibited propagation of peroxidation catalyzed by Fe2+ EDTA and lipid hydroperoxide containing liposomes. Eugenol inhibits XO-X-Fe+3 ADP mediated peroxidation by inhibiting the XO activity per se in addition to quenching various radical species.
 ...
PMID:Inhibition of xanthine oxidase-xanthine-iron mediated lipid peroxidation by eugenol in liposomes. 904 22

We examined the neuroprotective efficacy of eugenol against N-methyl-D-aspartate (NMDA)-, oxygen-glucose deprivation-, and xanthine/xanthine oxidase-induced neurotoxicity in primary murine cortical cultures. Eugenol (100-300 microM) attenuated NMDA (300 microM)-induced acute neurotoxicity by 20-60%. At the same concentration range, eugenol also inhibited NMDA (300 microM)-induced elevation in neuronal 45Ca2+ uptake by 10-30%. In the oxygen-glucose deprivation (50 min) neurotoxicity, eugenol (100-300 microM) prevented acute neuronal swelling and reduced neuronal death by 45-60% in a concentration-dependent fashion. Oxidative neuronal injury induced by xanthine/xanthine oxidase was also significantly reduced (75-90%) by eugenol (100- 300 microM) addition. These results suggest that eugenol may play a protective role against ischemic injury by modulating both NMDA receptor and superoxide radical.
 ...
PMID:Eugenol protects neuronal cells from excitotoxic and oxidative injury in primary cortical cultures. 914 82

The radical modulating activity of 2-methoxy-4-(2-propenyl)phenol (eugenol), 2-t-butyl-4-methoxy-phenol (BHA), and their dimers (bis-eugenol, bis-BHA) was investigated, using ESR spectroscopy. Eugenol produced radicals in alkaline solutions, and enhanced the radical intensity of both sodium-L-ascorbate and sodium 5,6-benzylidene-L-ascorbate. BHA has similar, but slightly lower activity, and their dimers were inactive. Their ability to scavenge the superoxide anion (O2-), generated by hypoxanthine and xanthine oxidase reaction, was in the order of eugenol > bis-eugenol > BHA > bis-BHA. The relative radical intensity among these compounds was paralleled by their cytotoxic activity. The present study demonstrates that eugenol and BHA were very reactive with radicals and their reactivity was considerably reduced by dimerization. The applicability of the dimerized eugenol in dentistry was discussed.
 ...
PMID:Interaction between eugenol-related compounds and radicals. 956 13

The ability of nine synthetic eugenol-related compounds to scavenge O2- (generated by the hypoxanthine-xanthine oxidase reaction) was compared with their radical generation and cytotoxic activity. ESR spectroscopy showed that eugenol (4-allyl-2-methoxyphenol), 2-allyl-4-methoxyphenol, 2-allyl-4-t-butylphenol and 2,4-dimethoxyphenol efficiently scavenged O2- and produced radicals under alkaline conditions. 2-allyl-4-t-butylphenol showed the highest cytotoxic activity and DNA-synthesis inhibitory activity, possibly due to the hydrophobic radical reactivity. 2-allyl-4-methoxyphenol and 2,4-dimethoxyphenol showed higher antioxidant activity than 3-t-butyl-4-hydroxyanisol (BHA), but all these compounds showed comparable cytotoxic activity with each other. These findings suggest a possible link between the cytotoxic activity and radical generation/scavenging activity in eugenol-related compounds.
 ...
PMID:Radical modulating activity and cytotoxic activity of synthesized eugenol-related compounds. 1106 7