Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P30044 (antioxidant enzyme)
 8,037 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Oxidative stress plays a central role in the pathogenesis of Parkinson's disease (PD). L-DOPA, the gold standard in PD therapy, may paradoxically contribute to the progression of the disease because of its pro-oxidant properties. The issue, however, is controversial. In this study, we evaluated peripheral markers of oxidative stress in normal subjects, untreated PD patients and PD patients treated only with L-DOPA. We also measured platelet and plasma levels of L-DOPA, 3-O-methyldopa (the long-lasting metabolite of the drug), and dopamine. We found that isolated platelets of treated PD patients form higher amounts of 2,3-dihydroxybenzoate, an index of hydroxyl radical generation, than platelets of controls or untreated patients. In treated patients, platelet levels of 2,3-dihydroxybenzoate were positively correlated with platelet levels of L-DOPA, 3-O-methyldopa, and with the score of disease severity. Disease severity was correlated with platelet and plasma levels of L-DOPA, as well as with the daily intake of the drug. No significant differences in platelet levels of cytosolic and mitochondrial isoforms of the antioxidant enzyme superoxide dismutase were found between PD patients, either treated or untreated, and controls. Our findings lend further support to the hypothesis that L-DOPA might promote free radical formation in PD patients.
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PMID:Peripheral markers of oxidative stress in Parkinson's disease. The role of L-DOPA. 1046 18

The present study was carried out to study the effect of gentisic acid (2,5-dihydroxybenzoic acid (2,5-DHBA)) on the tumor promotion related events of carcinogenesis in murine skin. Benzoyl peroxide (BPO) (20 mg/0.2 ml/animal) and ultraviolet radiations (UVR) (0.420 J/m2/s) were used to induce tumor promotion response and oxidative stress and caused significant depletion in the detoxification and antioxidant enzyme armory with concomitant elevation in malondialdehyde (MDA) formation, hydrogen peroxide (H2O2) generation, ornithine decarboxylase (ODC) activity and unscheduled DNA synthesis. However, gentisic acid pretreatment at two different doses restored the levels of the above said parameters (P < 0.05) in a dose-dependent manner except in the case of ODC activity. Therefore, we propose that it might suppress the promotion stage via inhibition of oxidative stress but may not affect the polyamine biosynthetic pathway.
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PMID:Modulatory effect of gentisic acid on the augmentation of biochemical events of tumor promotion stage by benzoyl peroxide and ultraviolet radiation in Swiss albino mice. 1545 5