Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:1.1.1.1 (alcohol dehydrogenase)
 9,284 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Single large doses of pyrazole (100-200 mg/kg) given either i.p. or orally caused a decrease in brain norepinephrine and 3-methoxy-4-hydroxyphenylethylene glycol sulfate, but no change in dopamine beta-hydroxylase activity. The effects were enhanced by daily administration for 3 to 4 days. Concomitant administration of ethanol prevented the effects. With smaller doses (50 mg/kg/day) given orally for several days, there was little or no change for 3 days, but after 6 days there was an increase in both parameters. Dopamine beta-hydroxylase activity was also increased. The daily administration of ethanol alone (6.0 g/kg/day) for 6 days caused increased norepinephrine, but 3-methoxy-4-hydroxyphenylene glycol sulfate was diminished and dopamine beta-hydroxylase was unaffected. When the two drugs were given simultaneously, steady-state levels of norepinephrine were unaltered, but the sulfate metabolite was increased as was dopamine beta-hydroxylase. The results suggest that pyrazole and/or ethanol, administered daily for 6 days, leads to adaptive responses in catecholamine metabolism. Pyrazole (or a metabolite) has marked effects of its own, some or all of which are independent of its effects on alcohol dehydrogenase. When the two drugs are administered together, it is difficult to know whether the observed changes are independent or overlapping effects.
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PMID:Interactions of pyrazole and ethanol on norepinephrine metabolism in rat brain. 66 May 60

The relative role of genetic and environmental factors in the pathogenesis of Parkinson's disease (PD) has been the matter of investigation and debate, especially in the last 30 years. The possible interaction between genetic and environmental factors led to a great number of association studies between single nucleotide polymorphisms (SNPs) of many candidate genes and PD risk. In this study we summarized and critically reviewed the results of studies published on this issue, with especial reference to those reported in the last 5 years. Many studies provided conflicting findings and, when positive associations were identified, associations were weak. Polymorphisms related with activation or detoxification of drugs and xenobiotics, such as CYP1A1, CYP1A2, CYP19A1, CYP1B1, CYP2C9, CYP2C19, CYP2E1, CYP2D6, NAT2, GSTM1, GSTM3, GSTO1, GSTP1, PON1, PON2, ABCB1 and ADH genes have not been demonstrated convincingly a definitive association with the risk of developing PD. Nor did polymorphisms in genes related to dopamine or serotonin DRD, DAT, TH, DDC, DBH, MAO, COMT, SLC6A4, MTR, MTHFR, oxidative stress NOQ1, NOQ2, mEPHX, HFE, GPX, CAT, mnSOD, HFE, HO-1, HO-2, NFE2L2, KEAP1, inflammatory processes, ILs, TNF, ACT, NOS, HNMT, ABP1, HRHs, trophic and growth factors BDNF, FGF, or mitochondrial metabolism and function. In addition we analyzed other putative relations and genes associated with monogenic familial PD.Taking together the results of candidate gene association studies and genome wide association studies, only some SNPs of the MAPT, SNCA, HLA and GBA genes seem to be the most likely associated with PD risk.
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PMID:Genomic and pharmacogenomic biomarkers of Parkinson's disease. 2469 31