Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Target Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Query: EC:1.6.5.2 (
NQO1
)
6,196
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
The association between the quinone oxidoreductase gene (
NQO1
) polymorphism (609C/T) and schizophrenia was examined to replicate and extend the findings of a previous study (Hori et al., 2003). The study sample was 107 schizophrenia in-patients and 106 healthy controls. The distributions of the
NQO1
genotypes and alleles were not different between the schizophrenia patients and the controls. However, the frequency of the variant genotype was significantly higher in the subgroup with
tardive dyskinesia
(TD) than in the subgroup without (p=0.019). The subjects with allele T were significantly more frequent in the TD patients than in those without (odds ratio 2.256, 95% confidence interval 1.235-4.133). In addition, the Abnormal Involuntary Movement Scale (AIMS) score was significantly higher in the variant genotype group (T/T) than in other genotypic groups (C/C and C/T) (p=0.004). This study suggests that the
NQO1
gene polymorphism (609C/T) may confer susceptibility to the development of TD in schizophrenia, at least in the Korean population.
...
PMID:Quinone oxidoreductase (NQO1) gene polymorphism (609C/T) may be associated with tardive dyskinesia, but not with the development of schizophrenia. 1583 2
Several lines of evidence have indicated that free radicals may play a role in the pathophysiology of
tardive dyskinesia
(TD) (reviewed in Andreassen and Jorgensen, 2000). NAD(P)H: quinone oxidoreductase (
NQO1
) is an important enzyme in the human body that counteracts the oxidative stress-induced neuronal injury caused by the toxic free radicals such as dopamine-semiquinones. Taking the possible genetic predisposition to TD into account (Yassa and Ananth, 1981), the
NQO1
gene is a good candidate gene that may confer increased susceptibility to TD. Based on this hypothesis, Pae et al. (2004) reported a significant association between the Pro187Ser polymorphism in the
NQO1
gene and TD. In the present study, we attempted to replicate the findings of Pae et al. (2004) with the same polymorphism in 222 Japanese patients with schizophrenia. No significant difference was detected between patients with and without TD in the allelic distribution (chi2 = 0.070, d.f. = 1, p = 0.795) and in the genotypic distribution (chi2 = 0.910, d.f. = 2, p = 0.657). In addition, there was no significant difference in terms of total Abnormal Involuntary Movement Scale scores among the three genotype groups (p = 0.49). Our results suggest that the
NQO1
gene polymorphism does not confer an increased risk of TD.
...
PMID:No association between a functional NAD(P)H: quinone oxidoreductase gene polymorphism (Pro187Ser) and tardive dyskinesia. 1677 88
This study investigated whether there was an interaction between the
NQO1
Pro187Ser and MnSOD Ala-9Val gene polymorphisms in the development of
tardive dyskinesia
(TD). The combined genotypes of T/T in
NQO1
Pro187Ser and Val/Val in MnSOD Ala-9Val polymorphisms were found to be independently associated with a significantly higher risk of TD. However, further adequately powered studies will be needed to confirm these preliminary findings.
...
PMID:Additive effect between quinine oxidoreductase gene (NQO1: Pro187Ser) and manganese superoxide dismutase gene (MnSOD: Ala-9Val) polymorphisms on tardive dyskinesia in patients with schizophrenia. 1897 34