Genetic association analysis of the glutathione peroxidase (GPX1) gene polymorphism (Pro197Leu) with tardive dyskinesia

Shinkai, Takahiro; Müller, Daniel J.; Luca, Vincenzo De; Shaikh, Sajid; Matsumoto, Chima; Hwang, Riudi; King, Nicole; Trakalo, Joseph; Potapova, Natalia; Zai, Gwyneth; Hori, Hiroko; Ohmori, Osamu; Meltzer, Herbert Y.; Nakamura, Jun; Kennedy, James L.

doi:10.1016/j.psychres.2004.06.023

Cited by 29 publications

(25 citation statements)

References 38 publications

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“…Although DRD2 gene polymorphisms (Bakker et al, 2008) and, to a degree, COMT gene polymorphisms (Bakker et al, 2008; Zai et al, 2010b) have been associated with TD, results for various enzymes involved in the oxidative stress cascade have been negative. This has included genetic variations in the pro-oxidative stress enzyme NQO1 (Zai et al, 2010a), and the antioxidant enzymes MnSOD (Zai et al, 2010a) and glutathione peroxidase (Shinkai et al, 2006). Although larger studies investigating additional polymorphisms are required to reach more definitive conclusions, these results may indicate that oxidative stress-related genetic polymorphisms may not be predominantly involved in the development of TD during antipsychotic treatment in humans.…”

Section: Discussionmentioning

confidence: 99%

BDNF Val66Met polymorphism and antipsychotic-induced tardive dyskinesia occurrence and severity: A meta-analysis

Miura

Zhang

Nitta

et al. 2014

Schizophrenia Research

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Background Tardive dyskinesia (TD) is a serious long-term consequence of antipsychotic treatment. Since brain-derived neurotrophic factor (BDNF) has potent neurotrophic activity, genetic alterations in the BDNF gene may affect antipsychotic-induced TD. Methods Searching PubMed and Web of Science until 05/31/13, we conducted a systematic review and a meta-analysis of the effects of BDNF Val66Met polymorphism on antipsychotic-induced TD. Pooled odds ratio was calculated to assess the effects of BDNF Val66Met polymorphism on TD occurrence. Additionally, pooled standardized mean differences (Hedges' g) were calculated to assess the effects on Abnormal Involuntary Movement Scale (AIMS) total score. Results Out of 699 potentially eligible hits, 6 studies (N = 1740, mean age = 46.0 ± 10.4 years; males = 73.1%; Asians = 80.5%, Caucasians = 19.5%; schizophrenia = 96.2%) were included in this meta-analysis. Pooling data from all studies, no significant associations were found between BDNF Val66Met polymorphism and TD (p = 0.82) or AIMS total scores (p = 0.11). However, in studies including only Caucasians (n = 339), Met allele carriers had significantly higher AIMS total scores (Hedges' g = 0.253, 95% confidence interval = 0.030 to 0.476, p = 0.026) and non-significantly higher TD occurrence (p = 0.127). Conversely, there was no association between BDNF and AIMS scores (p = 0.57) or TD (p=0.65) in Asians. Conclusion Although there was no significant association between BDNF Val66Met polymorphism and TD or AIMS scores across all patients, our results suggest that BDNF Val66Met polymorphism affects severity and, possibly, TD development in Caucasians. Since the number of studies and patients was still small, additional data are needed to confirm genotype-racial interactions. Furthermore, BDNF enhancing treatments for TD may require further study, especially in Caucasians.

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Section: Discussionmentioning

confidence: 99%

BDNF Val66Met polymorphism and antipsychotic-induced tardive dyskinesia occurrence and severity: A meta-analysis

Miura

Zhang

Nitta

et al. 2014

Schizophrenia Research

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“…Two antioxidant enzymes (glutathione peroxidase GPX1 and glutathione S-transferase GSTP1) involved in the detoxification of reactive oxygen species have been examined by Shinkai et al 241,242 with negative results. Nevertheless, evidence supporting this hypothesis was provided by studies investigating NAD(P)H quinone oxireductase (NQ01) and nitric oxide synthases (NOS1 and NOS3), three enzymes involved in the defence mechanism against oxidative stress.…”

Section: Prediction Of Side Effectsmentioning

confidence: 99%

Pharmacogenetics and pharmacogenomics of schizophrenia: a review of last decade of research

2007

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The last decade of research into the pharmacogenetics of antipsychotics has seen the development of genetic tests to determine the patients' metabolic status and the first attempts at personalization of antipsychotic treatment. The most significant results are the association between drug metabolic polymorphisms, mainly in cytochrome P450 genes, with variations in drug metabolic rates and side effects. Patients with genetically determined CYP2D6 poor metabolizer (PMs) status may require lower doses of antipsychotic. Alternatively, CYP2D6 ultrarapid matabolizers (UMs) will need increased drug dosage to obtain therapeutic response. Additionally, polymorphisms in dopamine and serotonin receptor genes are repeatedly found associated with response phenotypes, probably reflecting the strong affinities that most antipsychotics display for these receptors. In particular, there is important evidence suggesting association between dopamine 2 receptor (D2) polymorphisms (Taq I and À141-C Ins/Del) and a dopamine 3 receptor (D3) polymorphism (Ser9Gly) with antipsychotic response and drug-induced tardive dyskinesia. Additionally, there is accumulating evidence indicating the influence of a 5-HT2C polymorphism (À759ÀT/C) in antipsychotic-induced weight gain. Application of this knowledge to clinical practice is slowly gathering pace, with pretreatment determination of individual's drug metabolic rates, via CYP genotyping, leading the field. Genetic determination of patients' metabolic status is expected to bring clinical benefits by helping to adjust therapeutic doses and reduce adverse reactions. Genetic tests for the pretreatment prediction of antipsychotic response, although still in its infancy, have obvious implications for the selection and improvement of antipsychotic treatment. These developments can be considered as successes, but the objectives of bringing pharmacogenetic and pharmacogenomic research in psychiatric clinical practice are far from being realized. Further development of genetic tests is required before the concept of tailored treatment can be applied to psychopharmatherapy. This review aims to summarize the key findings from the last decade of research in the field. Current knowledge on genetic prediction of drug metabolic status, general response and drug-induced side effects will be reviewed and future pharmacogenomic and epigenetic research will be discussed.

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“…Our findings suggest that GPX1 Pro197Leu is not associated with the physiopathology and frequency of FMF. There are limited studies about the GPX1 Pro197Leu polymorphism in the literature (Hansen et al, 2005;Shinkai et al, 2004Shinkai et al, , 2006Wei et al, 2011). These studies conducted on the GPX1 Pro197Leu polymorphism mostly include malignancies; however, results concerning the relationship between malignancies and the GPX1 Pro197Leu polymorphism are contradictory.…”

Section: Discussionmentioning

confidence: 99%

“…These studies conducted on the GPX1 Pro197Leu polymorphism mostly include malignancies; however, results concerning the relationship between malignancies and the GPX1 Pro197Leu polymorphism are contradictory. In studies conducted on a group of diseases such as colorectal carcinoma, prostatic carcinoma, schizophrenia, and tardive dyskinesia, it has been stated that the GPX1 Pro197Leu polymorphism is not a major risk factor for these diseases (Hansen et al, 2005;Shinkai et al, 2004Shinkai et al, , 2006Choi et al, 2007).…”

Section: Discussionmentioning

confidence: 99%

Genetic polymorphisms of paraoxonase1 192 and glutathione peroxidase1 197 enzymes in familial Mediterranean fever

Öktem¹,

Anıl²,

Sütçü³

et al. 2014

Genet. Mol. Res.

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ABSTRACT. Familial Mediterranean fever (FMF) is an autosomal recessive disorder and is the most frequent of the periodic febrile inflammatory syndromes. The pathogenesis of the disease is not completely understood, even though the FMF gene has been identified. Oxidative stress and inflammation may play a role in the pathogenesis of FMF. We investigated gene polymorphisms of the antioxidative enzymes, glutathione peroxidase (GPX) and paraoxonase (PON) in FMF patients, and possible associations with FMF pathogenesis. Sixty FMF patients during an attack-free period and 51 healthy children as the control group were included in our study. PON1 Q/R192 and GPX1 Pro197Leu gene polymorphisms were assayed. Blood urea nitrogen, creatinine and serum lipid profile were also measured. PON1 Q/R192 genotype distribution was 52% QQ, 46% QR and 2% RR in the FMF group and 45% QQ, 45% QR and 10% RR in the control group (P > Familial Mediterranean fever 0.05). GPX1 Pro197Leu genotype distribution was 28% PP, 57% PL, 15% LL in the FMF group and 18% PP, 53% PL, 29% LL in the control group (P > 0.05). Blood urea nitrogen, serum creatinine, lipid levels, and the distribution of PON1 Q/R192 and GPX1 Pro197Leu genotypes were similar in the two groups. We conclude that the PON1 Q/R192 and GPX1 Pro197Leu gene polymorphisms are not important risk factors in the development of FMF. However, larger studies are warranted to validate these conclusions.

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Genetic association analysis of the glutathione peroxidase (GPX1) gene polymorphism (Pro197Leu) with tardive dyskinesia

Cited by 29 publications

References 38 publications

BDNF Val66Met polymorphism and antipsychotic-induced tardive dyskinesia occurrence and severity: A meta-analysis

BDNF Val66Met polymorphism and antipsychotic-induced tardive dyskinesia occurrence and severity: A meta-analysis

Pharmacogenetics and pharmacogenomics of schizophrenia: a review of last decade of research

Genetic polymorphisms of paraoxonase1 192 and glutathione peroxidase1 197 enzymes in familial Mediterranean fever

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