RGD Reference Report - Glutathione S-transferase mu, omega, pi, and theta class variants and smoking in Parkinson's disease. - Rat Genome Database

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Glutathione S-transferase mu, omega, pi, and theta class variants and smoking in Parkinson's disease.

Authors: Wahner, AD  Glatt, CE  Bronstein, JM  Ritz, B 
Citation: Wahner AD, etal., Neurosci Lett. 2007 Feb 21;413(3):274-8. Epub 2006 Dec 27.
RGD ID: 5490299
Pubmed: PMID:17194543   (View Abstract at PubMed)
PMCID: PMC1864949   (View Article at PubMed Central)
DOI: DOI:10.1016/j.neulet.2006.11.053   (Journal Full-text)

GSTs are a family of inducible phase II enzymes that may play a neuroprotective role in Parkinson's disease (PD). GSTs may also modify PD risk by metabolizing compounds in cigarettes, as cigarette smoking is generally found to be associated with a decrease in PD risk. Using a population-based case-control study design, we examined polymorphisms of the mu, omega, pi, and theta classes of GST to elucidate the main effects and smoking-GST interactions on PD risk. From three rural California counties, we recruited 289 incident idiopathic PD cases, clinically confirmed by our study neurologist, and 270 population controls, marginally matched by age, gender, and race. We assessed main gene polymorphism associations and evaluated interactions between smoking and GST polymorphisms as departures from a multiplicative scale adjusting for age, gender, and race. We also restricted analyses to Caucasian subjects to address the potential for population stratification (n=235 cases, 220 controls). Among Caucasians, we observed a risk reduction in subjects carrying at least one variant allele for GSTO1 (OR=0.68, 95% CI: 0.47-0.98) and also GSTO2 (OR=0.64, 95% CI: 0.44-0.93); both genes were in strong linkage disequilibrium. No main gene effects were observed for the remaining polymorphisms. We noted a multiplicative interaction between ever having smoked regularly and GSTO1 (OR(interaction)=0.55, 95% CI: 0.33-0.92) and GSTO2 (OR(interaction)=0.54, 95% CI: 0.32-0.90). Results were similar when combining all races. These findings and the paucity of similar studies suggest a need for further inquiry into the association between GSTs, smoking, and PD risk.



RGD Manual Disease Annotations    Click to see Annotation Detail View

  
Object SymbolSpeciesTermQualifierEvidenceWithNotesSourceOriginal Reference(s)
GSTO1HumanParkinson's disease susceptibilityIAGP DNA:polymorphism:exon:p. A140D (rs4925) (human)RGD 
GSTO2HumanParkinson's disease susceptibilityIAGP DNA:polymorphism: : -183 A>G (rs2297235)(human)RGD 
Gsto1RatParkinson's disease susceptibilityISOGSTO1 (Homo sapiens)DNA:polymorphism:exon:p. A140D (rs4925) (human)RGD 
Gsto1MouseParkinson's disease susceptibilityISOGSTO1 (Homo sapiens)DNA:polymorphism:exon:p. A140D (rs4925) (human)RGD 
Gsto2RatParkinson's disease susceptibilityISOGSTO2 (Homo sapiens)DNA:polymorphism: : -183 A>G (rs2297235)(human)RGD 
Gsto2MouseParkinson's disease susceptibilityISOGSTO2 (Homo sapiens)DNA:polymorphism: : -183 A>G (rs2297235)(human)RGD 

Objects Annotated

Genes (Rattus norvegicus)
Gsto1  (glutathione S-transferase omega 1)
Gsto2  (glutathione S-transferase omega 2)

Genes (Mus musculus)
Gsto1  (glutathione S-transferase omega 1)
Gsto2  (glutathione S-transferase omega 2)

Genes (Homo sapiens)
GSTO1  (glutathione S-transferase omega 1)
GSTO2  (glutathione S-transferase omega 2)


Additional Information