Title of article
Parkinsonʹs disease, pesticides, and glutathione transferase polymorphisms
Author/Authors
Alessandra Menegon، نويسنده , , Philip G Board and Michael W Parker، نويسنده , , Anneke C. Blackburn، نويسنده , , George D Mellick، نويسنده , , David G Le Couteur، نويسنده ,
Issue Information
روزنامه با شماره پیاپی سال 1998
Pages
3
From page
1344
To page
1346
Abstract
Background
Parkinsonʹs disease is thought to be secondary to the presence of neurotoxins, and pesticides have been implicated as possible causative agents. Glutathione transferases (GST) metabolise xenobiotics, including pesticides. Therefore, we investigated the role of GST polymorphisms in the pathogenesis of idiopathic Parkinsonʹs disease.
Methods
We genotyped by PCR polymorphisms in four GST classes (GSTM1, GSTT1, GSTP1, and GSTZ1) in 95 Parkinsonʹs disease patients and 95 controls. We asked all patients for information about pesticide exposure.
Findings
The distribution of the GSTP1 genotypes differed significantly between patients and controls who had been exposed to pesticides (controls vs patients: AA 14 [54%] of 26 vs seven [18%] of 39; AB 11 [42%] of 26 vs 22 [56%] of 39; BB 1 [4%] of 26 vs six [15%] of 39; AC 0 vs four [10%] of 39, p=0.009). No association was found with any of the other GST polymorphisms. Pesticide exposure and a positive family history were risk factors for Parkinsonʹs disease.
Interpretation
GSTP1-1, which is expressed in the blood-brain barrier, may influence response to neurotoxins and explain the susceptibility of some people to the parkinsonism-inducing effects of pesticides.
Journal title
The Lancet
Serial Year
1998
Journal title
The Lancet
Record number
578638
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