Chemical-related sensitivity is associated with gene variants PDF Print E-mail

 A cross-sectional study of self-reported chemical-related sensitivity is associated with gene variants of drug-metabolizing enzymes (Eckart Schnakenberg et al, 2007)

 A cross-sectional study of self-reported chemical-related sensitivity
is associated with gene variants of drug-metabolizing enzymes

Eckart Schnakenberg*1, Karl-Rainer Fabig2, Martin Stanulla4, Nils Strobl3,
Michael Lustig3, Nathalie Fabig2 and Werner Schloot3

Published: 10 February 2007
Environmental Health 2007, 6:6 doi:10.1186/1476-069X-6-6
Received: 6 March 2006
Accepted: 10 February 2007

Abstract

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Background: N-acetyltransferases (NAT) and glutathione S-transferases (GST) are involved in
the metabolism of several ubiquitous chemical substances leading to the activation and
detoxification of carcinogenic heterocyclic and aromatic amines. Since polymorphisms within these
genes are described to influence the metabolism of ubiquitous chemicals, we conducted the present
study to determine if individuals with self-reported chemical-related sensitivity differed from
controls without self-reported chemical-related sensitivity with regard to the distribution of
genotype frequencies of NAT2, GSTM1, GSTT1, and GSTP1 polymorphisms.
Methods: Out of 800 subjects who answered a questionnaire of ten items with regard to their
severity of chemical sensitivity 521 unrelated individuals agreed to participate in the study.
Subsequently, genetic variants of the NAT2, GSTM1, GSTT1, and GSTP1 genes were analyzed.
Results: The results show significant differences between individuals with and without selfreported
chemical-related sensitivity with regard to the distribution of NAT2, GSTM1, and GSTT1
gene variants. Cases with self-reported chemical-related sensitivity were significantly more
frequently NAT2 slow acetylators (controlled OR = 1.81, 95% CI = 1.27–2.59, P = 0.001). GSTM1
and GSTT1 genes were significantly more often homozygously deleted in those individuals reporting
sensitivity to chemicals compared to controls (GSTM1: controlled OR 2.08, 95% CI = 1.46–2.96, P
= 0.0001; GSTT1: controlled OR = 2.80, 95% CI = 1.65–4.75, P = 0.0001). Effects for GSTP1 gene
variants were observed in conjunction with GSTM1, GSTT1 and NAT2 gene.
Conclusion: The results from our study population show that individuals being slow acetylators
and/or harbouring a homozygous GSTM1 and/or GSTT1 deletion reported chemical-related
hypersensitivity more frequently.

 
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