Ethnic differences in the prevalence of the homozygous deleted genotype of glutathione s-transferase theta

Heather H. Nelson, John K. Wiencke, David C. Christiani, T. J. Cheng, Zheng Fa Zuo, Brian S. Schwartz, Byung Kook Lee, Margaret R. Spitz, Min Wang, Xiping Xu, Karl T. Kelsey

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327 Scopus citations

Abstract

In humans the glutathione S-transferase (GST) genes encode four classes of proteins (GST) important in the detoxification of reactive electrophiles. Recently, a gene deletion polymorphism was discovered within the GST class θ locus that leads to a functional deficiency in GST θ activity within circulating red blood cells. In this study we have examined the ethnic distribution of this polymorphism using a polymerase chain reaction (PCR)-based genotyping method. Five different ethnic groups were studied: North American Caucasians, African-Americans, Mexican- Americans, Chinese and Koreans. The prevalence of the null genotype was highest among Chinese (64.4%), followed by Koreans (60.2%), African-Americans (21.8%) and Caucasians (20.4%), whereas the prevalence was lowest among Mexican-Americans (9.7%). Interestingly, the prevalence of the deleted genotype in Caucasians differed significantly when 257 individuals drawn from a nation wide organization were compared with 185 people from the New England area (23.7 versus 15.7%, P < 0.05, χ2 test). These results indicate that there are major differences in the prevalence of this trait attributable to ethnicity and that ethnic origin even among Caucasians should be considered in studies of gene-environment interaction involving this polymorphism.

Original languageEnglish (US)
Pages (from-to)1243-1246
Number of pages4
JournalCarcinogenesis
Volume16
Issue number5
DOIs
StatePublished - May 1995

Bibliographical note

Funding Information:
We would like to thank Kathryn S.Springer for technical assistance. We also acknowledge the Carpenters Health and Safety Fund and Edward J.Gorman in J.D. for assistance in collection of the carpenter union samples, as well as all participants who donated blood for study. Supported by R01 ES06717, P42 ES04705, P01 06409, ES 00002 and CA 55769 from the NIEHS and NCI and KOI OH 00011 from NIOSH.

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