Glutathione S-transferase genotype and risk of systemic lupus erythematosus in Koreans

T. Y. Kang, A. El-Sohemy, M. C. Cornelis, K. M. Eny, Sang Cheol Bae

Research output: Contribution to journalArticle

25 Citations (Scopus)

Abstract

Oxidative stress caused by poor detoxification efficiency of reactive oxygen species (ROS) may play a role in the development of systemic lupus erythematosus (SLE). Glutathione S-transferase (GST) is involved in the detoxification of ROS and genetic polymorphisms of GSTM1, GSTT1 and GSTP1 are associated with altered enzyme activity. The aim of this study was to determine whether GSTM1 (deletion), GSTT1 (deletion) and GSTP1 (Ile 105 → Val 105 ) polymorphisms are associated with susceptibility to SLE or frequency of clinical manifestations according to the ACR diagnostic criteria. DNA was isolated from blood samples collected from 330 patients with SLE and 270 age- and sex-matched controls. GST genotypes were determined by polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) analysis. No associations were observed between GSTM1, GSTT1, and GSTP1 genotypes and risk of SLE. Among SLE patients, the GSTM1 null genotype was associated with a lower frequency of hematological disorders (P = 0.012), and a higher SSA(+)/SSB(-) autoantibody profile (P = 0.042). Compared to SLE patients with the GSTT1 non-null genotype, those with the GSTT1 null genotype had a lower frequency of discoid rash (P = 0.018), and nephritis (P = 0.033). Our findings suggest that genetic polymorphisms of GSTM1, GSTT1, and GSTP1 do not influence the risk of SLE, but a deletion of either GSTM1 or GSTT1 may influence certain clinical manifestations of the disease.

Original languageEnglish
Pages (from-to)381-384
Number of pages4
JournalLupus
Volume14
Issue number5
DOIs
StatePublished - 2005 Jun 13

Fingerprint

Glutathione Transferase
Systemic Lupus Erythematosus
Genotype
Genetic Polymorphisms
Reactive Oxygen Species
Nephritis
Exanthema
Restriction Fragment Length Polymorphisms
Autoantibodies
Oxidative Stress
Polymerase Chain Reaction
DNA
Enzymes

Keywords

  • Genotype
  • Glutathione
  • Oxidative stress
  • S-transferase
  • Systemic lupus erythematosus

Cite this

Kang, T. Y. ; El-Sohemy, A. ; Cornelis, M. C. ; Eny, K. M. ; Bae, Sang Cheol. / Glutathione S-transferase genotype and risk of systemic lupus erythematosus in Koreans. In: Lupus. 2005 ; Vol. 14, No. 5. pp. 381-384.
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Glutathione S-transferase genotype and risk of systemic lupus erythematosus in Koreans. / Kang, T. Y.; El-Sohemy, A.; Cornelis, M. C.; Eny, K. M.; Bae, Sang Cheol.

In: Lupus, Vol. 14, No. 5, 13.06.2005, p. 381-384.

Research output: Contribution to journalArticle

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AU - Kang, T. Y.

AU - El-Sohemy, A.

AU - Cornelis, M. C.

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AB - Oxidative stress caused by poor detoxification efficiency of reactive oxygen species (ROS) may play a role in the development of systemic lupus erythematosus (SLE). Glutathione S-transferase (GST) is involved in the detoxification of ROS and genetic polymorphisms of GSTM1, GSTT1 and GSTP1 are associated with altered enzyme activity. The aim of this study was to determine whether GSTM1 (deletion), GSTT1 (deletion) and GSTP1 (Ile 105 → Val 105 ) polymorphisms are associated with susceptibility to SLE or frequency of clinical manifestations according to the ACR diagnostic criteria. DNA was isolated from blood samples collected from 330 patients with SLE and 270 age- and sex-matched controls. GST genotypes were determined by polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) analysis. No associations were observed between GSTM1, GSTT1, and GSTP1 genotypes and risk of SLE. Among SLE patients, the GSTM1 null genotype was associated with a lower frequency of hematological disorders (P = 0.012), and a higher SSA(+)/SSB(-) autoantibody profile (P = 0.042). Compared to SLE patients with the GSTT1 non-null genotype, those with the GSTT1 null genotype had a lower frequency of discoid rash (P = 0.018), and nephritis (P = 0.033). Our findings suggest that genetic polymorphisms of GSTM1, GSTT1, and GSTP1 do not influence the risk of SLE, but a deletion of either GSTM1 or GSTT1 may influence certain clinical manifestations of the disease.

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