Glutathione-s-transferase M1 and T1 polymorphisms and associations with type 1 diabetes age-at-onset.
Bekris, L M ; Shephard, C ; Peterson, M ; Hoehna, J ; Van Yserloo, B ; Rutledge, E ; Farin, F ; Kavanagh, T J and Lernmark, Åke LU
(2005)
In Autoimmunity
38(8).
p.567-575
- Abstract
- Type 1 diabetes (T1D) is an autoimmune disease characterized by pancreatic beta cell destruction involving auto-reactive T-cells, pro-inflammatory cytokines, reactive oxygen species (ROS) and loss of insulin. Monozygotic twin studies show a 20-60% concordance with T1D indicating there may be an environmental component to the disease. Glutathione (GSH) is the major endogenous antioxidant produced by the cell. GSH participates directly in the neutralization of free radicals and plays a role in the immune response. Glutathione-s-transferases (GSTs) conjugate GSH to free-radicals or xenobiotics. GST activity depletes GSH levels and may either detoxify or enhance the toxicity of a compound. Glutathione-s-transferase mu 1 (GSTM1) and... (More)
- Type 1 diabetes (T1D) is an autoimmune disease characterized by pancreatic beta cell destruction involving auto-reactive T-cells, pro-inflammatory cytokines, reactive oxygen species (ROS) and loss of insulin. Monozygotic twin studies show a 20-60% concordance with T1D indicating there may be an environmental component to the disease. Glutathione (GSH) is the major endogenous antioxidant produced by the cell. GSH participates directly in the neutralization of free radicals and plays a role in the immune response. Glutathione-s-transferases (GSTs) conjugate GSH to free-radicals or xenobiotics. GST activity depletes GSH levels and may either detoxify or enhance the toxicity of a compound. Glutathione-s-transferase mu 1 (GSTM1) and glutathione-s-transferase theta 1 (GSTT1) have polymorphic homozygous deletion (null) genotypes resulting in complete absence of enzyme activity. GSTM1 and GSTT1 null genotypes in Caucasian populations have frequencies of approximately 40-60% and 15-20%, respect (Less)
Please use this url to cite or link to this publication:
https://lup.lub.lu.se/record/1133056
- author
- Bekris, L M
; Shephard, C
; Peterson, M
; Hoehna, J
; Van Yserloo, B
; Rutledge, E
; Farin, F
; Kavanagh, T J
and Lernmark, Åke
LU
- publishing date
- 2005
- type
- Contribution to journal
- publication status
- published
- subject
- keywords
- glutathione-s-transferase, Type 1 diabetes, polymorphism, GSTT1, GSTM1, age-at-onset
- in
- Autoimmunity
- volume
- 38
- issue
- 8
- pages
- 567 - 575
- publisher
- Taylor & Francis
- external identifiers
-
- scopus:30844448323
- ISSN
- 0891-6934
- DOI
- 10.1080/08916930500407238
- language
- English
- LU publication?
- no
- id
- f2d892ec-bd5a-4cc6-b616-5a8577f83995 (old id 1133056)
- date added to LUP
- 2016-04-01 15:44:19
- date last changed
- 2022-04-07 00:29:03
@article{f2d892ec-bd5a-4cc6-b616-5a8577f83995,
abstract = {{Type 1 diabetes (T1D) is an autoimmune disease characterized by pancreatic beta cell destruction involving auto-reactive T-cells, pro-inflammatory cytokines, reactive oxygen species (ROS) and loss of insulin. Monozygotic twin studies show a 20-60% concordance with T1D indicating there may be an environmental component to the disease. Glutathione (GSH) is the major endogenous antioxidant produced by the cell. GSH participates directly in the neutralization of free radicals and plays a role in the immune response. Glutathione-s-transferases (GSTs) conjugate GSH to free-radicals or xenobiotics. GST activity depletes GSH levels and may either detoxify or enhance the toxicity of a compound. Glutathione-s-transferase mu 1 (GSTM1) and glutathione-s-transferase theta 1 (GSTT1) have polymorphic homozygous deletion (null) genotypes resulting in complete absence of enzyme activity. GSTM1 and GSTT1 null genotypes in Caucasian populations have frequencies of approximately 40-60% and 15-20%, respect}},
author = {{Bekris, L M and Shephard, C and Peterson, M and Hoehna, J and Van Yserloo, B and Rutledge, E and Farin, F and Kavanagh, T J and Lernmark, Åke}},
issn = {{0891-6934}},
keywords = {{glutathione-s-transferase; Type 1 diabetes; polymorphism; GSTT1; GSTM1; age-at-onset}},
language = {{eng}},
number = {{8}},
pages = {{567--575}},
publisher = {{Taylor & Francis}},
series = {{Autoimmunity}},
title = {{Glutathione-s-transferase M1 and T1 polymorphisms and associations with type 1 diabetes age-at-onset.}},
url = {{http://dx.doi.org/10.1080/08916930500407238}},
doi = {{10.1080/08916930500407238}},
volume = {{38}},
year = {{2005}},
}