Record Details

Effect of <i style="">GSTM1</i> and <i style="">GSTT1</i> double deletions in the development of oxidative stress in diabetic nephropathy patients

NOPR - NISCAIR Online Periodicals Repository

View Archive Info
 
 
Field Value
 
Title Effect of GSTM1 and GSTT1 double deletions in the development of oxidative stress in diabetic nephropathy patients
 
Creator Datta, Sudip K
Kumar, Vivek
Ahmed, Rafat S
Tripathi, Ashok K
Kalra, Om Prakash
Banerjee, Basu Dev
 
Subject Diabetic nephropathy
Polymorphism
Glutathione S-transferase
GSTM1
GSTT1
Oxidative stress
 
Description 100-103
Association of diabetic nephropathy (DN) with the deletion of GSTT1 and GSTM1 genes is well reported. Oxidative stress (OS) has also been
associated with the development of DN. The present study was conducted to find
out, whether these deletions had any contributory role in the development of OS
in patients with DN. Pre-dialysis venous blood samples were obtained from 60 patients
with diabetic end-stage renal disease (stages 4 and 5). Reduced-glutathione
(GSH), glutathione S-transferase (GST) activity and malondialdehyde (MDA) levels
were measured for the assessment of OS. Genetic polymorphism analysis of DN
patients revealed the following distribution pattern: GSTM1 null 46.7%; GSTT1 null
55%; both null 30% and both positive 28.3%. Patients with both null genotypes
were found to have significantly increased levels of MDA and low GST activity
as compared to other genotypic groups. Lower GSH levels were observed in all
the genotypic groups as compared to both positives. Double deletions involving GSTT1 and GSTM1 may result in decreased GST levels, leading to increased OS
as reflected by increased MDA levels. As GST is a multi-functional enzyme
involved in xenobiotic metabolism, this double null genotype population has a greater
risk of development of DN. Further studies using increased sample size to find
out the allelic distribution and their role in the development of DN are in
progress
 
Date 2010-04-23T04:13:01Z
2010-04-23T04:13:01Z
2010-04
 
Type Article
 
Identifier 0975-0959 (Online); 0301-1208 (Print)
http://hdl.handle.net/123456789/8269
 
Language en_US
 
Publisher CSIR
 
Source IJBB Vol.47(2) [April 2010]