2009
DOI: 10.1016/j.ejim.2009.06.003
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The role of glutathione S- transferase M1 and T1 gene polymorphisms and oxidative stress-related parameters in Egyptian patients with essential hypertension

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Cited by 48 publications
(26 citation statements)
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“…These results were consistent with Sahar S. Bessa et al's study in Egyptian patients with essential hypertension [29], and Lakhdar R. et al's study in the patients with chronic obstructive pulmonary disease [30]. Not as we observed in healthy young adults (in them the GST activity performing as GSTM1 genotype dependent) [31], GSTT1 deletion significantly increased the GST activity ( P  = 0.034, <0.05) in the elderly.…”
Section: Discussionsupporting
confidence: 92%
“…These results were consistent with Sahar S. Bessa et al's study in Egyptian patients with essential hypertension [29], and Lakhdar R. et al's study in the patients with chronic obstructive pulmonary disease [30]. Not as we observed in healthy young adults (in them the GST activity performing as GSTM1 genotype dependent) [31], GSTT1 deletion significantly increased the GST activity ( P  = 0.034, <0.05) in the elderly.…”
Section: Discussionsupporting
confidence: 92%
“…The activity of erythrocyte SOD, GSH-Px, and catalase was not different depending on GSTM1 and GSTT1 polymorphisms and this result corresponds with some previous studies [24,27,33]. Bessa et al [33] found that the activity of SOD and GSH-Px did not change depending on GSTM1 and GSTT1 genotypes in patients with hypertension.…”
Section: Discussionsupporting
confidence: 89%
“…DNA damage is highly related to oxidative stress biomarkers and in the previous studies, oxidative stress-related parameters among patients with hypertension were lower in GSTM1 null genotype, which was expected [33]. However, studies on the correlation between the degree of DNA damage and GST polymorphism in patients with hypertension have been rarely conducted and, therefore, more studies are needed.…”
Section: Discussionmentioning
confidence: 86%
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“…A proposed pathway is that pulmonary exposure induces pulmonary oxidative stress, which leads to release of pro-thrombotic and inflammatory cytokines into the blood, as well as an increased level of reactive oxygen species (ROS) in the heart. [1], [3] This enhances expression of inflammatory cytokine-genes, which in turn induces systemic inflammation and systemic oxidative stress. Inflammation furthers progress of atherosclerosis and can potentially trigger acute plaque rupture.…”
Section: Introductionmentioning
confidence: 99%