Total antioxidant status and oxidative DNA damage in a South Indian population of essential hypertensives

Subash, Pramod; Premagurumurthy, K; Sarasabharathi, A.; Cherian, K.M.

doi:10.1038/jhh.2009.100

Cited by 24 publications

(28 citation statements)

References 32 publications

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“…This finding is consistent with the findings of other studies [21,33]. Reduced total antioxidant status (TAS) in hypertensive subjects compared to normotensive subjects has also been reported by some studies [25,34]. On evaluating the protein carbonyl content, we found a higher oxidative stress in hypertensive subjects (Fig.…”

Section: Discussionsupporting

confidence: 95%

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DNA Damage in Lymphocytes in Hypertensive Subjects in Bangladesh

Saiedullah¹,

Hayat²,

Zamir³

et al. 2013

J. Sci. Res.

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Oxidative stress due to imbalance between the production of reactive oxygen species and their dismutation is claimed to be higher in hypertensive subjects than normotensive subjects. In hypertensive subjects oxidative stress may damage deoxy-ribonucleic acids (DNA). In this study plasma superoxide dismutase (SOD) activities, protein carbonyl contents (PCCs) and extent of DNA damage in lymphocytes were measured in specimens obtained from 86 subjects to compare oxidative stress and oxidative DNA damage between normotensive and hypertensive subjects and to assess their relationship with the degree of blood pressure. Results were expressed as mean±SD. Two-tailed unpaired t test and Pearson's correlation test were done to compare or to determine the relationship between groups or variables. SOD activities were 2.85±0.12 unit/mg protein and 3.84±0.45 unit/mg protein (p<0.05) in hypertensive and normotensive groups respectively. PCCs were 4.77±0.36 nmol/mg protein and 3.75±0.23 nmol/mg protein in hypertensive and normotensive groups respectively. Olive tail moments (OTM) were 124.7±11.69 units and 108.9±9.27 units in hypertensive and normotensive groups respectively. The correlation coefficient of OTM was 0.3924 (p<0.05) for diastolic blood pressure and 0.3618 (p<0.05) for systolic blood pressure. Oxidative stress and DNA damage was higher in hypertensives than normotensives and DNA damage correlated positively with blood pressure.

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Section: Discussionsupporting

confidence: 95%

“…ROS occurs more frequently in hypertensive subjects than in normotensives [23][24][25]. A recent study in Chinese Han adults showed that oxidative stress is a reliable risk factors for developing hypertension [26].…”

Section: Introductionmentioning

confidence: 98%

DNA Damage in Lymphocytes in Hypertensive Subjects in Bangladesh

Saiedullah¹,

Hayat²,

Zamir³

et al. 2013

J. Sci. Res.

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“…DNA damage and DNA repair seem to be closely associated with aging as a result of endogenous factors, lifestyle, occupational or environmental exposure [30]. Some atherosclerosisrelated diseases, whose pathogenesis involves both inflammation and oxidative stress, lead to DNA-damage induction [31] and could explain the higher basal DNA damage found in our study in patients and in matched controls [32].…”

Section: Discussionsupporting

confidence: 46%

DNA Damage and Oxidative Stress in Patients with Chronic Obstructive Pulmonary Disease

Silva¹,

Rosa²,

Charlier³

et al. 2013

TOBIOMJ

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Abstract:Background: We aimed to assess the level of DNA damage and susceptibility to exogenous mutagens in peripheral blood cells of Chronic Obstructive Pulmonary Disease (COPD) patients and healthy individuals by comet assay. Oxidative stress was also evaluated by means of thiobarbituric acid reactive species (TBARS) in blood plasma.Methods: Case-control study enrolling 51 COPD patients and 51 controls. Peripheral blood was used to perform the alkaline (pH>13) and neutral (pH=8.5) comet assay. For the assessment of susceptibility to exogenous DNA damage, the cells were treated with methylmethane sulfonate (MMS) for 1-hour or 3-hour at 37° C. The percentage of residual DNA damage after 3-h MMS treatment was calculated using the value of 1-h MMS treatment for each subject as 100%. Lipid peroxidation was evaluated by measuring TBARS in blood plasma.Results: DNA damage in patients was significantly higher than in controls as measured by the neutral and alkaline comet assay. Residual DNA damage detected after MMS treatment increased in patients, in contrast to controls, indicating higher susceptibility to alkylation damage and/or repair inhibition. High susceptibility to exogenous DNA damage in COPD patients correlates with high amount of TBARS and low forced vital capacity and expiratory volume. Conclusion:The positive correlation between increased susceptibility to exogenous DNA damage and TBARS levels in COPD patients suggests the possible involvement of oxidative stress in damage induction and/or repair inhibition.

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“…Recently, antioxidant compounds such as luteolin, quercetin, rosmarinic acid, butin, and 7,8-dihydroxyflavone were shown to enhance oxidative DNA damage protection and repair (Silva et al 2008;Kang et al 2009;Zhang et al 2009a), suggesting these compounds may protect against oxidative stress-induced DNA damage, which occurs in several pathological conditions such as Alzheimer's disease, cancer, and hypertension (Zana et al 2006;Thompson 2006;Subash et al 2010).…”

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confidence: 99%