Establishment of non-invasive urinary biomarker for the early prediction of essential hypertension (EH) is important. We evaluated whether estimation of urinary DNA, serves as a marker to predict the extent of cellular oxidative stress in essential hypertension. A total of 180 South Indian subjects aged 30-65 were recruited for the study. Of these hypertensive subjects investigated, 30 were newly diagnosed and were not on any antihypertensive drugs, but had systolic blood pressure 140-160 mmHg and diastolic blood pressure 95-100 mmHg and 75 hypertensive patients who already on drug therapy for one year and 75 were South Indian normotensive healthy controls with blood pressure ≤ 120/80 mmHg. The 8-OHdG level in urine was significantly increased in hypertensive patients (both newly diagnosed and who already on drug therapy) compared with control group. The significant increase in 8-OHdG was observed in newly diagnosed hypertensive patients compared with hypertensive patients who already on drug therapy. There was a significant decrease in serum TAS value in essential hypertensive group when compared to control group. The urinary 8-OHdG was independently correlated with serum TAS. Decreased TAS levels, which reflect to increased oxidative stress, may be the reason of increased urinary 8-OHdG in South Indian hypertensive patients. Our preliminary data suggest that the competitive ELISA for 8-OHdG appears to be a simple method for quantifying the extent of oxidative stress.

To investigate the total antioxidant status (TAS) and the extent of oxidative DNA damage in total lymphocytes and their relation with essential hypertension. A total of 130 South Indian subjects aged 30-65 were recruited for the study. Of these hypertensive subjects investigated, 30 were newly diagnosed and were not on any antihypertensive drugs, but had systolic blood pressure (BP) ranging between 140 and 160 mm Hg and diastolic BP between 95 and 100 mm Hg; 50 hypertensive patients who were already on drug therapy for 1 year and 50 were normotensive controls with BP p120/80 mm Hg. DNA damage was significantly increased in hypertensive patients (both newly diagnosed and who were already on drug therapy) compared with control group. The major increase in DNA damage was observed in newly diagnosed hypertensive patients compared with hypertensive patients who were already on drug therapy. There was a significant decrease in plasma TAS value in essential hypertensive groups as compared to normotensive controls. Lymphocyte DNA damage was independently correlated with only TAS. Lymphocyte DNA damage was increased in hypertensive patients. The major increase in lymphocyte DNA damage was observed in newly diagnosed hypertensive patients compared with hypertensive patients who already on drug therapy. Decreased TAS levels, which reflect to increased oxidative stress, may be the reason of increased total lymphocyte DNA damage in South Indian hypertensive patients.