Research Highlight

DNA damage clue to hypertension

doi:10.1038/nindia.2010.86 Published online 22 June 2010

Patients with essential hypertension — high blood pressure with no identifiable cause — have impaired balance between oxidants and antioxidants. Until now, the mechanism underlying this abnormality and its effect on DNA level was unknown.

Researchers investigating the relationship between DNA damage in white blood cells (lymphocytes) and antioxidants have found that such damage is more extensive in patients with essential hypertension than in those with normal blood pressure.

In addition, the researchers also found that oxidative DNA damage can be significantly lowered through antihypertensive drugs over a period of time. This revelation could help to design better treatment protocols for hypertension patients with significant DNA damage.

The researchers studied 130 patients from south India — 30 newly diagnosed with essential hypertension and currently not on drugs, 50 with essential hypertension and on drugs for one year, and 50 control subjects with normal blood pressure. Using a method called alkaline comet assay, the researchers analysed DNA damage in these groups.

The results showed that DNA damage was significant in the hypertensive patients (particularly in newly diagnosed patients, but less among those on drugs), as compared with the control group. A significant decrease in plasma total antioxidant status was also observed in the hypertensive groups. The researchers say that lower total antioxidant status levels, which point towards increased oxidative stress, could be the reason behind higher lymphocyte DNA damage in the patients.

They emphasize that because oxidative damage is closely related to the development and complication of essential hypertension, this area of study requires larger clinical trials with hypertensive drugs.


  1. Subhash, P. et al. Total antioxidant status and oxidative DNA damage in a South Indian population of essential hypertensives. J. Hum. Hypertens. 24, 475-482 (2010) | Article | PubMed |