Lymphocyte DNA damage and total antioxidant status in patients with white-coat hypertension and sustained hypertension.
OBJECTIVE
We assessed lymphocyte DNA damage and total antioxidant status (TAS) in patients with white-coat hypertension (WCH) and sustained hypertension (SHT).


METHODS
The study included 23 patients (14 females, 9 males; mean age 46+/-6 years) with WCH, 21 patients (13 females, 8 males; mean age 45+/-7 years) with newly diagnosed SHT, and 19 age- and sex-matched healthy volunteers as controls. All subjects underwent echocardiographic examination, office blood pressure measurements, and 24-hour ambulatory blood pressure monitoring. DNA damage was assessed by the alkaline comet assay in peripheral lymphocytes, and plasma TAS levels were determined using an automated measurement method.


RESULTS
The two hypertensive groups had similar echocardiographic measurements and office systolic and diastolic blood pressures. The mean daytime and nighttime pressures were significantly higher in the SHT group (p<0.05). Patients with WCH had similar daytime and nighttime pressures compared to the controls (p>0.05). Patients with SHT had significantly increased lymphocyte DNA damage (p<0.001, for both WCH and control groups) and decreased TAS level (p=0.012 vs WCH group; p<0.001 vs controls). Patients with WCH did not differ significantly from the control group with regard to lymphocyte DNA damage (p=0.052), but had significantly lower TAS levels (p<0.001). In the SHT group, lymphocyte DNA damage was correlated with TAS (r= -0.818, p<0.001), age (r=0.453, p=0.039), total cholesterol (r=0.550, p=0.010), and LDL-cholesterol (r=0.539, p=0.012). In multiple linear regression analysis, lymphocyte DNA damage was independently correlated with serum TAS level (beta= -0.717, p<0.001). In the WCH group, lymphocyte DNA damage was only correlated with serum TAS level (r= -0.458, p=0.028).


CONCLUSIONS
Decreased TAS showing increased oxidative stress and increased lymphocyte DNA damage may contribute to target organ damage in patients with WCH.
Yildiz
Ali
A
Department of Cardiology, Medicine Faculty of Harran University, Sanliurfa, Turkey. ghcayildiz@yahoo.com
Gür
Mustafa
M
Yilmaz
Remzi
R
Demirbağ
Recep
R
Celik
Hakim
H
Aslan
Mehmet
M
Koçyiğit
Abdurrahim
A