H. Negishi et al., The relation of oxidative DNA damage to hypertension and other cardiovascular risk factors in Tanzania, J HYPERTENS, 19(3), 2001, pp. 529-533
Citations number
28
Categorie Soggetti
Cardiovascular & Respiratory Systems","Cardiovascular & Hematology Research
Objectives To clarify the mechanism of involvement of oxidative stress in h
ypertensives, we investigated the relationship between the marker of oxidat
ive DNA damage, urinary 8-hydroxy-2'-deoxyguanosine (8-OHdG), and cardiovas
cular risk factors, such as hypertension and serum glycosylated hemoglobin
(HbA(1c)), among Tanzanians aged 46-58 years who were not on antihypertensi
ve medication.
Design and methods Sixty subjects (males/females, 28/ 32) were selected ran
domly from the subjects who completed a 24h urine collection in our epidemi
ological study at Dar es Salaam, Tanzania in 1998, The subjects were divide
d into two groups, hypertensive subjects (systolic blood pressure (SBP) gre
ater than or equal to 140 mmHg and/or diastolic blood pressure (DBP) greate
r than or equal to 90 mmHg) and normotensive subjects (SBP < 140 mmHg and D
BP < 90 mmHg) or hyperglycemic subjects (HbA(1c) greater than or equal to 6
.0%) and normoglycemic subjects (HbA(1c) < 6.0%), Biological markers from u
rine and blood were analyzed centrally in the WHO Collaborating Center.
Results The mean levels of HbA(1c) and 8-OHdG were significantly higher in
the hypertensive subjects than in the normotensive subjects (P < 0.05). Uri
nary 8-OHdG was significantly higher in hyperglycemic subjects than in norm
oglycemic subjects. HbA(1c) was positively correlated with the 24-h urinary
8-OHdG excretions (r= 0.698, P < 0.0001).
Conclusions These findings suggest oxidative DNA damage is increased in hyp
ertensive subjects, and there is a positive correlation between the level o
f blood glucose estimated as HbA(1c) and oxidative DNA damage. Hyperglycemi
a related to insulin resistance in hypertension in Tanzania is associated w
ith increased urinary 8-OHdG. <(c)> 2001 Lippincott Williams & Wilkins.