Effect of vitamin C supplementation on oxidative DNA damage in an experimental model of lead-induced hypertension

Attri, J; Dhawan, V; Mahmood, S; Pandhi, P; Parwana, HK; Nath, R

HERO ID

81459

Reference Type

Journal Article

Year

2003

Language

English

PMID

14520025

HERO ID 81459
In Press No
Year 2003
Title Effect of vitamin C supplementation on oxidative DNA damage in an experimental model of lead-induced hypertension
Authors Attri, J; Dhawan, V; Mahmood, S; Pandhi, P; Parwana, HK; Nath, R
Journal Annals of Nutrition and Metabolism
Volume 47
Issue 6
Page Numbers 294-301
Abstract Aims: Chronic exposure to lead results in sustained hypertension in humans and experimental animals. We investigated the possible role of reactive oxygen species (ROS) and their impact on DNA damage in lead-induced hypertension. Further the effect of short-term supplementation of vitamin C is also demonstrated. Methods: Male Wistar rats were treated with either lead acetate (100 ppm) alone or lead acetate plus vitamin C (20 mg/rat/day). The control rats were fed regular rat chow. Blood pressure, antioxidants, total antioxidant status as measured by ferric-reducing antioxidant power, nitric oxide (NO) metabolites, malondialdehyde (MDA) and 8-hydroxy 2-deoxyguanosine were determined after 0, 1, 2 and 3 months. Results: The lead-exposed group showed a significant rise in blood pressure, lipid peroxidation (MDA) and a substantial oxidative damage to the DNA. A significant fall in NO metabolites, total antioxidant levels and ferric-reducing antioxidant power was also observed in this group. Concomitant administration of vitamin C ameliorated hypertension, normalized NO levels and abrogated lipid peroxidation. Also, it completely prevented oxidative damage to the DNA. Conclusions: These findings point to enhanced ROS-mediated inactivation and sequestration of NO which can potentially contribute to hypertension, lipid peroxidation, reduced antioxidant status and oxidative DNA damage. The beneficial effects of vitamin C on these parameters support the role of increased ROS activity in the pathogenesis of these abnormalities in this model.
Doi 10.1159/000072402
Pmid 14520025
Wosid WOS:000185848400006
Is Certified Translation No
Dupe Override No
Is Public Yes
Language Text English
Keyword blood pressure; nitric oxide; oxidative stress; DNA damage