Dna damage and oxidative stress in passively smoking children
Zalata, A., Yahia, S., El-Bakary, A. (2006). Dna damage and oxidative stress in passively smoking children. EKB Journal Management System, 26(1), 33-46. doi: 10.21608/besps.2006.37421
Adel Zalata; Sohier Yahia; Amal El-Bakary. "Dna damage and oxidative stress in passively smoking children". EKB Journal Management System, 26, 1, 2006, 33-46. doi: 10.21608/besps.2006.37421
Zalata, A., Yahia, S., El-Bakary, A. (2006). 'Dna damage and oxidative stress in passively smoking children', EKB Journal Management System, 26(1), pp. 33-46. doi: 10.21608/besps.2006.37421
Zalata, A., Yahia, S., El-Bakary, A. Dna damage and oxidative stress in passively smoking children. EKB Journal Management System, 2006; 26(1): 33-46. doi: 10.21608/besps.2006.37421

Dna damage and oxidative stress in passively smoking children

Bulletin of Egyptian Society for Physiological Sciences
Article 3, Volume 26, Issue 1, June 2006, Page 33-46  XML PDF (424.35 K)
Document Type: Original Article
DOI: 10.21608/besps.2006.37421
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Authors
Adel Zalata* 1; Sohier Yahia2; Amal El-Bakary3
1Department of Biochemistry, Mansoura University
2Department of Pediatrics, Mansoura University
3Department of Forensic Medicine and Clinical Toxicology, Mansoura University
Abstract
Tobacco smoking is the greatest single cause of preventable illness and
premature death in killing half of all people who continue to smoke for most of their
life. Passive smoking causes lung cancer in non-smokers .Genetic markers are used to
detect early biological responses in an attempt to link carcinogen exposure to
initiating events in the carcinogenesis process.
The present study was conducted on 66 children. Their ages ranged 1-8 years.
Twenty children were control, and 46 children were selected from the Outpatient
Clinic of Mansoura University Children Hospital. Patients were classified into two
test groups. Group 1 comprised of 22 children exposed to light passive smoking.
Group 2 included 24 children exposed to heavy passive smoking. Urinary
cotinine/creatinine ratio was determined asa marker of exposure to passive smoking
for those children.
Heparinized blood samples were collected and used for separation of
lymphocytes. Lymphocytes were used for the comet assay and blood sera were used
for measurement of glutathione peroxidase activity (GPX), malondialdehyde (MDA)
and tochopherol fractions (α, γ, δ).
There is significant increase in the number of cases showing underweight, chest
problems and other presentations as gastroenteritis in exposed children. Passive
smoking increases clinical complications. There is significant increase in comet assay
% (P<0.001), and MDA (P<0.001), and significant decrease in GPX activity
(P<0.001) and tochopherol fractions (P<0.001) in group 1 and group 2 compared
with control.
There is significant correlation between the comet assay and GPX activity
(P<0.001), MDA (P<0.001), tochopherol fractions (P<0.001) and cotinine /
creatinine ratio (P<0.001). Stepwise regression analysis showed that comet assay
results could be explained by the changes of MDA, αtochopherol and
cotinine/creatinine ratio. In conclusion, exposure of children to tobacco smoke could
cause oxidative stress with increased DNA damage which may have a role in certain
diseases of children.
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