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Antioxidant status in newborns and infants suffering from congenital heart defects
Władysław Rokicki1, Adam Strzałkowski, Barbara Kłapcińska
1Department of Pediatric Cardiology Medical University of Silesia, Katowice.
Insights
Infants with congenital heart defects (CHD) show an antioxidant imbalance, with lower vitamin E and altered glutathione peroxidase activity. Oxidative stress is linked to CHD in infants, highlighting potential therapeutic targets.
Area of Science:
- Biochemistry
- Pediatrics
- Cardiology
Background:
- Free radicals are implicated in tissue damage, but their role in infant congenital heart defects (CHD) is understudied.
- Congenital heart defects (CHD) affect newborns and infants, necessitating research into associated pathophysiological mechanisms.
Purpose of the Study:
- To evaluate the antioxidant status in newborns and infants with CHD.
- To investigate the relationship between oxidative stress markers and CHD in infants.
Main Methods:
- Assessed antioxidant enzyme activities (superoxide dismutase, catalase, glutathione peroxidase) in blood.
- Measured levels of low molecular weight antioxidants (vitamin E, uric acid, selenium) and malondialdehyde (MDA) as a lipid peroxidation marker.
- Compared 23 infants with CHD (14 acyanotic, 9 cyanotic) against 18 healthy controls.
Main Results:
- All infants, including controls, had low blood selenium.
- Infants with CHD exhibited lower plasma vitamin E, significantly so in acyanotic cases.
- Glutathione peroxidase activity was lowest in cyanotic infants, correlating with highest MDA levels (lipid peroxidation).
- Uric acid levels were higher in cyanotic infants, potentially offering protection against oxidative damage.
Conclusions:
- Enhanced oxidative stress, resulting from an imbalance between prooxidant and antioxidant reactions, is associated with congenital heart defect pathology in infants.
- Specific antioxidant deficiencies (e.g., vitamin E) and altered enzyme activities (e.g., glutathione peroxidase) are observed in infants with CHD.
Abstract:
There is a common view that free radicals may play an important role in tissue damage resulting from circulatory insufficiency, cardiosurgery etc. There are very few data concerning the involvement of free radical reactions in the newborns and infants suffering from congenital heart defects (CHD). Antioxidant status was evaluated in 41 newborns and infants under 1 year of age, among them 23 suffering from CHD (14 with left-to-right shunt and 9 with cyanotic heart defect) and 18 healthy controls. The study based on the assessment of activities of antioxidant enzymes in blood (superoxide dismutase, catalase and glutathione peroxidase), levels of low molecular weight antioxidants (vitamin E, uric acid and selenium) and the concentration of malondialdehyde (MDA) as a marker of lipid peroxidation. All subjects had low blood selenium concentration as compared to the level considered as being adequate. Infants suffering from CHD had lower, as compared to healthy controls, plasma vitamin E concentration. The difference was significant in the case of acyanotic ones. The activities of superoxide dismutase and catalase in infants with CHD were not significantly different from the respective values recorded in healthy controls. The activity of glutathione peroxidase in whole blood was the lowest in infants with cyanotic heart defect in whom lipid peroxidation, as evaluated by MDA level, was the most enhanced. Significantly higher plasma concentration of uric acid which may be interpreted as a positive mechanism enabling better protection of red blood cells from peroxidative damage was found in this group of infants. It is concluded that enhanced oxidative stress due to imbalance between prooxidant and antioxidant reactions appears to be associated with congenital heart defect pathology in infants.
