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. 1994 Mar;70(2):F107-11.
doi: 10.1136/fn.70.2.f107.

Lipid peroxidation as a measure of oxygen free radical damage in the very low birthweight infant

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Lipid peroxidation as a measure of oxygen free radical damage in the very low birthweight infant

T E Inder et al. Arch Dis Child Fetal Neonatal Ed. 1994 Mar.

Abstract

(ABSTRACTOxygen free radical mediated tissue injury is implicated as a major factor in the pathogenesis of the long term complications seen in the premature infant, and direct evidence of their role in the development of these long term problems is lacking. A prospective observational study of 78% of very low birthweight infants admitted to a level III neonatal intensive care unit in 1992 was undertaken to determine the relationship between lipid peroxidation products, antioxidant activity, and outcome. Lipid peroxidation (malondialdehyde-thiobarbituric acid, MDA-TBA) and antioxidant activity (vitamin E and glutathione peroxidase activity) were measured in 22 very low birthweight infants in the cord blood and the infant's blood at 24 hours, 48 hours, and 1 week of age and correlated with outcome measures. The normal range for these measures was established in the cord blood samples of 48 consecutive healthy full term infants. The concentration of MDA-TBA at 1 week correlated with the number of days of oxygen treatment and number of days of positive pressure ventilatory support. Controlling for gestational age and antenatal complications simultaneously the MDA-TBA concentration remained significantly associated with the number of days of oxygen treatment and the number of days of positive pressure ventilatory support. Glutathione peroxidase was low in the premature and full term infants consistent with the low concentrations of selenium known to be present in southern New Zealand. There was evidence of a quadratic relationship between vitamin E at 1 week and the total number of days of supplementary oxygen requirement, with both high and low values associated with increased oxygen requirement. This association, however, did not remain after controlling for gestational age and antenatal complications. These results support the role of oxygen free radicals in mediating tissue damage associated with the development of chronic lung disease in the premature infant.

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