Prevention of bronchopulmonary dysplasia by administration of bovine superoxide dismutase in preterm infants with respiratory distress syndrome

Rosenfeld, Warren; Evans, Hugh E.; Concepcion, Luzminda; Jhaveri, Ramesh; Schaeffer, H; Friedman, Alexander

doi:10.1016/s0022-3476(84)80307-8

Cited by 138 publications

(43 citation statements)

References 23 publications

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“…Nonetheless, the antioxidant enzymes CAT, SOD, and GPx, when added together to formula, were shown to provide increased protection against oxidative stress and lipid damage, likely working with other systems in the HM. This suggests that the addition of these protective agents to formulas may help reduce the harmful effects of excess oxidative stress and inflammatory-induced reactive oxygen species, resulting in reduced symptoms, faster recovery, and normal development, as has been shown previously with SOD given intramuscularly (29). Consistent with these results is the report of Van ZoerenGrobben et al (7), who found that healthy breast-fed PT infants had higher antioxidant capacity in plasma compared with formula-fed infants.…”

Section: Discussionsupporting

confidence: 71%

Milk from Mothers of Both Premature and Full-Term Infants Provides Better Antioxidant Protection than Does Infant Formula

et al. 2002

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Section: Discussionsupporting

confidence: 71%

Milk from Mothers of Both Premature and Full-Term Infants Provides Better Antioxidant Protection than Does Infant Formula

et al. 2002

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“…In a study of humans exposed to increased inspired oxygen tensions for prolonged periods, administering bovine superoxide dismutase (SOD) subcutaneously in infants with respiratory distress syndrome palliated bronchopulmonary dysplasia (1). However, a detailed morphologic study done in newborn rats developing bronchovascular dysplasia as a result of early exposure to oxygen did not demonstrate any 1. Abbreviations used in this paper: G6PD, glucose-6-phosphate dehydrogenase; GPX, glutathione peroxidase, GR, glutathione reductase, SOD, superoxide dismutase.…”

Section: Introductionmentioning

confidence: 99%

Transgenic mice with expression of elevated levels of copper-zinc superoxide dismutase in the lungs are resistant to pulmonary oxygen toxicity.

White¹,

Avraham²,

Shanley³

et al. 1991

J. Clin. Invest.

134

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To test the hypothesis that increases in lung superoxide dismutase can cause tolerance to pulmonary oxygen toxicity, we studied transgenic mice which constitutively express elevated levels of the human copper-zinc SOD (CuZnSOD). Upon exposure to hyperoxia (> 99% 02, 630 torr) the transgenic CuZnSOD mice showed increased survival, decreased morphologic evidence of lung damage such as edema and hyaline membrane formation, and reduction in the number of lung neutrophils. During continuous exposure to oxygen, both control and transgenic animals who successfully adapted to hyperoxia showed increased activity of lung antioxidant enzymes such as glutathione peroxidase (GPX), glutathione reductase (GR), and glucose-6-phosphate dehydrogenase (G6PD), whereas superoxide dismutase activity remained unchanged. The results show that expression of elevated levels of CuZnSOD decreases pulmonary oxygen toxicity and associated histologic damage and mortality. (J. Clin.

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“…42 The repetitive subcutaneous administration of bovine SOD in a small randomized study in the pre-surfactant era yielded promising results. 43 In this group of relatively mature infants, SOD administration was not able to reduce the total days of oxygen therapy or mechanical ventilation but significantly reduced the days on CPAP and radiographic as well as clinical signs of BPD without major side effects. In a small study, the intratracheal application of recombinant human SOD (rhSOD) in two different dosages every 48 hours up to seven doses was well tolerated by VLBW infants and led to an increased SOD concentration in tracheal aspirate fluid and serum.…”

Section: Methylxanthinesmentioning

confidence: 72%

Prevention and treatment of bronchopulmonary dysplasia: current status and future prospects

Thomas

Speer

2007

J Perinatol

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This review summarizes the existing evidence for potential non-ventilatordependent strategies to prevent or ameliorate bronchopulmonary dysplasia (BPD). Oxygen plays an important pathogenetic and therapeutic role for BPD. Targeting infants with lower saturation of peripheral oxygen levels than traditionally used seems justified. Inhaled nitric oxide has not proven effective on pulmonary outcome in extremely low birth weight infants. Diuretics can ameliorate lung function transiently. High intramuscular doses of vitamin A reduce the risk of BPD. Prophylactic application of natural surfactant may also confer benefits. Recently, early administration of caffeine has been shown to decrease risk of BPD. However, assessment of long-term effects is needed before routine use can be recommended. Owing to potential short-and long-term effects, postnatal corticosteroids should be restricted to the most severe manifestations of BPD. Superoxide dismutase and a1-proteinase inhibitor have not shown efficacy in preventing BPD. The potential role of anti-inflammatory therapies like Clara Cell 10 kDa protein has yet to be defined.

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Prevention of bronchopulmonary dysplasia by administration of bovine superoxide dismutase in preterm infants with respiratory distress syndrome

Cited by 138 publications

References 23 publications

Milk from Mothers of Both Premature and Full-Term Infants Provides Better Antioxidant Protection than Does Infant Formula

Milk from Mothers of Both Premature and Full-Term Infants Provides Better Antioxidant Protection than Does Infant Formula

Transgenic mice with expression of elevated levels of copper-zinc superoxide dismutase in the lungs are resistant to pulmonary oxygen toxicity.

Prevention and treatment of bronchopulmonary dysplasia: current status and future prospects

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