Nutrient Deficiencies in the Premature Infant

Shah, Malika D.; Shah, Shilpa

doi:10.1016/j.pcl.2009.08.001

Cited by 56 publications

(51 citation statements)

References 98 publications

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“…Conversely, serum or plasma levels of non-enzymatic antioxidants, including vitamin A (De Vriese et al 2001) and b-carotene (Oostenbrug et al 1998), decrease throughout pregnancy, while levels of a-tocopherol increase (Oostenbrug et al 1998, De Vriese et al 2001. Together these gestational changes in antioxidant capacity appear to place the preterm newborn at an increased risk of ROSinduced injury (Shah & Shah 2009). DHA has previously been shown to enhance glutathione reductase levels in response to oxidative stress in human fibroblast cells (Arab et al 2006).…”

Section: Discussionmentioning

confidence: 99%

Differential effects of docosahexaenoic acid on preterm and term placental pro-oxidant/antioxidant balance

2013

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Docosahexaenoic acid (DHA) supplementation in pregnancy may confer some clinical benefits; however, this compound can exert pro-oxidant effects. In this study, we investigated the effects of DHA on pro-oxidant/antioxidant balance in term and preterm placental explants, assessing oxidative stress marker concentrations, antioxidant capacity and pro-inflammatory cytokine production. Term (nZ8) and preterm (nZ9) placental explants were exposed to lipopolysaccharide (LPS, 1 ng/ml), DHA (1, 10 and 100 mM), and DHA and LPS simultaneously or pre-treated with DHA for 24 h prior to LPS treatment. The production of malondialdehyde (MDA, lipid peroxidation), 8-hydroxy-2-deoxy guanosine (8-OHdG, oxidative DNA damage) and pro-inflammatory cytokines (tumour necrosis factor a (TNFa), interleukin 6 and interferon-g) and total antioxidant capacity were measured. DHA at a concentration of 100 mM induced oxidative stress in term placentas, while at all the three concentrations, it induced oxidative stress in preterm placentas. DHA and LPS resulted in reduced MDA levels in term (P!0.005) and preterm (PZ0.004) placentas and reduced 8-OHdG levels in preterm placentas (PZ0.035). DHA pre-treatment, but not co-treatment with LPS, reduced 8-OHdG levels (P!0.001) in term placentas. DHA increased antioxidant capacity only in term placentas (P!0.001), with lower antioxidant capacity being observed overall in preterm placentas compared with term placentas (P%0.001). In term placentas, but not in preterm ones, DHA co-treatment and pre-treatment reduced LPS-induced TNFa levels. The ability of DHA to alter placental pro-oxidant/antioxidant balance is dependent on the DHA concentration used and the gestational age of the placental tissue. DHA has a greater capacity to increase oxidative stress in preterm placentas, but it offers greater protection against inflammation-induced oxidative stress in term placentas. This appears to be a result of DHA altering placental antioxidant capacity. These data have implications for the timing and concentration of DHA supplementation in pregnancy.

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Section: Discussionmentioning

confidence: 99%

Differential effects of docosahexaenoic acid on preterm and term placental pro-oxidant/antioxidant balance

2013

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“…Nutritional requirements are higher for premature infants because most glucose, protein, mineral and fatty acid stores are accelerated in the third trimester of pregnancy. 2 Because of the late accretion of these important nutrients, the more premature the infant is at birth, the more deficient the nutrient stores.…”

Section: Introductionmentioning

confidence: 99%

Evaluation of human milk fortification from the time of the first feeding: effects on infants of less than 31 weeks gestational age

2011

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Objective: To determine whether human milk fortification from the time of the first feeding significantly improves weight gain and bone mineral status in infants of <31 weeks estimated gestational age as compared with delayed or standard human milk fortification.Study Design: This was a retrospective pre-post design. In all, 95 infants born at <31 weeks estimated gestational age were compared. There were 53 infants in the early fortification group (EFG) and 42 infants in the delayed fortification group (DFG). They were compared with regard to weight gain at 34 weeks postmenstrual age (PMA), and their serum levels of calcium, phosphorus and alkaline phosphatase levels were compared as an indicator of bone mineral status. The practice change of fortifying all human milk given to preterm infants at <34 weeks PMA commenced in June 2009. The usual practice of fortification took place once an infant had reached a feeding volume of 50 to 100 ml kg À1 per day. The new practice fortified all human milk with a powdered human milk fortifier to 24 calories per ounce, starting with the first feeding, no matter how small the volume.Result: There were no differences in weight gain between the EFG and the DFG. The group that received fortification from the time of the first feeding were significantly less likely to have alkaline phosphatase levels >500 U l À1 from 33 weeks PMA onward. There was no incidence of feeding intolerance with early fortification.Conclusion: Fortification of human milk from the time of the first feeding does not affect weight gain at 34 weeks PMA, but is related to a lower incidence of elevated alkaline phosphate levels and does not cause feeding intolerance.

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“…Comparison of erythrocytes, plasma, and bronchoalveolar lavage fluids from preterm and term infants identified GSH, GPx, and SOD deficiencies that correlated with the degree of prematurity (66,85). Deficiencies of nonenzymatic antioxidants, including alpha tocopherol and vitamin A, have also been documented in serum samples from premature infants (46,64,98). Finally, indirect evaluation of antioxidant capacities using fetal tissue and serum samples from premature infants confirms elevated markers of oxidative stress and a reduced antioxidant potential (31, 41, 58, 77, 95).…”

Section: Human Studiesmentioning

confidence: 99%

Developmental Regulation of Antioxidant Enzymes and Their Impact on Neonatal Lung Disease

Berkelhamer

Farrow

2014

Antioxidants & Redox Signaling

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Significance: Deficient antioxidant defenses and compromised ability to respond to oxidative stress burden the immature lung. Routine neonatal therapies can cause increased oxidative stress with subsequent injury to the premature lung. Novel therapeutic approaches to protect the premature lung are greatly needed. Recent Advances: Live cell imaging with targeted redox probes allows for the measurement of subcellular oxidative stress and for comparisons of oxidative stress across development. Comprehension of subcellular and cell-typespecific responses to oxidative stress may influence the targeting of future antioxidant therapies. Critical Issues: Challenges remain in identifying the optimal cellular targets, degree of enzyme activity, and appropriate antioxidant therapy. Further, the efficacy of delivering exogenous antioxidants to specific cell types or subcellular compartments remains under investigation. Treatment with a nonselective antioxidant could unintentionally compromise cellular function or impact cellular defense mechanisms and homeostasis. Future Directions: Genetic and/or biomarker screening may identify infants at the greatest risk for oxidative lung injury and guide the use of more selective antioxidant therapies. Novel approaches to the delivery of antioxidant enzymes may allow cell type-or cellular organelle-specific therapy. Improved comprehension of the antioxidant enzyme regulation across cell type, cell compartment, gender, and developmental stage is critical to the design and optimization of therapy.

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Nutrient Deficiencies in the Premature Infant

Cited by 56 publications

References 98 publications

Differential effects of docosahexaenoic acid on preterm and term placental pro-oxidant/antioxidant balance

Differential effects of docosahexaenoic acid on preterm and term placental pro-oxidant/antioxidant balance

Evaluation of human milk fortification from the time of the first feeding: effects on infants of less than 31 weeks gestational age

Developmental Regulation of Antioxidant Enzymes and Their Impact on Neonatal Lung Disease

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