BACKGROUNDParenteral nutrition (PN) is associated with bronchopulmonary dysplasia in premature infants. In animals, PN leads to alveolar loss following stimulation of apoptosis by oxidative stress (oxidized redox potential). Peroxides and aldehydes generated in PN can induce hypo-alveolarization. The implication of peroxides, which is reduced by light protection, is demonstrated. The implication of aldehydes from omega-6 fatty acids oxidation is expected. The hypothesis is that composition and light exposure of PN influences bronchopulmonary dysplasia development. Since SMOFLipid (SMOF) contains a lower amount of omega-6 fatty acids than Intralipid (IL), the aim was to compare, the impacts of PN compounded with SMOF or IL, photo-protected or not, on alveolar development.MATERIALS AND METHODSThree-day-old Guinea pigs received PN, photo-protected or not, made with SMOF or IL through a jugular vein catheter. After 4 days, lungs were sampled for determinations of redox potential of glutathione, apoptosis (caspase-3, caspase-8, and caspase-9) and alveolarization index (histology: number of intercepts/mm).RESULTSCompared with IL, SMOF induces a greater oxidation of redox potential (-200 ± 1 versus [vs] -205 ± 1 mV), apoptosis (caspase-3: 0.27 ± 0.04 vs 0.16 ± 0.02; caspase-9: 0.47 ± 0.03 vs 0.30 ± 0.03), and a lower alveolarization index (27.2 ± 0.8 vs 30.0 ± 0.9). Photo-protection prevented activation of caspase-9 and was statistically without effect on redox potential, caspase-3, and alveolarization index.CONCLUSIONIn our model, SMOF is pro-oxidant and induces hypo-alveolarization following exaggerated apoptosis. These results highlight the need for further studies before introducing SMOFLipid in standard neonatal care.

Peroxides are generated in parenteral nutrition (PN). Infusion of PN or H2O2 in the first week of life of animals alters later in life their hepatic energy metabolism. Glutathione addition in PN prevented pulmonary oxidative stress induced by PN in newborn guinea pigs (GP). Hypothesis: Addition of glutathione into PN prevents the long-term impact of PN on activities of key enzymes of energy metabolism (glucokinase (GK), phosphofructokinase (PFK) and acetyl-CoA carboxylase (ACC)). 4 groups (N=48) of 3-day old GP were used. Control: no manipulation, fed ad libitum all time; PN: animals nourished exclusively with a complete PN via a catheter; PN+ 6 or 12 µM GSSG; GSSG was used as pro-GSH. After 4 days, hepatic redox potential was measured in half of GP. The other half started oral diet. At 16 weeks of age, liver was collected for determination of GSH, GSSG and redox potential (capillary electrophoresis, Nernst's equation), activities (U: nmol/min/mg prot) of PFK, GK (calorimetric method), and ACC (method with radioactive tracer). Data (mean±sem) were analyzed by ANOVA, p<0.05. Immediately after treatments, there was no difference between groups for redox potential (mV) (-231±1). Four months later, redox potential, GSH and GSSG (nmol/mg prot) were lower in PN groups independently of GSSG addition, relatively to control (respectively, PN groups: -235±1, 69±2, 0.8±0.1 vs. Control: -229±2, 81±5, 1.8±0.3). ACC activity was higher in PN group (4.5±0.3 U) and greater in NP+GSSG groups (5.7±0.3 U) relatively to control (3.2±0.2 U). GK and PFK activities did not differ. PN early in life induces later in liver reduction of redox potential and higher activity of a key enzyme of lipogenesis (ACC). In contrast to beneficial effect previously observed in lungs, addition of GSSG into PN did not prevent the long-term effects of PN on the liver.

Background: The immaturity of glutathione metabolism is believed to explain the oxidative stress observed in premature neonates on total parenteral nutrition [TPN]. Animal studies report that peroxides contaminating TPN induce the low glutathione levels as a consequence of the inhibition of the generation of substrates for its synthesis. We hypothesize that older children receiving long-term TPN have low levels of glutathione with the consequence to have an increased oxidative stress. Methods: Total glutathione and oxidative stress markers [hydroperoxides and isoprostane-F2α] were measured in urine, plasma or erythrocytes from 6 children aged 77 ± 24 months treated with TPN for a mean duration of 28 ± 7 months and from 7 control children aged of 87 ± 21 months. Results: In the TPN group, glutathione was lower [p<0.01] whereas hydroperoxide and isoprostane-F2α were higher [p<0.01] than in control group. Plasma isoprostane-F2α was negatively correlated with erythrocytes glutathione [r2 = 0.60, p<0.01]. Ascorbate levels were similar in erythrocyte, but higher [p<0.05] in urine of the TPN group. Conclusion: Similar to premature infants, oxidative stress is increased in children on long-term TPN. The oxidative stress is associated with low glutathione.

Peroxides contaminating parenteral nutrition (PN) are associated with oxidized redox potential of glutathione in blood of preterm newborns (<30 wks) and in lungs of animal. An oxidized redox and the peroxides are associated to bronchopulmonary dysplasia in preterm newborns and induce loss of alveoli in animals. Glutathione detoxifies peroxides and normalises redox potential. The low glutathione in preterm newborns limits capacity to detoxify peroxides. Glutathione is derived from liver where methionine is transformed in cysteine of which availability limits the glutathione synthesis. Peroxides inhibit this transformation. Hypothesis: Addition of glutathione into PN compensates for the low hepatic capacity to supply glutathione, and consequently preserves the lung integrity.

Background: Ascorbylperoxide (AscOOH) is a hydrogen peroxide–dependent by‐product of ascorbic acid that contaminates parenteral nutrition. In a guinea pig model, it caused oxidized redox potential, increased apoptosis, and decreased alveolarization. AscOOH detoxification is carried out by glutathione peroxidase (GPX). We hypothesize that extremely preterm infants have limited capacity for AscOOH detoxification. Our objective was to determine if there is an association between an early level of urinary AscOOH and later development of bronchopulmonary dysplasia (BPD) or death. Materials and Methods: This prospective cohort study included 51 infants at <29 weeks of gestation. Baseline clinical characteristics and clinical outcomes data were collected. Urine samples were collected on days 3, 5, and 7 of life for urinary AscOOH. Blood samples on day 7 were collected for total plasma glutathione, GPX, and glutathione reductase. χ 2 , Student's t test, Spearman correlation ( r ), linear regression (adjusted r 2 ), and repeated‐measure analysis of variance were used as appropriate. P < .05 was considered significant. Results: Urinary AscOOH increased over time ( P = .001) and was higher in infants who later developed BPD or died ( P = .037). Compared with adults and full‐term infants, total plasma glutathione concentration was low (median, 1.02 µmol/L; 25th–75th percentiles, 0.49–1.76 µmol/L), whereas GPX and glutathione reductase activities were sufficient (3.98 ± 1.25 and 0.36 ± 0.01 nmol/min/mg of protein, respectively). Conclusion: Extremely preterm infants have low glutathione levels, which limit their capacity to detoxify AscOOH. Higher first‐week urinary AscOOH levels are associated with an increased incidence of BPD or death.

Infants born <30 weeks of gestation suffer from major oxidative stress because their parenteral nutrition (PN) is contaminated with peroxides. This oxidative stress in early life is suspected to be an important inducer of several health complications observed in adults, following epigenetic modifications. Peroxides as well as the oxidized redox potential reduce the activity of the methionine adenosyltransferase, leading to a lower generation of S-adenosylmethionine (SAM), the substrate for DNA methylation. The recent proposition to change the lipid emulsion of PN from Intralipid (low n-3 fatty acid) to SMOFLipid (high n-3 fatty acid) is questionable. Indeed, n-3 fatty acids are more prone to oxidation and to peroxides generation. Compared to Intralipid (IL), SMOFLipid (SM) is suspected to induce greater oxidative stress and lower DNA methylation.

Background: The oxidation of the methionine adenosyltransferase (MAT) by the combined impact of peroxides contaminating parenteral nutrition (PN) and oxidized redox potential of glutathione is suspected to explain its inhibition observed in animals. A modification of MAT activity is suspected to be at origin of the PN-associated liver disease as observed in newborns. We hypothesized that the correction of redox potential of glutathione by adding glutathione in PN protects the MAT activity. Aim: To investigate whether the addition of glutathione to PN can reverse the inhibition of MAT observed in animal on PN. Methods: Three days old guinea pigs received through a jugular vein catheter 2 series of solutions. First with methionine supplement, (1) Sham (no infusion); (2) PN: amino acids, dextrose, lipids and vitamins; (3) PN-GSSG: PN+10 μM GSSG. Second without methionine, (4) D: dextrose; (5) D+180 μM ascorbylperoxide; (6) D+350 μM H2O2. Four days later, liver was sampled for determination of redox potential of glutathione and MAT activity in the presence or absence of 1 mM DTT. Data were compared by ANOVA, p<0.05. Results: MAT activity was 45±4% lower in animal infused with PN and 23±7% with peroxides generated in PN. The inhibition by peroxides was associated with oxidized redox potential and was reversible by DTT. Correction of redox potential (PN+GSSG) or DTT was without effect on the inhibition of MAT by PN. The slope of the linear relation between MAT activity and redox potential was two fold lower in animal infused with PN than in others groups. Conclusion: The present study suggests that prevention of peroxide generation in PN and/or correction of the redox potential by adding glutathione in PN are not sufficient, at least in newborn guinea pigs, to restore normal MAT activity.

Bronchopulmonary dysplasia, a main complication of prematurity, is characterized by an alveolar hypoplasia. Oxidative stress is suspected to be a trigger event in this population who has a low level of glutathione, a main endogenous antioxidant, and who receives high oxidative load, particularly ascorbylperoxide from their parenteral nutrition. Hypothesis: the addition of glutathione (GSSG) in parenteral nutrition improves detoxification of ascorbylperoxide by glutathione peroxidase and therefore prevents exaggerated apoptosis and loss of alveoli.Methods: Ascorbylperoxide is assessed as substrate for glutathione peroxidase in Michaelis-Menten kinetics. Three-days old guinea pig pups were divided in 6 groups to receive, through a catheter in jugular vein, the following solutions: 1) Sham (no infusion); 2) PN(-L): parenteral nutrition protected ! against light (low ascorbylperoxide); 3) PN(+L): PN without photo-protection (high ascorbylperoxide); 4) 180 mu M ascorbylperoxicle; 5) PN(+L)+10 mu M GSSG; 6) ascorbylperoxyde +10 mu M GSSG. After 4 days, lungs were sampled and prepared for histology and biochemical determinations. Data were analysed by AN OVA. p < 0.05Results: The Km of ascorbylperoxide for glutathione peroxidase was 126 +/- 6 mu M and Vmax was 384 +/- 2.5 nmolimini U. The presence of GSSG in intravenous solution has prevented the high GSSG, oxidized redox potential of glutathione, activation of caspase-3 (apoprosis marker) and loss of alveoli induced by PN( + L) or ascorbylperoxide.Conclusion: A correction of the low glutathione levels observed in newborn animal on parenteral nutrition, protects lungs from toxic effect of ascorbylperoxide. Premature infants having a low level of glutathione, this finding is of high importance because it provides hope in a possible prevention of bronchopulmonary dysplasia. (C) 2015 Published by Elsevier Inc.

OBJECTIVES To assess the effect of early exposure to O2 and parenteral nutrition (PN) on oxidative stress at 36 weeks post-menstrual age (PMA) and on bronchopulmonary dysplasia (BPD) in extremely preterm infants. STUDY DESIGN A prospective observational study including 116 infants <29 weeks of gestation. Baseline clinical characteristics, FiO2 on day 7, duration of PN and clinical outcomes data were collected. In 39 infants, whole blood glutathione (GSH) and oxidized glutathione (GSSG) at 36 weeks PMA were measured and the redox potential was calculated using Nernst equation. Student's t-test, Chi-square, Spearman correlation, ANOVA, and logistic regression analyses were used as appropriate. P < 0.05 was considered significant. RESULTS FiO2 ≥25% was associated with higher level of GSSG (0.29 ± 0.04 versus 0.18 ± 0.02 nmol/mg of protein), a more oxidized redox potential (-191 ± 2 versus -198 ± 2 mV) and more BPD (90% versus 45%). PN duration >14 days was also associated with higher level of GSSG (0.26 ± 0.03 versus 0.13 ± 0.02 nmol/mg of protein), a more oxidized redox potential (-193 ± 5 versus -203 ± 2 mV) and more BPD (89% versus 24%). In logistic regression model, each 1% increase in FiO2 and each day increase in PN duration resulted in an increase in the OR for BPD by 1.57 (1.09 -2.28) and 1.17 (1.03 -1.33) respectively. CONCLUSION Early O2 supplement and PN have additive effects that were associated with prolonged oxidative stress and increased risk of BPD. Strategies targeting judicious use of O2 and decreasing the duration or developing a safer formulation of PN can be targeted to decrease BPD.

Transhumance sheep and goat production have been a common and traditional practice in Greece, with its origins dating back to ancient times. Despite the diminishing number of transhumance farms, it remains an essential activity in less-favoured and mountainous areas of the country. This article applies DEA (Data Envelopment Analysis) in a sample of transhumance farms in Greece in order to assess the technical efficiency of sheep and goat transhumance flocks and determine the factors that affect their performance. The effect of EU subsidies on the technical efficiency of transhumance farms is assessed and the type of farms that benefit most is investigated. Results accrued reveal that the overall technical efficiency of transhumance farms in Greece is quite low and it is affected by herd size. EU subsidies have a significant impact on the technical efficiency of only the low-efficiency, small-sized farms.

Background: Bronchopulmonary dysplasia is one of the main complications associated with extreme prematurity. Oxidative stress is suspected to be a trigger event of this lung disease, which is characterized by impaired alveolar development. Peroxides, mainly ascorbylperoxide and H2O2, are known contaminant of parenteral nutrition. We hypothesize that these oxidant molecules induce bronchopulmonary dysplasia development. The aim was to determine if the infusion of ascorbylperoxide, whether in presence or absence of H2O2, is associated with oxidative stress, apoptosis and loss of alveoli in the lungs of newborn guinea pigs.Method: Three-day-old guinea pigs received parenteral solutions containing 0, 20, 60 or 180 mu M ascorbylperoxide in the presence or not of 350 mu M H2O2 (concentrations similar to those measured in parenteral nutrition). After 4 days, the lungs were collected for determination of glutathione's redox potential, caspase-3 activation (an apoptosis marker), alveolarization index (by histology), activation of Nrf2 and NF kappa B (biological markers of oxidative stress), and IL-6 and PGJ(2) levels (markers of NF kappa B activation). Groups were compared by ANOVA, p < 0.05.Results: Loss of alveoli was associated with ascorbylperoxide in a dose-dependent manner, without an influence of H2O2. The dose-dependent activation of caspase-3 by ascorbylperoxide was lower in the presence of H2O2. Ascorbylperoxide induced an increase of redox potential in a dose-dependent manner, which reached a plateau in presence of H2O2. Nrf2 and NF kappa B were activated by H2O2 but not by ascorbylperoxide.Conclusion: Results suggest that ascorbylperoxide, generated in parenteral nutrition, is involved in the development of bronchopulmonary dysplasia, independently of the increase of the redox potential. This study underlines the importance of developing a safer formulation of parenteral nutrition. (C) 2014 The Authors. Published by Elsevier B.V.

In preterm infants, the antioxidant defenses are still poorly developed. The two major sources of oxidants during intensive care stay are oxygen and parenteral nutrition (PN) which is contaminated with peroxides. We hypothesize that early O2 supplementation and longer PN duration increase the risk for oxidative stress associated diseases such as bronchopulmonary dysplasia (BPD), retinopathy of prematurity (ROP) and necrotizing enterocolitis (NEC). To assess the effect of early oxygen (on day 7 and 28) and the PN duration on oxidative stress markers at 36 weeks corrected age and on oxidative stress related diseases. A prospective observational study including all infants <29 weeks GA without major congenital anomalies admitted to our NICU during one year period (116 infants). During the first week of life, in fifty-one out of 116 infants, consent for blood sample at 36 corrected age (CA) was obtained. GSH and GSSG (nmol/mg protein) were measured by capillary electrophoresis and were used for redox potential (mV) calculation using Nernst equation -expressed as mean (sem). BPD was defined as the need of O2 supplement at 36 weeks CA. Significant ROP was defined as any ROP stage 3 or higher or that required laser or anti-VEGF treatment. Cases of NEC grade 2 or higher according to Bell's criteria were included. Student's t test or χ2 were used, as appropriate, *=P<0.05, **=P<0.01. Basline chracteristics was similar in the consent group and the whole cohort. FiO2 ≥25 on day 7 and 28 of life and PN duration >14 days resulted in higher GSSG concentration and more oxidized redox potential at 36 weeks CA indicating prolonged oxidative stress. FiO2 ≥25 early on life and PN duration >14 days increased the incidence of BPD, significant ROP and NEC (Table 1). Early life exposure to oxidants is associated with prolonged oxidative stress and higher incidence of oxidative stress-related diseases. These results suggest that strategies targeting judicious O2 use and either decreasing the duration or using safer formulation PN will help decreasing the incidence of BPD, ROP and NEC.

Background The antioxidant defenses are poorly developed in preterm infants. Oxygen and parenteral nutrition (PN) which is contaminated with peroxides are two major sources of oxidants. Objective To assess the effect of early oxygen (on day 7 and 28) and the PN duration on oxidative stress markers at 36 weeks post menstrual age (PMA) and on the incidence of neonatal morbidities. Design/methods A prospective observational study including 120 infants less than 29 weeks gestational age without major congenital anomalies. Consent for blood sample at 36 weeks PMA was obtained for 51 infants. GSH and GSSG (nmol/mg protein) were measured by capillary electrophoresis and were used for redox potential (mV) calculation using Nernst equation, and expressed as mean (± sem). BPD was defined as the need of O2 supplement at 36 weeks PMA. ROP that required either laser or anti-VGF treatment and NEC grade 2 or higher according to Bell’s criteria were included. Student’s t test or Chi squared were used as appropriate, * = p < 0.05, **= p < 0.01. Results FiO2 ≥ 25% on day 7 and 28 of life and PN duration > 14 days resulted in higher GSSG concentration, more oxidised redox potential at 36 weeks PMA and increased the incidence of BPD, ROP and NEC Conclusions Early life exposure to oxidants is associated with prolonged oxidative stress and higher incidence of neonatal morbidities. These results suggest that strategies targeting judicious O2 use and either decreasing the duration or using safer formulation PN will help decreasing the incidence of BPD, ROP and NEC.

Neonatal total parenteral nutrition (TPN) is associated with animals with low glucose tolerance, body weight, and physical activity at adulthood. The early life origin of adult metabolic perturbations suggests a reprogramming of metabolism following epigenetic modifications induced by a change in the pattern of DNA expression. We hypothesized that peroxides contaminating TPN inhibit the activity of DNA methyltransferase (DNMT), leading to a modified DNA methylation state. Three groups of 3-d-old guinea pigs with catheters in their jugular veins were compared: (i) control: enterally fed with regular chow; (ii) TPN: fed exclusively with TPN (dextrose, amino acids, lipids, multivitamins, contaminated with 350 ± 29 μmol/l peroxides); (iii) H2O2: control + 350 μmol/l H2O2 intravenously. After 4 d, infusions were stopped and animals enterally fed. Half the animals were killed immediately after treatments and half were killed 8 wk later (n = 4–6 per group) for hepatic determination of DNMT activities and of 5′-methyl-2′-deoxycytidine (5MedCyd) levels, a marker of DNA methylation. At 1 wk, DNMT and 5MedCyd were lower in the TPN and H2O2 groups as compared with controls. At 9 wk, DNMT remained lower in the TPN group, whereas 5MedCyd was lower in the TPN and H2O2 groups. Administration of TPN or H2O2 early in life in guinea pigs induces a sustained hypomethylation of DNA following inhibition of DNMT activity.

In preterm neonates, peroxides contaminating total parenteral nutrition (TPN) contribute to oxidative stress, which is suspected to be a strong inducer of hepatic complications related to prematurity. Recently, others reported that hexapeptides derived from human milk (HM) exerted free radical–scavenging activities in vitro. Therefore, the aim of this study was to assess the capacity of these hexapeptides to limit the generation of peroxides in TPN and to prevent TPN-induced hepatic oxidative stress. At 3 d of life, guinea pigs were infused, through a catheter in jugular vein, with TPN containing or not peptide-A (YGYTGA) or peptide-B (ISELGW). Peroxide concentrations were measured in TPN solutions, whereas glutathione, glutathionyl-1,4-dihydroxynonenal (GS-HNE) and mRNA levels of interleukin-1 (IL-1) and tumor necrosis factor-α (TNFα) were determined in liver after 4 d of infusion. The addition of peptide-A to TPN allowed a reduction in peroxide contamination by half. In vivo, peptide-A or peptide-B corrected the hepatic oxidative status induced by TPN. Indeed, both peptides lowered the hepatic redox potential of glutathione and the level of GS-HNE, a marker of lipid peroxidation. As compared with animals infused with TPN without peptide, the hepatic mRNA levels of IL-1 and TNFα were lower in animals infused with TPN containing peptide-A or peptide-B. These results suggest that the addition of YGYTGA or ISELGW to TPN will reduce oxidative stress in newborns. The reduction in mRNA of two proinflammatory cytokines could be important for the incidence of hepatic complications related to TPN.

Background & aims: The absence of light protection of neonatal total parenteral nutrition (PN) contributes to the generation of 4-hydroxynonenal and peroxides. 4-Hydroxynonenal is suspected to be involved in PN-related liver complications. Aims: To find a practical modality to reduce 4-hydroxynonenal in PN and assess in vivo the impact of PN containing low 4-hydroxynonenal concentration.Methods: Six modalities of delivering PN were compared for the in vitro generation of peroxides and 4-hydroxynonenal: 1) MV-AA-L: light-protected (-L) solution containing multivitamin (MV) mixed with amino acids + dextrose (AA); 2) MV-AA+L: MV-AA without photo-protection (+L); 3) MV-LIP+L: MV mixed with lipid emulsion (LIP). LIP was a)Intralipid20%(R) or b) Omegaven (R). Hepatic markers of oxidative stress (glutathione, F-2 alpha-isoprostanes, GS-HNE) and inflammation (mRNA of TNF-alpha and IL-1) were measured in newborn guinea pigs infused during 4-days with MV-AA+L compounded with Intralipid20%(R) or Omegaven (R).Results: Hydroperoxides and 4-hydroxynonenal were the lowest in MV-AA L and the highest in MV-LIP+L. MV-AA+L with Omegaven (R) was associated with the lowest levels of markers of oxidative stress and inflammation.Conclusion: Compared to Intralipid20%(R), Omegaven (R) reduces oxidative stress associated with PN and prevents liver inflammation. These findings offer an alternative strategy to light protection of PN, which in the clinical setting is a cumbersome modality. (C) 2012 Elsevier Ltd and European Society for Clinical Nutrition and Metabolism. All rights reserved.

Premature newborn infants on total parenteral nutrition (TPN) are at risk of oxidative stress because of peroxides contaminating TPN and low glutathione level. Low cysteine availability limits glutathione synthesis. In this population, the main source of cysteine derives from the hepatic conversion of methionine. The first enzyme of this conversion, methionine adenosyltransferase (MAT), contains redox-sensitive cysteinyl residues. We hypothesize that inhibition of MAT by peroxides contaminating TPN leads to a lower availability of cysteine for glutathione synthesis. At 3 days of life, animals were fitted with a jugular catheter for intravenous infusion. Four groups were compared by ANOVA (P<0.05): (1) Control, without surgery, fed regular chow; (2) Sham, fitted with an obstructed catheter, fed orally regular chow; (3) TPN, fed exclusively TPN (dextrose, amino acids, fat, vitamins) containing 350 μM peroxides; (4) H2O2, fed regular chow orally and infused with 350 μM H2O2. Four days later, MAT activity and glutathione in liver and blood were lower in TPN and H2O2 groups. The redox potential was more oxidized in blood and liver of the TPN group. In conclusion, peroxides generated in TPN inhibit methionine adenosyltransferase activity with, among consequences, a low level of glutathione and a more oxidized redox potential.

Objectives: The smallest premature neonates often receive blood transfusions early in life. Nonrestrictive transfusion policies are linked to deleterious outcomes. Exposure of total parenteral nutrition (TPN) to ambient light generates oxidation products associated with haemolysis in vitro. Shielding TPN from light limits oxidation. Our hypothesis was protecting TPN from light decreases haemolysis and therefore the need for early blood transfusions.Methods: Comparison of haemolysis between animals fed enterally and those receiving TPN, and exploratory case-control retrospective analysis of transfusion counts in premature infants receiving light-exposed or light-protected TPN. The statistical analysis was analysis of variance and longitudinal binomial regression model adjusting for potential covariables of transfusion counts.Results: In animals, TPN is associated with higher (P < 0.05) haemolysis compared with enteral feeds; photoprotection induces lower peroxide load with no effect on the level of haemolysis. In premature infants, light-exposed (n = 76) or light-protected (n = 57) populations exhibited similar clinical characteristics. Initial haematocrit, gestational age, and index of disease severity had a significant effect on the number of transfusions. When adjusting for these covariables, photoprotection was no longer significant.Conclusions: Even though peroxides are associated in vitro with haemolysis, shielding TPN from light to reduce infused peroxides does not significantly decrease the need for early transfusions in premature infants.