Evaluation of oxidant and antioxidant status in infants with hyperbilirubinemia and kernicterus

Doğan, Murat; Peker, Erdal; Kırımi, Ercan; Sal, Ertan; Akbayram, Sinan; Erel, Özcan; Ocak, Ali Rıza; Tuncer, Oğuz

doi:10.1177/0960327111401638

Cited by 22 publications

(14 citation statements)

References 32 publications

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“…Previous research shows that UCB has oxidant effects, while ω-3 PUFA demonstrates antioxidant properties [ 7 , 12 ]. To further examine this, the effects of UCB and ω-3 PUFA on SOD and CAT enzyme activity in neurons was evaluated.…”

Section: Resultsmentioning

confidence: 99%

“…Bilirubin encephalopathy is a serious complication of neonatal jaundice [ 7 ]. High concentrations of UCB in the blood can easily cross the blood-brain barrier and damage neurons, resulting in neurological disability or even death [ 15 ].…”

Section: Discussionmentioning

confidence: 99%

“…Excessive UCB levels have neurotoxic effects though several potential mechanisms: (1) UCB can disrupt the cell and mitochondria membranes, leading to phagocytic recognition and cell death; (2) UCB can induce the loss of myelin basic protein, resulting in lack of myelin sheath formation and increased reactivity of astroglia and microglia; (3) UCB-copper (Cu) system and the resulted ROS are responsible for oxidative DNA damage; (4) UCB stimulates the pro-inflammatory cytokines release; (5) UCB inhibits the nerve growth factor- and brain-derived neurotrophic factor-induced activation of pro-survival signals; and (6) UCB can activate caspase-3 and promote apoptosis [ 6 ]. Although the mechanism by which neurotoxicity is induced by UCB is not well understood, the oxidative stress and apoptosis induced by UCB may contribute to considerable neurological damage [ 7 ]. The destructive process is gradually caused by the gathering, bonding, and deposition of UCB on the neurons.…”

Section: Introductionmentioning

confidence: 99%

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Neuroprotective Effect of ω-3 Polyunsaturated Fatty Acids on Bilirubin Encephalopathy In Vitro and In Vivo

Song

2018

Med Sci Monit

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BackgroundBilirubin encephalopathy is a serious complication in neonatal jaundice and is associated with high mortality and disability in newborns. The present study aimed to investigate the neuroprotective effects of omega-3 polyunsaturated fatty acids (ω-3 PUFA) on bilirubin encephalopathy in vitro and in vivo.Material/MethodsThe cytotoxicity of unconjugated bilirubin (UCB) to neurons and neuroprotection of ω-3 PUFA were investigated using MTT assays and apoptosis evaluations. Superoxide dismutase (SOD) and catalase (CAT) enzyme activity were measured to investigate the anti-oxidative effect of ω-3 PUFA. The differences between eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) were also compared. The in vivo neuroprotective effect of DHA was demonstrated in neonatal rats with bilirubin encephalopathy by bilirubin monitoring, neuron-specific enolase (NSE) monitoring, H&E staining of brain tissue, and apoptosis rate evaluations.ResultsOmega-3 PUFA reduced the rate of apoptosis induced by UCB and increased SOD and CAT enzyme activity for anti-oxidation. DHA did not reduce the bilirubin in the serum of neonatal rats with bilirubin encephalopathy, but did reduce the damage caused by bilirubin with decreased NSE and apoptosis rate as well as improved neuron morphology.ConclusionsOmega-3 PUFA, particularly DHA, can reduce neurological damage in neonatal rats with bilirubin encephalopathy by increasing anti-apoptosis and anti-oxidation effects against UCB, providing a theoretical basis for the clinical treatment of bilirubin encephalopathy in newborns.

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Section: Resultsmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Neuroprotective Effect of ω-3 Polyunsaturated Fatty Acids on Bilirubin Encephalopathy In Vitro and In Vivo

Song

2018

Med Sci Monit

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“…Previous studies have revealed a significant imbalance of pro-oxidants and antioxidants in patients with CKD and diabetes [15,16,19,24,25]. It is also well known that bilirubin shows an antioxidant capacity, as in neonatal patients with increased bilirubin levels [26][27][28].…”

Section: Discussionmentioning

confidence: 99%

Establishing reference values and evaluation of an in-house ferric reducing antioxidant power (FRAP) colorimetric assay in microplates

Üstündağ¹,

Huysal²,

Kahvecioğlu³

et al. 2016

Eur Res J

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Objectives. The total antioxidant capacity (TAC) of a sample can be measured with a ferric reducing antioxidant power (FRAP) assay. There are commercially available kits for FRAP assays, however they are more expensive than in-house kits. We aimed to evaluate a FRAP direct measurement method under our laboratory conditions using a microplate reader and establish reference values to use in future research projects. Methods. An inhouse microplate adaptation of the FRAP method was evaluated. Reference values of FRAP were established for one hundred and twenty subjects aged between 25-55 years. FRAP levels were estimated in 30 serum samples with high glucose concentration, 44 hyperbiluribinemic neonatals and 16 patients receiving renal replacement therapy (RRT). Results. The mean FRAP level was 890±235 µmol/L. The median TAC level was 904 µmol/L. This method was found to be linear up to at least 2000 µmol/L. The intra-and inter-assay coefficients of variation were 2.7-6.7% and 5.3-10.1%, respectively. The mean FRAP level was lower than normal in diabetes and RRT patients and higher in hyperbiluribinemic neonatals (687±209 µmol/L, 609±250 µmol/L and 945±187 µmol/L, respectively). Conclusions. Our reference values give comparable results with the literature. This method is simple, reliable, and inexpensive. It could be used for studies of oxidative stressrelated diseases.Eur Res J 2016;2(2):126-131

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“…Some studies reported lower concentration of MDA in babies with high bilirubin concentration of 20 mg/dl [41] or even 25 mg/dl [42]. Other studies declared contrary results, suggesting that this issue is still unsolved [43,44]. Researches focusing on the influence of bilirubin on total plasma antioxidant capacity (TPAC) also give inconsistent outcomes [45].…”

Section: Is Bilirubin Only a Toxic Waste Product?mentioning

confidence: 99%

Two Faces of Heme Catabolic Pathway in Newborns: A Potential Role of Bilirubin and Carbon Monoxide in Neonatal Inflammatory Diseases

Osiak

Wątroba²,

Kapka‐Skrzypczak

et al. 2020

Oxidative Medicine and Cellular Longevity

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In an infant’s body, all the systems undergo significant changes in order to adapt to the new, extrauterine environment and challenges which it poses. Fragile homeostasis can be easily disrupted as the defensive mechanisms are yet imperfect. The activity of antioxidant enzymes, i.e., superoxide dismutase, catalase, and glutathione peroxidase, is low; therefore, neonates are especially vulnerable to oxidative stress. Free radical burden significantly contributes to neonatal illnesses such as sepsis, retinopathy of premature, necrotizing enterocolitis, bronchopulmonary dysplasia, or leukomalacia. However, newborns have an important ally—an inducible heme oxygenase-1 (HO-1) which expression rises rapidly in response to stress stimuli. HO-1 activity leads to production of carbon monoxide (CO), free iron ion, and biliverdin; the latter is promptly reduced to bilirubin. Although CO and bilirubin used to be considered noxious by-products, new interesting properties of those compounds are being revealed. Bilirubin proved to be an efficient free radicals scavenger and modulator of immune responses. CO affects a vast range of processes such as vasodilatation, platelet aggregation, and inflammatory reactions. Recently, developed nanoparticles consisting of PEGylated bilirubin as well as several kinds of molecules releasing CO have been successfully tested on animal models of inflammatory diseases. This paper focuses on the role of heme metabolites and their potential utility in prevention and treatment of neonatal diseases.

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Evaluation of oxidant and antioxidant status in infants with hyperbilirubinemia and kernicterus

Cited by 22 publications

References 32 publications

Neuroprotective Effect of ω-3 Polyunsaturated Fatty Acids on Bilirubin Encephalopathy In Vitro and In Vivo

Neuroprotective Effect of ω-3 Polyunsaturated Fatty Acids on Bilirubin Encephalopathy In Vitro and In Vivo

Establishing reference values and evaluation of an in-house ferric reducing antioxidant power (FRAP) colorimetric assay in microplates

Two Faces of Heme Catabolic Pathway in Newborns: A Potential Role of Bilirubin and Carbon Monoxide in Neonatal Inflammatory Diseases

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