Abstract
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.
Highlights
A healthy infant is born with a concentration of bilirubin below 5 mg/dl [1]; serum bilirubin concentration rises quickly, up to 12 mg/dl within first 4-5 days
Bilirubin is a compound with known antioxidant properties [6,7,8]; an increase in its concentration may be necessary to maintain a proper oxidative balance in the perinatal period or maybe not bilirubin but Oxidative Medicine and Cellular Longevity another compound formed in the heme catabolic pathway—carbon monoxide (CO) is the hero of the perinatal period? This review work explores both of these options
They modulate inflammation and ameliorate generation of noxious free radicals. As it was presented above, aggravated inflammatory reactions and increased oxidative stress are often implicated in the pathology of typical neonatal diseases
Summary
A healthy infant is born with a concentration of bilirubin below 5 mg/dl [1]; serum bilirubin concentration rises quickly, up to 12 mg/dl within first 4-5 days. HbF is intensively eliminated and exchanged by HbA, leading to the low HbF concentration observed in adults (around 1% of total Hb) [3]. The increased hemoglobin catabolism is consistent with increased degradation of heme. This process is physiologically justified because unique properties of HbF only function during prenatal period, the mechanism of gene silencing responsible for the reduced synthesis of HbF is not fully understood [4]. Some researchers have wondered whether the observed increase in bilirubin is only a side effect of the metabolic changes at newborn infants or such growth brings specific benefits [5]. Bilirubin is a compound with known antioxidant properties [6,7,8]; an increase in its concentration may be necessary to maintain a proper oxidative balance in the perinatal period or maybe not bilirubin but Oxidative Medicine and Cellular Longevity another compound formed in the heme catabolic pathway—CO is the hero of the perinatal period? This review work explores both of these options
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