Influence of bilirubin on the antioxidant capacity of plasma in newborn infants.
ABSTRACT In vitro, bilirubin is a strong antioxidant, but in vivo its capacity to act as a scavenger of toxic oxygen radicals remains poorly documented. The aim of this study was to evaluate of bilirubin had antioxidant properties in jaundiced infants. The antioxidant capacity of neonatal plasma was measured in Trolox equivalents (TEAC, mmol/l) and correlated in vitro with plasma bilirubin concentrations (r2 = 0.99). Plasma TEAC was compared before and after exchange transfusions for neonatal hyperbilirubinemia (250-435 mumol/l). The antioxidant properties of the paired blood samples before and after exchange transfusions (TEAC: 1.67 +/- 0.12 vs. 1.37 +/- 0.09 mmol/l, n = 11) varied in proportion to the serum bilirubin levels. The changes in other antioxidants were not large enough to account for the magnitude of change in antioxidant capacity. Therefore, in vivo, the plasma antioxidant capacity of jaundiced newborn infants is related to the level of bilirubin.
- SourceAvailable from: Kalyan Goswami[Show abstract] [Hide abstract]
ABSTRACT: Bilirubin is an end product of heme metabolism, which is under disposal of tissues like liver, intestine and kidney. Clinically hyperbilirubinemia appears as jaundice or icterus. Jaundice can usually be detected when the serum bilirubin level exceeds 2.0 to 2.5 mg/dl. Determination of total and direct bilirubin levels helps the physician to know the underlying pathogenic mechanism. Hence accurate and unbiased estimation of bilirubin becomes mandatory. The problem of finding an accurate and specific method of bilirubin assay has been a challenge for over 50 years for many workers. Historically, Ehrlich in 1883 treated bilirubin in urine with diazo reagent and described formation of a red – blue coloured pigment. Later, Van den Bergh and Muller found that bilirubin in normal serum reacted with Ehrlich's diazo reagent (diazotized sulfanilic acid). We shall discuss here the further evolution of methods of bilirubin estimation till the modern era and also will cover the various aspects of interpretation and quality control measures.
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ABSTRACT: Diabetes is a chronic metabolic disease which is characterized by absolute or relative deficiencies in insulin secretion and/or insulin action. The key roles of oxidative stress and inflammation in the progression of vascular complications of this disease are well recognized. Accumulating epidemiologic evidence confirms that physical inactivity is an independent risk factor for insulin resistance and type II diabetes. This paper briefly reviews the pathophysiological pathways associated with oxidative stress and inflammation in diabetes mellitus and then discusses the impact of exercise on these systems. In this regard, we discuss exercise induced activation of cellular antioxidant systems through "nuclear factor erythroid 2-related factor." We also discuss anti-inflammatory myokines, which are produced and released by contracting muscle fibers. Antiapoptotic, anti-inflammatory and chaperon effects of exercise-induced heat shock proteins are also reviewed.Experimental Diabetes Research 01/2012; 2012:941868. DOI:10.1155/2012/941868 · 3.54 Impact Factor
Article: Cerebroprotective functions of HO-2.[Show abstract] [Hide abstract]
ABSTRACT: The constitutive isoform of heme oxygenase, HO-2, is highly expressed in the brain and in cerebral vessels. HO-2 functions in the brain have been evaluated using pharmacological inhibitors of the enzyme and HO-2 gene deletion in in vivo animal models and in cultured cells (neurons, astrocytes, cerebral vascular endothelial cells). Rapid activation of HO-2 via post-translational modifications without upregulation of HO-2 expression or HO-1 induction coincides with the increase in cerebral blood flow aimed at maintaining brain homeostasis and neuronal survival during seizures, hypoxia, and hypotension. Pharmacological inhibition or gene deletion of brain HO-2 exacerbates oxidative stress induced by seizures, glutamate, and inflammatory cytokines, and causes cerebral vascular injury. Carbon monoxide (CO) and bilirubin, the end products of HO-catalyzed heme degradation, have distinct cytoprotective functions. CO, by binding to a heme prosthetic group, regulates the key components of cell signaling, including BK(Ca) channels, guanylyl cyclase, NADPH oxidase, and the mitochondria respiratory chain. Cerebral vasodilator effects of CO are mediated via activation of BK(Ca) channels and guanylyl cyclase. CO, by inhibiting the major components of endogenous oxidant-generating machinery, NADPH oxidase and the cytochrome C oxidase of the mitochondrial respiratory chain, blocks formation of reactive oxygen species. Bilirubin, via redox cycling with biliverdin, is a potent oxidant scavenger that removes preformed oxidants. Overall, HO-2 has dual housekeeping cerebroprotective functions by maintaining autoregulation of cerebral blood flow aimed at improving neuronal survival in a changing environment, and by providing an effective defense mechanism that blocks oxidant formation and prevents cell death caused by oxidative stress.Current pharmaceutical design 02/2008; 14(5):443-53. · 3.29 Impact Factor