Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P30044 (antioxidant enzyme)
 8,037 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

It is an honor, and indeed fitting, to have a chapter on pulmonary oxygen toxicity included in a Festschrift for Dan Gilbert, whose contributions to the free radical theory of oxygen toxicity have been a catalyst to the last half-century of investigation in this field. There is cellular damage that results in pulmonary edema and even death if the increase in reactive oxygen species produced in the lung during exposure to hyperoxia is not counterbalanced by an increase in the cell's antioxidant defense systems. In this chapter experimental evidence will substantiate the importance of post-transcriptional regulation of antioxidant enzyme gene expression in animal models of pulmonary oxygen toxicity and tolerance to hyperoxia with special emphasis given to the role of manganese superoxide dismutase (MnSOD) synthesis, specific activity, and RNA half-life and to a proposed function of a MnSOD RNA-binding protein as a positive regulator in the control of translational efficiency.
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PMID:Post-transcriptional regulation of lung antioxidant enzyme gene expression. 1086 32

Bilirubin is a potent antioxidant, however, uncertainty surrounds its physiological importance. Individuals with Gilbert's syndrome (GS) have increased circulating bilirubin and a reduced prevalence of cardiovascular disease (CVD). The aim of this study was to investigate mechanisms that may link bilirubin to protection from CVD seen in GS by examining markers of antioxidant and oxidative stress status and the susceptibility of serum to oxidation. Nine individuals with GS and twelve controls, matched for age, height and weight, were assessed for plasma antioxidant status, red blood cell antioxidant enzyme activities, plasma malondialdehyde, the susceptibility of serum to copper (Cu(2+)) induced oxidation and blood lipid profile. Individuals with GS had significantly elevated unconjugated bilirubin (GS: 26.0+/-6.4; control: 9.7+/-3.0 micromol/L; P<0.001), increased trolox equivalent antioxidant capacity (GS: 1.59+/-0.07; control: 1.52+/-0.07 mmol/L trolox Equ; P=0.035) and ferric reducing ability of plasma (GS: 1.09+/-0.16; control: 0.92+/-0.14 mmol/L Fe(2+) Equ; P=0.024). The lag phase of serum oxidation was significantly longer in the GS group (GS: 121.4+/-10.5; control: 106.8+/-14.6 min; P=0.020) and was positively correlated with the bilirubin concentration (r=0.451, P=0.040). A trend toward elevated HDL:LDL ratio was observed in GS (GS 0.96+/-0.31; control: 0.73+/-0.21; P=0.072). In summary, individuals with GS have an increased circulating antioxidant status and an improved resistance to serum oxidation which may partially explain their reduced prevalence of CVD.
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PMID:Improved resistance to serum oxidation in Gilbert's syndrome: a mechanism for cardiovascular protection. 1815 9