title: [Biological specificity of the neonate and infant heart, with reference to selenium and glutathione peroxidase--the study to clarify the cause of vulnerability of neonate and infant heart].
abstract: Selenium (Se) is known to be an integral part in glutathione peroxidase (GSHPx). There are some reports serum Se levels are lower in infants than in adults and GSHPx activity is parallel to Se levels. There may be reasons why myocardial reperfusion injury occurs more easily in infants than in adults by reperfusion of ischemic myocardium. Serum and myocardial Se levels and GSHPx activity in experimental rats were measured to clarify the vulnerability of infant heart. Wistar rats were divided into three groups. First, infant rats 8-12 days after birth (infant rats), second, adult rats fed Se-deficient diet for two months (Se-deficient rats), and third, adult rats fed normal diet for two months (control rats). Serum Se levels, serum GSHPx activity and myocardial GSHPx activity in both infant and Se-deficient rats were significantly lower than that in control rats (p less than 0.01). However myocardial Se levels in infant rats were significantly higher than that in both Se-deficient and control rats (p less than 0.01). The lipid peroxide levels in heart mitochondria of Se-deficient rats were significantly higher than that in control rats (p less than 0.01). These results suggest that in infant heart Se does not manifest an effective function for a integral part of GSHPx despite its high level, its reason is not clear, and this phenomenon generates more oxygen-derived free radicals after reoxygeneration of the ischemic myocardium.
authors.affiliation: Second Department of Surgery, Fukui Medical School, Japan.
authors.forename: Y
authors.initials: Y
authors.lastname: Chiba
authors.forename: R
authors.initials: R
authors.lastname: Muraoka
authors.forename: H
authors.initials: H
authors.lastname: Noguchi
authors.forename: A
authors.initials: A
authors.lastname: Ihaya
authors.forename: T
authors.initials: T
authors.lastname: Kimura
authors.forename: Y
authors.initials: Y
authors.lastname: Hiramatsu
authors.forename: K
authors.initials: K
authors.lastname: Morioka
mesh_terms: D000818:Animals; D000831:Animals, Newborn / Q000378:metabolism*; D005609:Free Radicals; D005979:Glutathione Peroxidase / Q000378:metabolism*; D008054:Lipid Peroxides / Q000378:metabolism; D008929:Mitochondria, Heart / Q000378:metabolism; D009206:Myocardium / Q000378:metabolism*; D010100:Oxygen / Q000378:metabolism; D051381:Rats; D011919:Rats, Inbred Strains; D012643:Selenium / Q000097:blood / Q000172:deficiency / Q000378:metabolism*
chemical_list: D005609:Free Radicals; D008054:Lipid Peroxides; D005979:Glutathione Peroxidase; D012643:Selenium; D010100:Oxygen