title: Suppression of regucalcin mRNA expression in the hearts of rats administered with free radical compound: the administration-induced death is accelerated in regucalcin transgenic rats.
abstract: The expression of regucalcin, a regulatory protein in the intracellular signaling system, in the hearts of rats was investigated. Regucalcin expression was examined using reverse transcription-polymerase chain reaction and Western blot analysis. Regucalcin mRNA and its protein levels in the hearts of male and female rats were significantly decreased with increasing age (50 weeks old) as compared with that of 5-week-old rats. The effect of 1,1-diphenyl-2-picryl-hydrazyl (DPPH), a compound that produces free radical, on regucalcin mRNA expression in the hearts of female rats (5 weeks old) was examined. Heart regucalcin mRNA levels were significantly decreased at 60 or 180 min after a single intraperitoneal administration of DPPH (0.5 mg /100 g body weight), suggesting that free radical stress has a suppressive effect on the gene expression. Normal (wild) female rats died at approximately 300 min after a single intraperitoneal administration of DPPH (0.5 mg/100 g), while regucalcin transgenic (TG) female rats died at approximately 150 min after the administration. Heart regucalcin protein in DPPH-administered rats was greater in regucalcin TG rats than in normal (wild) rats. This study demonstrates that the death of regucalcin TG rats is accelerated after the administration of free radical compound, indicating that overexpression of regucalcin does not have effects as the suppressor for free radical stress and the scavenger for free radical in rats.
authors.affiliation: Laboratory of Endocrinology and Molecular Metabolism, Graduate School of Nutritional Sciences, University of Shizuoka, Shizuoka 422-8526, Japan.
authors.forename: Tania
authors.initials: T
authors.lastname: Akhter
authors.forename: Taeko
authors.initials: T
authors.lastname: Nakagawa
authors.forename: Akiko
authors.initials: A
authors.lastname: Kobayashi
authors.forename: Masayoshi
authors.initials: M
authors.lastname: Yamaguchi
mesh_terms: D000818:Animals; D030801:Animals, Genetically Modified; D001713:Biphenyl Compounds; D002135:Calcium-Binding Proteins / Q000037:antagonists & inhibitors* / Q000235:genetics / Q000378:metabolism; D002265:Carboxylic Ester Hydrolases; D003643:Death; D015536:Down-Regulation; D005260:Female; D005609:Free Radicals / Q000633:toxicity*; D015870:Gene Expression / Q000187:drug effects; D006321:Heart / Q000503:physiopathology*; D047908:Intracellular Signaling Peptides and Proteins / Q000037:antagonists & inhibitors* / Q000235:genetics / Q000378:metabolism; D008297:Male; D018384:Oxidative Stress / Q000235:genetics*; D010851:Picrates / Q000008:administration & dosage; D012333:RNA, Messenger / Q000037:antagonists & inhibitors / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley
chemical_list: D001713:Biphenyl Compounds; D002135:Calcium-Binding Proteins; D005609:Free Radicals; D047908:Intracellular Signaling Peptides and Proteins; D010851:Picrates; D012333:RNA, Messenger; C004931:1,1-diphenyl-2-picrylhydrazyl; D002265:Carboxylic Ester Hydrolases; C513325:Rgn protein, rat