Search PubMed⌕ Search

Biomedical subjects

K Hiraga

Publications and source records attributed to K Hiraga.

At least 163 records · Page 9Linked to original sources
PubMed1981

Effect of butylated hydroxytoluene on the lipid composition of rat liver.

Hepatic lipids were studied in Sprague-Dawley male rats given butylated hydroxytoluene(BHT) at a level of 1.20% for 1 week. BHT significantly increased cholesteryl esters and phospholipids but decreased triglycerides, non-esterified fatty acids and diglycerides. BHT also increased phosphatidylethanolamine or decreased phosphatidylinositol and lysophosphatidylcholine. Fatty acid composition of each lipid class was also changed by BHT-feeding. The decrease in 16 : 1/16 : 0, 18 1/18 : 0 and 20 : 4/18 :2 ratios of total lipids, non-esterified fatty acids or phospholipids of BHT-given rats suggests that BHT decreases the activity of fatty acid desaturase in the liver.

Animals↗
PubMed1981

Effects of four bisphenolic antioxidants on prothrombin levels of rat plasma.

Male Sprague--Dawley rats were fed 2,2'-methylenebis(4-ethyl-6-tert-butylphenol), 2,2'-methylenebis(4-methyl-6-tert-butylphenol), 4,4'-butylidenebis(3-methyl-6-tert-butylphenol) or 4,4'-methylenebis(2,6-di-tert-butylphenol) at a level of 1.135 mmol/100 g in the diet for 1 week. The prothrombin and kaolin-partially thromboplastin time (PTT) indices were significantly decreased to 32% and 37% of control values in rats given 2,2'-methylenebis(4-methyl-6-tert-butylphenol). A slight decrease in prothrombin index of rats given 4,4'-butylidenebis(3-methyl-6-tert-butylphenol) was also observed.

Animals↗
PubMed1981

Effects of four bisphenolic antioxidants on lipid contents of rat liver.

Hepatic lipids were studied in Sprague-Dawley male rats given, 2,2'-methylenebis(4-ethyl-6-tert-butylphenol), 2,2'-methylenebis(4-methyl-6-tert-butylphenol), 4,4'-butylidenebis(3-methyl-6-tert-butylphenol) or 4,4'-methylenebis(2,6-di-tert-butylphenol) at a level of 1.135 mmol% for 1 week. 4,4'-Butylidenebis(3-methyl-6-tert-butylphenol) induced fatty liver and increased triglyceride, diglyceride and cholesteryl-ester concentrations, 7.1-, 5.8- and 6.1-fold, respectively. Plasma triglycerides, total cholesterol and non-esterified fatty acids were markedly decreased. It would appear that the fatty liver resulted mainly from defective fat excretion from the liver. The other bisphenols produced a little change in liver lipids.

Animals↗
PubMed1981

Haemorrhagic toxicosis in rats given butylated hydroxytoluene.

Vascular permeability, platelet function, blood coagulation and fibrinolytic activity were examined in Sprague-Dawley male rats given 1.20% butylated hydroxytoluene (BHT) in the diet for 1 week. BHT significantly increased the leakage of Evans blue from blood into epididymus. BHT inhibited the ADP-induced platelet aggregation and decreased the platelet factor 3 availability. Plasma prothrombin, factors IX, X, VII and VIII were decreased in rats given BHT. Fibrinolytic activity was little influenced by BHT-feeding.

Animals↗
PubMed1981

Defective glycine cleavage system in nonketotic hyperglycinemia. Occurrence of a less active glycine decarboxylase and an abnormal aminomethyl carrier protein.

The activities of then glycine cleavage system in the liver and brain of patient with nonketotic hyperglycinemia was extremely low as compared with those of control human liver and brain. The activities of glycine decarboxylase (P-protein) and the aminomethyl carrier protein (H-protein), two of the four protein components of the glycine cleavage system, were considerably reduced in both the liver and brain; the extent of reduction was greater in the H-protein. The activity of the T-protein was normal. Purified H-protein from the patient did not react with lipoamide dehydrogenase, and titration of thiol groups with [2,3-14C]N-ethylmaleimide suggested that this H-protein is devoid of lipoic acid. This structural abnormality in the H-protein is considered to constitute the primary molecular lesion in this patient with non-ketotic hyperglycinemia. Immunochemical studies using an antibody specific for P-protein showed that the patient was due to reduction of the catalytic activity of the protein rather than a decrease in the actual amount of the P-protein. Partial inactivation of P-protein could result secondarily from impaired metabolism of glycine resulting from deficiency in the activity of H-protein. However, the H-protein from the patient could stimulate the P-protein catalyzed exchange of the carboxyl carbon of glycine with 14CO2, although the specific activity of the purified H-protein from the patient was only 4% of that of control human H-protein. The content of H-protein in the liver of the patient was approximately 35% of that of control human liver.

Amino Acid Metabolism, Inborn Errors↗
PubMed1981

Effects of butylated hydroxytoluene (BHT) on the level of glutathione and the activity of glutathione-S-transferase in rat liver.

Oral administration of 500 mg/kg of butylated hydroxytoluene (BHT) daily for three days elevated the total glutathione (GSH) level and the activities of GSH-S-transferase for CDNB and DCNB and GSSG reductase in the rat liver. BHT-alcohol, which is a metabolite of BHT, also elevated the level or activity of these components. The induction of these components with BHT-alcohol was slightly less than that with BHT. However, BHT or BHT-alcohol in doses used had no effect on GSH peroxidase activity.

Animals↗
PubMed1980

The mitochondrial glycine cleavage system. Purification and properties of glycine decarboxylase from chicken liver mitochondria.

Glycine decarboxylase, tentatively called P-protein and considered a constituent of the glycine cleavage system, was purified to apparent homogeneity from chicken liver mitochondria. P-protein is a homodimer having a Mr = approximately 200,000 and consisting of identical subunits with Mr = approximately 100,000. Each subunit appears to contain an equimolar pyridoxal 5'-phosphate which is bound to the protein, possibly through a protonated aldimine linkage. The isoelectric point of P-protein was 7.2. P-protein could bind glycine, showing a Kd of 33 mM for it, and could catalyze glycine decarboxylation even though the rate of decarboxylation catalyzed by P-protein alone was extremely low. The product of glycine decarboxylation was methylamine and the Km for glycine. Methylamine could bind to P-protein, giving a Kd value of 63 mM, and it inhibited the glycine decarboxylation. P-protein alone could also slightly catalyze the exchange of carboxyl carbon of glycine with CO2 and the exchange appeared to obey a ping-pong mechanism. Both glycine decarboxylation and the glycine-CO2 exchange catalyzed by P-protein were stimulated 100-fold or more by the addition of lipoic acid, which is a functional group of H-protein. We may define P-protein as glycine decarboxylase although P-protein alone exhibits only very low catalytic activities.

Amino Acid Oxidoreductases↗