title: Dietary (+)-catechin and BHT markedly increase alpha-tocopherol concentrations in rats by a tocopherol-omega-hydroxylase-independent mechanism.
abstract: The effects of dietary (+)-catechin (CAT) and BHT on plasma and tissue concentrations of alpha-tocopherol (alpha-T), gamma-tocopherol (gamma-T) and cholesterol (C) were studied in male Sprague-Dawley rats. The rats were fed the compounds during a 4-wk period at concentrations of 2 g/kg in standardized diets, low but adequate in vitamin E, with 2 g/kg cholesterol. The CAT-regimen did not affect weight gain, feed intake or organ weights. BHT did not affect feed intake but lowered the body weight and the amount of liver lipids and increased the weights of livers and lungs relative to the body weight. Rats consuming CAT had 2.5-3.5-fold increased plasma, liver and lung alpha-T concentrations, but C concentrations remained unchanged. BHT-feeding resulted in 2.4- and 1.7-fold elevation in alpha-T but approximately 50% decrease in gamma-T concentrations in blood plasma and liver, respectively. BHT also lowered total C in the liver without affecting the concentration of C in the liver lipids. To investigate whether the alpha-T-sparing action of the studied compounds was due to the inhibition of tocopherol-omega-hydroxylase, HepG2 cells were incubated with CAT or BHT in the presence of delta-tocopherol (delta-T) and the 3'- and 5'-delta-carboxychromanol metabolites in the media were analyzed by GC/MS. Neither CAT nor BHT inhibited tocopherol-omega-hydroxylase activity in hepatocyte cultures; CAT was also inactive in a rat microsomal assay. In conclusion, both dietary CAT and BHT markedly increased alpha-T concentrations in plasma and organs of Sprague-Dawley rats by a mechanism that apparently does not involve inhibition of tocopherol-omega-hydroxylase, a key enzyme in tocopherol catabolism.
authors.affiliation: Department of Food Science, Swedish University of Agricultural Sciences, S-750 07 Uppsala, Sweden. Jan.Frank@lmv.slu.se
authors.forename: Jan
authors.initials: J
authors.lastname: Frank
authors.forename: Torbjörn
authors.initials: T
authors.lastname: Lundh
authors.forename: Robert S
authors.initials: RS
authors.lastname: Parker
authors.forename: Joy E
authors.initials: JE
authors.lastname: Swanson
authors.forename: Bengt
authors.initials: B
authors.lastname: Vessby
authors.forename: Afaf
authors.initials: A
authors.lastname: Kamal-Eldin
mesh_terms: D000818:Animals; D000975:Antioxidants / Q000008:administration & dosage*; D001835:Body Weight; D002084:Butylated Hydroxytoluene / Q000008:administration & dosage*; D002392:Catechin / Q000008:administration & dosage*; D002478:Cells, Cultured; D002784:Cholesterol / Q000032:analysis / Q000097:blood; D004032:Diet; D004149:Dioxoles / Q000008:administration & dosage; D004791:Enzyme Inhibitors / Q000494:pharmacology; D022781:Hepatocytes / Q000201:enzymology; D017705:Lignans / Q000008:administration & dosage; D008055:Lipids / Q000032:analysis; D008099:Liver / Q000033:anatomy & histology / Q000737:chemistry; D008168:Lung / Q000033:anatomy & histology; D008297:Male; D006899:Mixed Function Oxygenases / Q000037:antagonists & inhibitors / Q000378:metabolism*; D009929:Organ Size; D051381:Rats; D017207:Rats, Sprague-Dawley; D024502:alpha-Tocopherol / Q000032:analysis / Q000097:blood*; D024504:gamma-Tocopherol / Q000097:blood
chemical_list: D000975:Antioxidants; D004149:Dioxoles; D004791:Enzyme Inhibitors; D017705:Lignans; D008055:Lipids; D002084:Butylated Hydroxytoluene; D024504:gamma-Tocopherol; D002392:Catechin; D002784:Cholesterol; D006899:Mixed Function Oxygenases; C479073:tocopherol-omega-hydroxylase; D024502:alpha-Tocopherol; C054125:sesamin