title: Release of fructose and hexose phosphates from perivascular cells induced by low density lipoprotein and acceleration of protein glycation in vitro.
abstract: We investigated whether low density lipoprotein (LDL) under oxidative stress might induce the release of fructose, glucose-6-phosphate and fructose-6-phosphate from perivascular cells, and also whether these substances might accelerate the formation of advanced glycation end products (AGE) from proteins in vitro. When vascular smooth muscle cells were incubated with LDL in Ham's F10 at 37 degrees C for 48 h. release of all these substances was increased dose-dependently by oxidized LDL. Fructose release was increased in a dose-dependent manner by glucose. Indomethacin (20 microM) significantly (P < 0.01) suppressed the release of fructose (25.4 +/- 15.7% of control) and hexose phosphates (29.4 +/- 4.0) with the inhibition of release of lactate dehydrogenase (35.5 +/- 4.9) as well as probucol, whereas an aldose reductase inhibitor, epalrestat, significantly (P < 0.001) inhibited only the fructose release (0.9 +/- 0.8). Release of fructose and hexose phosphates from vascular endothelial cells was also induced by oxidized LDL. AGE immunoreactivities and AGE-related fluorescence formed from proteins and glucose were significantly increased (P < 0.001) in the presence of small amounts of the cellular glucose metabolites (6.6%) with glucose (93.4%). These data suggest that release of potent AGE initiators, fructose and hexose phosphates, from perivascular cells induced by oxidized LDL may be an important phenomenon for vascular complications.
authors.affiliation: Diabetes Center, Yatsushiro Health Insurance General Hospital, Japan.
authors.forename: H
authors.initials: H
authors.lastname: Takeda
authors.forename: T
authors.initials: T
authors.lastname: Higashi
authors.forename: T
authors.initials: T
authors.lastname: Nishikawa
authors.forename: Y
authors.initials: Y
authors.lastname: Sato
authors.forename: Y
authors.initials: Y
authors.lastname: Anami
authors.forename: T
authors.initials: T
authors.lastname: Yano
authors.forename: M
authors.initials: M
authors.lastname: Kasho
authors.forename: S
authors.initials: S
authors.lastname: Kobori
authors.forename: M
authors.initials: M
authors.lastname: Shichiri
mesh_terms: D000449:Aldehyde Reductase / Q000037:antagonists & inhibitors; D000818:Animals; D001013:Aorta, Thoracic; D002478:Cells, Cultured; D004730:Endothelium, Vascular / Q000166:cytology / Q000187:drug effects / Q000378:metabolism*; D004791:Enzyme Inhibitors / Q000494:pharmacology; D005632:Fructose / Q000378:metabolism*; D006023:Glycoproteins / Q000378:metabolism*; D006031:Glycosylation; D006600:Hexosephosphates / Q000378:metabolism*; D006801:Humans; D007700:Kinetics; D007770:L-Lactate Dehydrogenase; D008077:Lipoproteins, LDL / Q000494:pharmacology*; D009131:Muscle, Smooth, Vascular / Q000166:cytology / Q000187:drug effects / Q000378:metabolism*; D010084:Oxidation-Reduction; D018384:Oxidative Stress; D010972:Platelet Activating Factor / Q000032:analysis*; D011341:Probucol / Q000494:pharmacology; D011817:Rabbits; D012236:Rhodanine / Q000031:analogs & derivatives / Q000494:pharmacology; D053778:Thiazolidines; D017392:Thiobarbituric Acid Reactive Substances; D014471:Umbilical Veins
chemical_list: D004791:Enzyme Inhibitors; D006023:Glycoproteins; D006600:Hexosephosphates; D008077:Lipoproteins, LDL; D010972:Platelet Activating Factor; D053778:Thiazolidines; D017392:Thiobarbituric Acid Reactive Substances; C099252:oxidized low density lipoprotein; D005632:Fructose; C038131:epalrestat; D012236:Rhodanine; D000449:Aldehyde Reductase; D007770:L-Lactate Dehydrogenase; D011341:Probucol