title: Stimulatory effect of phospholipase A2 treatment on glucose utilization in human erythrocytes.
abstract: We examined whether modification of membrane phospholipids of human erythrocytes by hydrolysis with phospholipase A2 (PLA2 from bee venom) would affect glucose utilization, chosen as a typical model of intracellular metabolism, and, if so, intended to clarify the mechanism of the alteration of glycolysis. Treatment of erythrocytes with PLA2 induced a marked shape change (i.e., crenation) and significantly increased the rate of lactate production from glucose. Available evidence indicated that there is no relevance of this cell-shape change to the alteration of glycolysis. The lack of a detectable effect of papain treatment on glycolysis in PLA2-treated cells suggested that the increase in glycolysis by PLA2 treatment might not be caused by the conformational change of band-3 protein through modulation of membrane phospholipids. The result of the measurement of lactate production in the presence and absence of ouabain did not support the idea that hydrolysis of phospholipids by PLA2 treatment makes plasma membranes leaky to Na+ and consequently enhances glycolysis through activation of Na+/K(+)-ATPase. The action of PLA2 on glycolysis was abolished by extraction of free fatty acids in the cell membrane with bovine serum albumin. Loading erythrocytes with free fatty acid (oleic acid, linoleic acid, or arachidonic acid) caused a significant increase in glycolysis. Analysis of glycolytic intermediates suggested that the enhancement of glycolysis was induced by activation of 6-phosphofructokinase. The data, thus, indicate that treatment of human erythrocytes with PLA2 significantly accelerates glucose utilization and suggest that the stimulation of glycolysis is caused by activation of 6-phosphofructokinase through liberation of free fatty acids of membrane phospholipids by PLA2.
authors.affiliation: Department of Clinical Biochemistry, Faculty of Pharmacy, Meijo University, Nagoya, Japan.
authors.forename: I
authors.initials: I
authors.lastname: Miwa
authors.forename: Y J
authors.initials: YJ
authors.lastname: Duan
authors.forename: S
authors.initials: S
authors.lastname: Murase
authors.forename: H
authors.initials: H
authors.lastname: Fukatsu
authors.forename: A
authors.initials: A
authors.lastname: Tamura
authors.forename: J
authors.initials: J
authors.lastname: Okuda
mesh_terms: D000328:Adult; D004910:Erythrocyte Membrane / Q000187:drug effects / Q000378:metabolism; D004912:Erythrocytes / Q000187:drug effects* / Q000378:metabolism; D005230:Fatty Acids, Nonesterified / Q000494:pharmacology; D005260:Female; D005947:Glucose / Q000378:metabolism*; D006019:Glycolysis; D006801:Humans; D007773:Lactates / Q000032:analysis; D019344:Lactic Acid; D008297:Male; D008875:Middle Aged; D010206:Papain / Q000494:pharmacology; D010741:Phospholipases A / Q000494:pharmacology*; D054467:Phospholipases A2; D012710:Serum Albumin, Bovine / Q000494:pharmacology
chemical_list: D005230:Fatty Acids, Nonesterified; D007773:Lactates; D012710:Serum Albumin, Bovine; D019344:Lactic Acid; D010741:Phospholipases A; D054467:Phospholipases A2; D010206:Papain; D005947:Glucose