Oxidant-induced arachidonic acid release and impairment of fatty acid acylation in vascular smooth muscle cells

Oxidativedamage, which plays a major role in the early stages ofatherosclerosis, is associated with arachidonic acid (AA) release invascular smooth muscle cells (VSMC) as in other cell types. In thisstudy,H₂O₂was used to investigate mechanisms of AA release from VSMC on oxidativestress. Cell treatment with H₂O₂inhibited AA incorporation in an inverse relationship to prolongedH₂O₂-inducedAA release. Identical kinetics of inhibition of AA incorporation and AArelease were observed after cell treatment withAlF₄, a process not involvingphospholipase A₂(PLA₂) activation as recentlydescribed (A. Cane, M. Breton, G. Béréziat, and O. Colard.Biochem. Pharmacol. 53: 327-337, 1997). AA release was not specific, since oleic acid also increased inthe extracellular medium of cells treated withH₂O₂or AlF₄ as measured by gaschromatography-mass spectrometry. In contrast, AA and oleic acid cellcontent decreased after cell treatment. Oleoyl and arachidonoylacyl-CoA synthases and acyltransferases, assayed using a cell-freesystem, were not significantly modified. In contrast, a goodcorrelation was observed between decreases in AA acylation and cell ATPcontent. The decrease in ATP content is only partially accounted for bymitochondrial damage as assayed by rhodamine 123 assay. We concludethat oxidant-induced arachidonate release results from impairment offatty acid esterification and that ATP availability is probablyresponsible for free AA accumulation on oxidative stress by preventingits reesterification and/or transmembranetransport.

     

The action of cyclic-AMP on GA3 controlled responses III. Characteristics of barley endosperm acid phosphatase induction by gibberellic acid and cyclic 3', 5'-adenosine monophosphate

Studies on the induction of barley endosperm acid phosphataseby GA₃ and cyclic-AMP revealed (1) acid phosphatase inductionby GA₃ and cyclic-AMP is inhibited in a similar manner by ABA,cycloheximide and 6-methyl purine, (2) combinations of GA₃ andphosphodiesterase inhibitors such as caffeine and theophyllinepromoted the level of acid phosphatase induction obtainablewith the hormone alone, and (3) cyclic-AMP and GA₃ may be actingas triggers in the induction of this enzyme. Some of the implicationsof these results are discussed. (Received May 25, 1972; )     

Regulatory Defect of Glycolysis in Human Lipoma

A metabolic defect has been observed in extracts of lipomata in which citrate fails to inhibit the conversion of glucose-6-phosphate to glyceride-glycerol. Phospho-fructokinase extracted from lipomata was less sensitive to inhibition by citrate than the enzyme of normal adipose tissue. However, maximal rates of lipogenesis (from glucose or palmitate) and lipolysis (stimulated with isoprenaline) in lipomata were similar to those of normal adipose tissue. This work suggests that loss of negative feedback control of regulatory enzymes may be an early feature in the development of neoplasia.