The adaptation (tolerance) to chronic EtOH exposure was explained by the development of resistance to the disordering of the membrane phospholipids (PL). This phenomenon may be associated with changes in enzymes such as phospholipase A2 (PLA2) that govern PL metabolism. The data presented here, using the mouse inhalation model, supports and confirms previously reported findings that chronic exposure to EtOH substantially increased PLA2 activity in synaptosomal preparations from rat brain. We have previously reported that pretreatment with ganglioside GM1 reduced the intoxicating effect of EtOH in mice. The present study indicates that GM1 pretreatment both in vivo and in vitro reduced the EtOH-induced activation of PLA2 in synaptosomal preparations. Thus GM1 may exert its neuroprotective effects by influencing deacylation/reacylation of membrane phospholipids.
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[Anonymous], METHOD BIOCHEM ANAL, DOI DOI 10.1002/9780470110232.CH7