Involvement of Lipid Metabolism in the Action of Phospholipase A2 Neurotoxins
Abstract
A number of potent presynaptically-acting neurotoxins (PSNTXs) from snake venom were examined as regards the role of phospholipase A2 (PLA2) activity in altering acetylcholine (ACh) release and choline (Ch) uptake. Also, the effects of PSNTXs and snake venom cardiotoxins (CTXs) on Ca2+ metabolism and activation of tissue lipolysis were examined. The inclusion of BSA in the incubation medium at the time of toxin expose has allowed a clear distinction to be made between nonPSNTX PLA2s and the PSNTXs in synaptosome preparations. For those PSNTXs active on synaptosomes, PLA2 activity (judged by fatty acid analysis) may play an important role in the enhancement of ACh release and Inhibition of Ch uptake . CTXs, melittin and myotoxin a all cause Ca2+ release from the terminal cisternae of the sarcoplasmic reticulum through the Ca 2+ release channel. B-Butx also causes a transient release of Ca 2+ from the sarcoplasmic reticulum. Melittin and CTX both activate phospholipase C activity in cell cultures that appears to be specific for phosphatidylethanolamine over phosphatidylcholine and with no requirement for Ca2+. Presynaptic snake venom toxins; Phospholipase A2 toxins; Cardiotoxins, Lipids; Phospholipase C; Skeletal-muscle; Synaptosomes; Cell culture; Beta-bungarotoxin; Scutoxin; RA 1.
Document Details
- Document Type
- Technical Report
- Publication Date
- Apr 15, 1992
- Accession Number
- ADA252885
Entities
People
- Jeffrey E. Fletcher