AI Article Synopsis
- Crotoxin, a toxin from Crotalus durissus terrificus, disrupts neurotransmission at the neuromuscular junction using a triphasic mechanism that relies on its ability to break down phospholipids.
- The study focuses on the fatty acids released during crotoxin's action, comparing them to other phospholipases A(2), including its subunit CB.
- Findings indicate that crotoxin leads to greater release of palmitate and arachidonate than other phospholipases A(2), suggesting these fatty acids are linked to crotoxin's neurotoxic effects through processes like protein modification and cell signaling.
Article Abstract
Crotoxin, the main toxin of Crotalus durissus terrificus venom, exerts its lethal effect by blocking neurotransmission at the neuromuscular junction level through a triphasic mechanism. This effect seems to depend on its phospholipasic activity, suggesting that the mechanism of neurotransmission blockage may be related to fatty acids release in specific sites of the nervous terminal. In this work, we purified the fatty acids released by crotoxin's activity and this outline was compared with other phospholipases A(2), including CB, a subunit of crotoxin. Our results show a higher release of palmitate and arachidonate by crotoxin when compared to other phospholipases A(2). Since palmitate has a role in protein acylation processes and arachidonate participates in signal transduction events, these mechanisms may be related to the neurotoxic actions of crotoxin.
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| http://dx.doi.org/10.1016/s0041-0101(01)00186-6 | DOI Listing |
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