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Bungarus candidus (Malayan krait) venom contains a complex mixture of neurotoxins, primarily three-finger toxins (3FTxs) and phospholipase A2 enzymes (PLA2s), that induce rapid and severe neuromuscular paralysis. β-bungarotoxins act presynaptically to irreversibly damage motor nerve terminals, while α-neurotoxins act postsynaptically to block nicotinic acetylcholine receptors. This leads to flaccid paralysis and respiratory failure, potentially resulting in death if untreated. Antivenom is the primary treatment, but its effectiveness is limited once significant paralysis develops. The venom also contains other components like L-amino acid oxidase (LAAO), hyaluronidase, and acetylcholinesterase that contribute to the overall toxicity.
Presynaptic: Blocks acetylcholine release by damaging nerve terminals (β-bungarotoxins). Postsynaptic: Competitively inhibits nicotinic acetylcholine receptors (α-neurotoxins).
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