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Daboia siamensis phospholipase A2 toxins are a group of potent enzymes and proteins that serve as the primary toxic components in the venom of the Eastern Russell's viper [1, 4]. These toxins function as secreted phospholipases A2 (sPLA2), which catalyze the calcium-dependent hydrolysis of phospholipids in cellular membranes, leading to the release of fatty acids and lysophospholipids [2, 7]. This enzymatic process triggers a cascade of pathological events, including presynaptic neurotoxicity by blocking acetylcholine release, systemic myotoxicity, and severe acute kidney injury characterized by tubular necrosis [1, 5, 10]. Additionally, these toxins exhibit anticoagulant and pro-inflammatory properties that exacerbate the clinical severity of envenomation [3, 8]. Given their central role in the morbidity and mortality associated with Russell's viper bites, they are critical therapeutic targets for both traditional antibody-based antivenoms and emerging small-molecule inhibitors like varespladib [6, 7].
Competitive inhibition of the phospholipase A2 active site and antibody-mediated neutralization of the toxin's enzymatic and non-enzymatic domains.
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