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The Big Four venomous snakes of India—the Indian Cobra (Naja naja), Common Krait (Bungarus caeruleus), Russell’s Viper (Daboia russelii), and Saw-scaled Viper (Echis carinatus)—possess venoms containing a complex mixture of toxins categorized by molecular weight. Low-molecular-weight toxins, such as three-finger toxins (3FTxs) and disintegrins, are primarily responsible for neurotoxicity and the inhibition of platelet aggregation. Mid-molecular-weight toxins are dominated by phospholipase A2 (PLA2) enzymes, which cause local and systemic myotoxicity, hemolysis, and inflammation. High-molecular-weight toxins include snake venom metalloproteinases (SVMPs) and serine proteases (SVSPs), which induce systemic hemorrhage and coagulopathy by degrading the extracellular matrix and interfering with the clotting cascade. These toxins are the primary therapeutic targets of polyvalent antivenom, which consists of purified antibodies that bind and neutralize the venom components. Emerging therapies also include small-molecule inhibitors like varespladib and prinomastat, which specifically target PLA2 and SVMP activities, respectively, to mitigate tissue damage and improve patient survival.
Antibody-mediated neutralization of venom toxins; competitive inhibition of phospholipase A2; inhibition of zinc-dependent snake venom metalloproteinases
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