Blood Destruction II

Hemotoxic venoms in snakes evolved primarily through gene duplication and neofunctionalization of ancestral digestive enzymes like metalloproteinases, serine proteases, and phospholipases.

These components were co-opted and refined to disrupt prey circulatory systems by degrading endothelial linings, lysing red blood cells, and preventing clotting.

This evolutionary path favored snakes in ambush predation niches, especially vipers, where immobilizing prey quickly and initiating pre-digestion externally offered survival advantages.

Selective pressures led to regionally adapted venom profiles, with hemotoxicity being more common in terrestrial species inhabiting dense vegetation or burrows, where quick prey escape needed to be prevented without relying on rapid neurotoxic effects.