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Venomous snakes are capable of storing venom for years while maintaining functionality upon injection, with no known harmful impact to their own physiology; however, the mechanisms behind this are poorly understood. Several major components of venom, most notably SVMPs, are autolytic when active, suggesting the presence of an inhibitory environment during storage to preserve venom functionality. It is hypothesized that the venom gland is continuously acidified by vacuolar rotary proton pump mechanisms (V-ATPases) localized in mitochondria-rich cells found in small concentration within the venom gland secretory epithelium, keeping the venom inert at a pH of 5.4-5.6 during the production/storage period. Upon injection into prey, the venom is activated by the environmental pH of the prey tissue, around 7.2-7.4. I tested this hypothesis by developing a novel method of chemically inhibiting these acidifying mechanisms during venom production in vivo. When bafilomycin A1, a V-ATPase specific inhibitor was delivered in vivo with direct injections, pH of venom extracted 7 DPE (days post extraction) was increased to 6.0-6.5, showing altered venom profiles, signs of protein degradation, and decreased enzymatic functionality when compared to controls. The influences of inhibited V-ATPases during venom production may also extend to the secretion of venom proteins into the lumen, as components showing greatly reduced activity in vivo, while remaining relatively intact during artificial pH alteration in vitro.

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