In vivo and in vitro characterization of the biochemical and pathological changes induced by lionfish (Pterios volitans) venom in mice

Accidents caused by lionfish (Pterios volitans) envenomation are characterized by edema, intense pain, and necrosis at the site of sting. The mode of action and biochemistry of venoms are obviously complex and require a better knowledge and investigation to explore the toxic action and resulting biochemical changes. In the present study the LD₅₀ value of lionfish venom was found to be 42.5 μg/kg body weight (intraperitoneal injection) in Albino Swiss mice and was associated with reduced motor activity and asphyxiation followed by respiratory failure. The effect on vital organs revealed spongiosis in brain, vascular congestion in liver, cloudy swelling of renal tubules, congested blood vessels in renal tubules, and degeneration of myofibrils in heart. Whereas, the 10% of LD₅₀ (was 4.25 μg/kg b.w.), the sublethal dose showed reversible changes in the hematological (blood cell count, hematocrit, hemoglobin, mean corpuscular volume, mean corpuscular hemoglobin, and platelet count) parameters, serum enzymes (aspartate transaminase, alanine transaminase, alkaline phosphatase, lactate dehydrogenase, and creatinine phosphokinase), blood sugar, urea, creatinine, triglycerides, cholesterol, and total protein in mouse in vivo. The in vitro analysis of lionfish venom on mouse brain acetyl cholinesterase and Na⁺, K ⁺, ATPase showed significant increased activity in a dose-dependent manner (10 to 40 μg). Moreover, the lionfish venom was observed to have a protease with a molecular weight of 45 kDa. Hence, the present study suggests the presence of bioactive proteins and peptides with excellent target specificity, which could be trapped for drug development in near future.