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 LD(50) value of lionfish
venom was found to be 42.5 mug/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 LD(50) (was 4.25 mug/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 mug). 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.