Abstract
The venom of the marine snail,
Conus loroisii, was studied to assess its risk and lethal factors in regard of human welfare. The lethality of the crude venom (LD
50-5.0
mg/kg via i.p.) in mice was associated with reduced motor activity, asphyxiation, followed by respiratory failure. The effects on vital tissues revealed vascular congestion and inflammatory cell infiltration around the portal triad of the liver, spongiosis of the brain, hemorrhages/congested blood vessels in lung and endothelial cells of the renal tubule. Repeated measures of hematological profiles indicated that the venom significantly reduced erythrocytes (
P
<
0.001, GLM repeated measures), followed associated with depletion of hemoglobin, hematocrit, mean corpuscular volume, mean corpuscular hemoglobin and platelet count. Serum enzymes such as, glutamic-oxaloacetic transaminase, glutamic-pyruvic transaminase, lactate dehydrogenase and alkaline and acid phosphatases were altered significantly (
P
<
0.05, Friedman test), which in turn confirmed the damage of vital organ tissues. Dual effect of the venom on the activity of mouse brain acetylcholinesterase stand for concentration specific, whereas maximal inhibition (60.41%,
P
<
0.05, Wilcoxon signed rank test) in erythrocyte acetylcholinesterase did not show the dual activity observed in brain. The Ciphergen ProteinChip
® analysis of the envenomed serum further revealed that the venom causes changes in definite molecules involved in inflammatory process and ionic transport. In all, the venom of
C. loroisii is potentially lethal to mammals, through its rapid action on the central and peripheral nervous systems by blocking neurotransmission with selective interference of ionic channels/receptors.