Viper envenomations are characterized by prominent local and systemic manifestations including hematological alterations.
Snake venom metalloproteinases (SVMPs) and
phospholipase A2 (PLA2) plays crucial role in the pathophysiology of
hemorrhage by targeting/altering the platelets function which may result in
thrombocytopenia. Platelets undergo the classic events of mitochondria-mediated apoptotic pathway due to augmented endogenous
reactive oxygen species (ROS) levels. The observed
anticoagulant effects during viper envenomations could be due to exacerbated platelet apoptosis and
thrombocytopenia. Moreover,
antivenin treatments are ineffective against the
venom-induced oxidative stress; therefore, it necessitates an auxiliary
therapy involving
antioxidants which can effectively scavenge the endothelium-generated/endogenous ROS and protect the platelets. The present study explored the effects of
viper venom on platelet apoptosis and its amelioration by a
phytochemical crocin. The study evaluated the Vipera russelli
venom-induced apoptotic events including endogenous ROS generation, intracellular Ca(2+) mobilization, mitochondrial membrane depolarization, cyt-c translocation,
caspase activation and
phosphatidylserine externalization which were effectively mitigated when the
venom was pre-treated with
crocin. The study highlights one of the less studied features of
venom-induced secondary complications i.e. platelet apoptosis and sheds light on the underlying basis for
venom-induced
thrombocytopenia, systemic
hemorrhage and in vivo
anticoagulant effect.