Alleviation of viper venom induced platelet apoptosis by crocin (Crocus sativus): implications for thrombocytopenia in viper bites

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 Ca²⁺ 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.     

The turnover of [1-14C]eicosapentaenoic acid among individual phospholipids of human platelets

The incorporation of [1-¹⁴C] eicosapentaenoic acid (EPA) into the individual phospholipids of human platelets was studied using both isolated platelet suspensions and platelet-rich-plasma (PRP). With platelet suspensions, 47 and 38% of the newly-incorporated radio-activity was associated with phosphatidylcholine and phosphatidylinositol, respectively, with considerably lesser proportions residing in the phosphatidylethanolamine (8%) and phosphatidylserine (5%). A disproportionally high level of entry of [¹⁴C]EPA into phosphatidylinositol, relative to the minor contribution of this lipid to total platelet phospholipid was found also using PRP. Incubation of pre-labelled platelet suspensions with thrombin produced a substantial and rapid loss of [¹⁴C] EPA from platelet phospholipids which amounted to a net percentage (thrombin-dependent) decrease from phosphatidylinositol and phosphatidylcholine of 47 and 15%, respectively, within 1 min and 58 and 30% by 2.5 min. These results suggest a rapid turnover of EPA in human platelet phosphatidylinositol which may possibly bear relevance to the anti-aggregatory potential of this fatty acid.     

Nuclear medicine exposure in the United States, 2005-2007: preliminary results

Medical radiation exposure of the U.S. population has not been systematically evaluated for almost 25 years. In 1982, the per-capita dose was estimated to be 0.54 mSv and the collective dose 124,000 person-Sv. The preliminary estimates of the National Council on Radiation Protection and Measurements Scientific Committee 6-2 medical subgroup are that, in 2006, the per-capita dose from all medical exposure (not including radiotherapy) had increased almost 600% to 3.0 mSv and the collective dose had increased more than 700% to approximately 900,000 person-Sv. >Nuclear medicine accounted for only about 2% of all procedures but 26% of the total collective dose from diagnostic studies in medicine. In 1982, the estimated number of nuclear medicine procedures was about 7.5 million. The per-capita effective dose from nuclear medicine was 0.14 mSv and the collective dose was 32,000 person Sv. By 2005, the estimated number of procedures had increased to about 19.6 million. The per-caput effective dose increased to about 0.75 mSv and the collective dose to about 220,000 person Sv. There also has been a marked shift in the type of procedures being performed with cardiac scanning accounting for about 70% of procedures.     

Para‐tertiary butyl catechol (PTBC), an industrial antioxidant induces human platelet apoptosis

The catecholic derivative para‐tertiary butyl catechol (PTBC) is a conventional antioxidant and polymerization inhibitor, which exhibits melanocytotoxic effects and contact dermatitis often leading to occupational leucoderma or vitiligo. Although numerous industrial workers will be in constant exposure to PTBC and its chances of getting entry into blood are most expected, its effect on blood components is still undisclosed. As platelets play a prominent role in dermatitis, inflammation, and immunity, in this study we have evaluated the effect of PTBC on human platelets in vitro. Exposure of platelets to PTBC showed increased reactive oxygen species (ROS), intracellular calcium, cardiolipin oxidation, mitochondrial permeability transition pore ( MPTP) formation, activation of caspases, phosphatidylserine (PS) externalization and decreased mitochondrial membrane potential. In addition, there was a significant decrease in cellular glutathione level, increased γ‐glutamyltransferase (GGT) activity and cell death. These findings demonstrate that PTBC could induce toxic effects on blood components, which is often ignored field of research. Since dermal exposure of humans to toxic chemicals covers an important issue in various industries, there is a need of such work to understand and update the long‐term toxicities induced by PTBC usage in industrial sectors and public domain.