Modification of radiation induced lipid peroxidation by calmodulin antagonists.
It has been shown that calmodulin antagonists provide radio-protection in euoxic and sensitization in hypoxic conditions. This differential protection in euoxic conditions might have arisen from the interaction of calmodulin antagonists with oxygen free radicals. This possibility has been tested in the present communication. Radiation induced lipid peroxidation process in liposomes has been used for this purpose. Liposomes prepared from L-alpha-lecithin were irradiated with or without calmodulin antagonists. Calmodulin antagonists inhibited lipid peroxidation significantly. The inhibition was found to increase with increase in concentration of the drugs. These observations suggest that calmodulin antagonists have a capacity to scavenge oxygen free radicals involved in initiation and/or propagation of lipid peroxidation process. This may be the reason for their differential radioprotection in euoxic conditions in biological systems.
Kale
R K
RK
Radiation Biology Laboratory, School of Life Sciences, Jawaharlal Nehru University, New Delhi, India.
Sitasawad
S L
SL
D002147:Calmodulin / Q000037:antagonists & inhibitors*; D002746:Chlorpromazine / Q000494:pharmacology; D005609:Free Radicals; D015227:Lipid Peroxidation / Q000187:drug effects* / Q000528:radiation effects; D008081:Liposomes; D010713:Phosphatidylcholines; D011398:Promethazine / Q000494:pharmacology; D011837:Radiation-Protective Agents / Q000494:pharmacology*; D014273:Triflupromazine / Q000494:pharmacology; D014291:Trimeprazine / Q000494:pharmacology
D002147:Calmodulin; D005609:Free Radicals; D008081:Liposomes; D010713:Phosphatidylcholines; D011837:Radiation-Protective Agents; D014291:Trimeprazine; D011398:Promethazine; D014273:Triflupromazine; D002746:Chlorpromazine