Effect of cryopreservation on lipid peroxidation in chick cornea.

A mechanism suggested to cause injury to the preserved organs in vitro is the generation of oxygen free radicals either during preservation or after transplantation due to reperfusion. Methods to suppress generation of oxygen free radicals may lead to improved methods of organ preservation. In this study, increase in the levels of lipid peroxidation in chick cornea after cryopreservation is reported. Addition of fetal bovine serum (FBS) in cryopreservation medium was found to prevent lipid peroxidation. Addition of FBS was also found to be protective towards corneal viability during cryopreservation.

Divalent cations and radiation induced lipid peroxidation.

Response of Co2+, Cu2+, Fe2+, Ni2+ and Mn2+ against radiation induced lipid peroxidation has been examined. Liposomes prepared from L-alpha-lecithin were irradiated with or without divalent cations, Co2+ and Cu2+ inhibited lipid peroxidation in concentration dependent manner. On the other hand Fe2+, Ni2+ and Mn2+ enhanced the peroxidation. The enhancement of peroxidation due to Ni2+ was biphasic in nature. Higher concentration of Mn2+ decreased the peroxidation. Except Cu2+ no other cation studied could change the non-linear pattern of radiation induced lipid peroxidation. The pro- or antioxidant effect of divalent cations may be due to their reactivity towards oxygen and oxygen free radicals, and at least in part to their hard/soft acid character.

Non-linear pattern of radiation induced lipid peroxidation is not affected by vitamin E, Fe2+ ions and molecular oxygen.

Results of the present study on liposomes have clearly shown that non-linear pattern of radiation-induced lipid peroxidation was not changed even in the presence of vitamin E, Fe2+ ions or molecular oxygen. These results are important from biological point of view as lipid peroxidation is used as a measure of membrane damage.

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.