Effect of mercuric chloride on phospholipid peroxidation in rat

Individual molecular species of mercuric chloride induced phospholipid peroxide formed in rat brain, liver and kidney were determined using the multi-channel UV-high-performance liquid chromatography (HPLC) combined with potentiometric determination. Mercuric chloride (0.5 mg/kg/day) was administered subcutaneously to rats for 3 days. In accordance with a specified time schedule following administration (0.5, 1, 3 and 5 days), rats were decapitated and the phospholipids of brains, livers and kidneys were extracted and purified. The samples were then injected into the HPLC and the ratio (235 nm/203 nm) of peak area of each phospholipid was calculated. The peroxide value of each sample was determined using the calibration curve of the auto-oxidized standard phospholipids which were analyzed by both potentiometric determination and UV HPLC. Kidney phospholipid peroxides were easier induced than those in other organs reached their maximum peak (20.5 meq./kg) at 1 day after initial administration. Phospholipid peroxides in kidney and brain showed similar movement, while those in liver showed their maximum peak 3 days later. Of the phospholipids, phosphatidylserine and phosphatidylethanolamine seemed to be more susceptible to lipid peroxidation induced by mercuric chloride, the common feature of these two phospholipids being that both of them have primary amine group(s) on their polary heads and both are located on the cytosolic side of cell membrane. These results may be explained by mechanisms that relate to the interaction between mercurials and cell membranes or that between mercurials and primary amine groups of phospholipids. Further study is necessary to clarify the specific mechanisms involved in the induction of lipid peroxidation by mercurials and the interaction of mercurials with phospholipids.