Erythrocyte alterations in praseodymium-induced lecithin:cholesterol acyltransferase (LCAT) deficiency in the rat: comparison with familial LCAT deficiency in man.

The intravenous administration of praseodymium nitrate (PrN) to rats was associated with parallel decreases in plasma lecithin: cholesterol acyltransferase (LCAT) activity and erythrocyte osmotic fragility at low doses (20 and 40 mg/kg) while higher doses (80 mg/kg) resulted in increases in both. Erythrocyte membranes from rats with PrN-induced LCAT deficiency exhibited small increases in cholesterol content, but not other alterations (e.g., in phospholipid profiles and sulfhydryl group latency) which characterize erythrocytes in familial LCAT deficiency in man. The administration of PrN caused a time- and dose-dependent accumulation of praseodymium in liver with hepatic levels being substantially greater in animals given the high (protective) as compared with the low (toxic) doses of PrN. Hepatic levels of glutathione were not altered by PrN administration, but hexobarbital sleeping time was markedly prolonged in animals receiving a toxic dose of PrN. It is suggested that dose-dependent alterations in the subcellular distribution of praseodymium may explain the paradoxical pathophysiological effects of high and low doses of PrN.