Abstract
The owl monkey (Aotus trivirgatus), a species of New World monkey represented by several different karyotypes, develops hemolytic anemia in captivity. Susceptibility to anemia varies as a function of karyotype, and the hemolytic process responds to vitamin E. Since the plasma concentration of vitamin E in these owl monkeys was normal, it was hypothesized that the anemia may reflect a lipid abnormality in the red blood cell (RBC) membrane which was stabilized by supplemental tocopherol and that the basic RBC lipids would differ as a function of owl monkey karyotype. To test this hypothesis the RBC membrane cholesterol, phospholipid, fatty acids, and free cholesterol to phospholipid ratio (FC/PL) were compared between (a) anemic and nonanemic owl monkeys, (b) owl monkeys of different karyotypes, and (c) between different primate species. As a species, the owl monkey exhibited a unique RBC phospholipid profile, having reduced proportions of phosphatidylserine (PS) and phosphatidylethanolamine (PE) and more phosphatidylcholine (PC) and sphingomyelin (Sph) when compared to other primates, including man. As a function of karyotype, owl monkeys of karyotype VI (anemia resistant) had a normal polyunsaturated fatty acid (PUFA) profile in RBC phospholipids and less RBC membrane cholesterol contributing to a normal FC/PL ratio, whereas RBCs from susceptible and overtly anemic owl monkeys revealed low levels of PUFA and increased RBC membrane cholesterol that led to an elevated FC/PL ratio. The etiology of these lipid alterations and their association with anemia remains to be elucidated.