Abstract
Arginase activity in red blood cells (RBC) of various mammalian species including man was determined. In nonprimate species, the activity generally fell below the level of detectability of the assay: less than 1.0 mumol urea/g hemoglobin per hr. Activities in higher nonhuman primates were equal to or of the same order of magnitude as those in man (approximately 950 mumol/g hemoglobin per hr). RBC arginase deficiency with normal liver arginase activity has been shown to segregate as an autosomal codominant trait in Macaca fascicularis established and bred in captivity. This study confirms the presence of this polymorphism in wild populations trapped in several geographic areas and demonstrates the absence of immunologically cross-reactive material in the RBC of RBC arginase-deficient animals. These data when taken together suggest that the expression of arginase in RBC is the result of a regulatory alteration, has evolved under positive selective pressure, and is not an example of the vestigial persistence of an arcane function. The expression of arginase in the RBC results in a marked drop in the arginine content of these cells.
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Selected References
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