Lack of protein 4.1a in red blood cells of the hereditarily anemic Belgrade laboratory (b/b) rat

We have demonstrated that the red blood cell (RBC) membrane of the heredita rily anemic Belgrade laboratory (b/b) rat contains protein 4.1b isoform, on ly. The evidence are given that the synthesis of protein 4.1 in the b/b rat reticulocytes is the same as in normal rat. When haemolytic anaemia was in duced in normal rat by in vivo phenyhydrazine treatment the same phenomenon , i.e., the absence of protein 4.1 a in the RBC membrane was observed. The increase of 4.1 a isoform was monitored in RBCs during the recovery of norm al rat after phenyhydrazine treatment. Hence, the portion of membrane prote in 4.1a isoform is increasing during rat RBC aging. Likewise, when the RBC life span is prolonged (but not normalised) in the b/b rats by iron-dextran treatment protein 4.1a is present in small portion in the RBC membrane. Al l these data indicate that the lack of protein 4.1a isoform in the b/b rat is due to the presence of young RBCs in the circulation. (C) 1999 Wiley-Lis s, Inc.