Peroxiredoxin I deficiency attenuates phagocytic capacity of macrophage in clearance of the red blood cells damaged by oxidative stress

• Main Author: Ying-Hao Han1,8,#, Taeho Kwon1,7,#, Sun-Uk Kim1,2,#, Hye-Lin Ha1, Tae-Hoon Lee1,3, Jin-Man Kim4, Eun-Kyeong Jo5, Bo Yeon Kim6, Do Young Yoon7 & Dae-Yeul Yu1,*
• Format: Article
• Language: English
• Published: Korean Society for Biochemistry and Molecular Biology 2012-10-01
• Series: BMB Reports
• Subjects: Heinz body; Hemolytic anemia; Macrophage; Peroxiredoxin; Phagocytosis
• Online Access: http://www.jbmb.or.kr/jbmb/pdf.php?data=MTMwMTIyMTdAcGRmX3JhaW50cmFjZV9sZWV5c0AlNUI0NS0xMCU1RDEyMTAyOTIxMTVfJTI4NTYwLTU2NCUyOUJNQl8xMi0wODIucGRm

The role of peroxiredoxin (Prx) I as an erythrocyte antioxidantdefense in red blood cells (RBCs) is controversial. Here weinvestigated the function of Prx I by using Prx I–⁄– and Prx I/II–⁄–mice. Prx I–⁄– mice exhibited a normal blood profile. However,Prx I/II–⁄– mice showed more significantly increased Heinz bodyformation as compared with Prx II–⁄– mice. The clearance rate ofHeinz body-containing RBCs in Prx I–⁄– mice decreasedsignificantly through the treatment of aniline hydrochloride (AH)compared with wild-type mice. Prx I deficiency decreased thephagocytic capacity of macrophage in clearing Heinz bodycontainingRBCs. Our data demonstrate that Prx I deficiency didnot cause hemolytic anemia, but showed that further increasedhemolytic anemia symptoms in Prx II–⁄– mice by attenuatingphagocytic capacity of macrophage in oxidative stress damagedRBCs, suggesting a novel role of Prx I in phagocytosis ofmacrophage.