Myeloperoxidase(MPO)is a peroxidase abundantly expressed in neutrophils.The MPO oxidant system is believed to be a main contributor to the microbicidal activity of neutrophils and inflammatory tissue injury.Recent evidence demonstrates that MPO is involved in cellular homeostasis and is an important factor in the initiation and progression of various inflammatory diseases.However,few consequences result from the MPO-deficient patients and knockout mice indicate the activation of compensatory mechanisms.In this study,we identify a zebrafish mutant with completely Mpx deficiency through genetic screening by sudan black(SB)staining.Further characterizing shows significant reduce of mpx transcript,but normal expression of other hematopoiesis markers in the mutant embryos.Injecting the mRNA of mpx to the mutant embryos can partly restore the enzymatically active detected by diaminobenzidine(DAB)staining.The Mpx-deficient mutant simulates the phenotype of related human disorder,and provides an excellent model for investigating the further function of MPO and the compensatory mechanisms.