The balance of reduction-oxidation (redox) has been shown acting an important role in vascular growth. However, most studies have done in adult animals under pathological conditions, and very limited information about oxidative stress and vascular development during embryogenesis. Here, we report a novel biological function of prdx1 (peroxiredoxin1) that play critical roles in vascular formation during zebrafish development. Prdx1 belongs to a member of the peroxiredoxin family of antioxidant enzymes. We showed prdx1 is expressed in developing vessels and knockdown of prdx1 by morpholino injection impairs the growth of ISV (intersegmental vessel) and CVP (caudal vein plexus), suggesting the role of prdx1 in promoting vessels growth. We further showed the reduction of ISV cells is due to a decrease of cell proliferation and migration, but not results from cell death in non-endothelial cells. The molecular evidence of vascular defects in prdx1MO is related to the decreased expression of vascular markers, flt4, mrc1, stabilin and ephrinb2. Loss of prdx1 results in vascular defects suggest the antioxidant function is important, thus, we test if oxidative stress could cause vascular defects in H2O2-treated embryos. Our data showed H2O2 treatment impaired CVP formation and caused mild ISV defects. While H2O2-treated embryo combined with knockdown of prdx1, synergetic effects are observed. In addition, exogenous N-acetylcysteine (NAC) treatment rescues the vascular defects in prdx1MO. Those data suggested the oxidative stress indeed can disturb vascular development. We further showed the different regulation pattern of antioxidant genes SOD1, SOD2 and catalase in prdx1 morphants from H2O2-treated embryos. To confirm the role of prdx1 in vasculature, we overexpressed prdx1 in the embryos and found overexpression of prdx1 promotes ISV and CVP growth. Meanwhile, overexpression of prdx1 can rescue the loss of prdx1. Those data suggest prdx1 functions in vascular development necessary and sufficient. Interestingly, we found the increased expression of blood markers (gata1, globin and lmo2) coincident with the decreased expression of endothelial markers flk1 and fli in prdx1 MO, suggested prdx1 likely regulate hemangioblast fate decision at earlier developmental stage. We further demonstrated prdx1 likely interacts with Notch to control cell fate switch. Together, we showed prdx1 play novel and critical roles in vascular growth during zebrafish development.