Plays a role in cuticle biogenesis (PubMed:11514595, PubMed:19406744, PubMed:23028364, PubMed:25480962, PubMed:18460651). In complex with doxa-1 and tsp-15, produces reactive oxygen species (ROS), which are probably used by mlt-7 for tyrosine cross-linking, thus stabilizing cuticular extracellular matrix (PubMed:11514595, PubMed:19406744, PubMed:23028364). May regulate the production of ROS by playing a role in modulating proline catabolism (PubMed:27974198). Required in combination with mlt-7 for correct formation of cross-links in cuticle collagens (PubMed:19406744). Association with the GTPase rho-1 promotes ROS production and this interaction may be modulated by memo-1, in order to control the oxidative stress response and longevity (PubMed:28085666). H(+) + NADH + O2 = H2O2 + NAD(+) H(+) + NADPH + O2 = H2O2 + NADP(+) Peroxidase activity is inhibited by aminobenzohydrazide. Interacts with doxa-1 and tsp-15 (PubMed:23028364). Interacts with rho-1 (PubMed:28085666). Expressed in hypodermal cells. RNAi-mediated knockdown results in a blistered cuticle phenotype (PubMed:23028364, PubMed:25480962). Resistant to iodide toxicity (PubMed:25480962). RNAi-mediated knockdown in combination with proline supplementation suppresses the effects of exogenous proline alone and increases reactive oxygen species production and reduces the expression of skn-1 transcriptional targets including gst-4 following infection by P.aeruginosa (PubMed:27974198). RNAi-mediated knockdown rescues the enhanced longevity and increased reactive oxygen species production defects in memo-1 mutants (PubMed:28085666). RNAi-mediated knockdown suppresses the nuclear localization of transcription factor skn-1 in memo-1 RNAi mutants (PubMed:28085666). In the N-terminal section; belongs to the peroxidase family.