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Increased transcriptional levels of genes encoding antioxidant enzymes play important protective roles in coping with excessive accumulation of reactive oxygen species (ROS) in plants exposed to various abiotic stresses. To fully elucidate different evolutions and functions of ROS-scavenging enzymatic genes, we isolated iron superoxide dismutase (FeSOD), dehydroascorbate reductase (DHAR) and monodehydroascorbate reductase (MDHAR) from white clover for the first time and subsequently tested dynamic expression profiles of these genes together with previously identified other antioxidant enzyme genes including copper zinc superoxide dismutase (Cu/ZnSOD), manganese superoxide dismutase (MnSOD), glutathione reductase (GR), peroxidase (POD), catalase (CAT), and ascorbate peroxidase (APX) in response to cold, drought, salinity, cadmium stress and exogenous abscisic acid (ABA) or spermidine (Spd) treatment. The cloned fragments of FeSOD, DHAR and MDHAR genes were 630, 471 and 669 bp nucleotide sequences encoding 210, 157 and 223 amino acids, respectively. Phylogenetic analysis indicated that both amino acid and nucleotide sequences of these three genes are highly conservative. In addition, the analysis of genes expression showed the transcription of GR, POD, MDHAR, DHAR and Cu/ZnSOD were rapidly activated with relatively high abundance during cold stress. Differently, CAT, APX, FeSOD, Cu/ZnSOD and MnSOD exhibited more abundant transcripts compared to others under drought stress. Under salt stress, CAT was induced preferentially (3-12 h) compared to GR which was induced later (12-72 h). Cadmium stress mainly up-regulated Cu/ZnSOD, DHAR and MDHAR. Interestingly, most of genes expression induced by ABA or Spd happened prior to various abiotic stresses. The particular expression patterns and different response time of these genes indicated that white clover differentially activates genes encoding antioxidant enzymes to mitigate the damage of ROS during various environmental stresses.

Retinal neovascularization is typically accompanied by hypoxia-induced oxidative injury in the vascular system. This study developed an ultrasmall (6–8 nm) platinum (Pt) nanozyme loaded mitochondria-targeted liposome (Pt@MitoLipo) to alleviate hypoxia and eliminate excess reactive oxygen species (ROS) for effective retinal neovascularization disease therapy. Pt nanozymes possess superoxide dismutase (SOD) and catalase (CAT) cascade enzyme-like activities, which convert cytotoxic O 2 •− and H 2 O 2 into nontoxic H 2 O and O 2. Triphenylphosphonium (TPP)-conjugated liposomes were coated on the surface of Pt nanozymes to increase their biocompatibility and help them penetrate the cell membrane, escape from the lysosomal barrier, and target mitochondria, thus achieving precise scavenging of mitochondrial O 2 •− and relief from hypoxia. Using an oxygen-induced retinopathy (OIR) mouse model, we demonstrated that Pt@MitoLipo nanozymes significantly suppressed hypoxia-induced abnormal neovascularization and facilitated avascular normalization of the retina in vivo without any noticeable toxicity. This study provides a promising way to break through cellular barriers and target scavenging mitochondrial O 2 •− and illustrates the potential of ROS-scavenging and hypoxia relief in retinal neovascularization disease therapy. [Display omitted] [ABSTRACT FROM AUTHOR]

• A nanoplatform (CS-CDs@155) for rheumatoid arthritis accurate monitoring and amelioration was fabricated. • CS-CDs@155 effectively scavenges intracellular reactive oxygen species and downregulates pro-inflammatory cytokines. • CS-CDs@155 realize macrophage subphenotype identification via miRNA-155 ratiometric imaging. • CS-CDs@155 regulate the polarization of proinflammatory macrophages. Accurate monitoring and effective antioxidant treatment strategies are highly desirable in rheumatoid arthritis (RA) amelioration. Herein, cerium (Ce) and selenium (Se) co-doped carbon dots (CS-CDs) integrated superoxide dismutase (SOD)-like and glutathione peroxidase (GPx)-like self-cascading catalytic activity are engineered. In this self-cascading nanozymes system, Ce active center catalyzes ·O 2 − to H 2 O 2 by mimicking SOD, and the adjacent Se component sequentially decomposes the H 2 O 2 by mimicking GPx, achieving enhanced catalytic and superior reactive oxygen species (ROS)-scavenging activities. CS-CDs further load cyanine-5 (Cy5)-labeled anti-miRNA-155 to realize macrophage subphenotype identification via miRNA-155 ratiometric imaging for RA accurate monitoring, and regulate the polarization of pro-inflammatory macrophages for synergistic RA amelioration. Comprehensive in vitro and in vivo experiments validate the advanced RA monitoring and therapy performance of the self-cascading nanozymes. This work not only offers a rationally designed self-cascading nanozyme with simple structures and intriguing ROS-scavenging capacity, but also opens up a strategy for accurate RA monitoring and synergistic amelioration. [ABSTRACT FROM AUTHOR]

Manganese superoxide dismutase (Mn-SOD) is an essential enzyme involved in the detoxification of reactive oxygen by dismutation of the superoxide radical anion. In this study, full-length complementary DNA (cDNA) and genomic DNA of Mn-sod genes were cloned from Pyropia haitanensis ( phsod), and its expression was monitored using quantitative polymerase chain reaction (qPCR). Scavenging of reactive oxygen species under heat shock was analyzed as well. The full-length cDNA of the phsod gene consists of 935 bp (GenBank accession number: EU715988) with an open reading frame of 675 bp, which encodes 224 amino acids. The length of the genomic sequence is 1416 bp and includes four exons and three introns. A highly conserved Mn-SOD signature (DVWEHAYY) was found. The transit peptide in the N-terminal helps protein targeting to the mitochondria. Results showed that the expression levels of phsod increased 3.4 times compared to controls and then suddenly decreased under a heat shock of 35°C for 30 min. After heat shock exposure and return to normal cultivation temperature, the expression levels of phsod decreased within 1 h of release from the heat shock and then increased within 3 h. SOD activity correlated with the expression of the phsod gene and, as expected, the concentration of ·O2- showed negative correlations with SOD activity. [ABSTRACT FROM AUTHOR]