Explore the vast range of titles available.

Acute oxidative stress induced by ischemia-reperfusion or inflammation causes serious damage to tissues, and persistent oxidative stress is accepted as one of the causes of many common diseases including cancer. We show here that hydrogen (H 2 ) has potential as an antioxidant in preventive and therapeutic applications. We induced acute oxidative stress in cultured cells by three independent methods. H 2 selectively reduced the hydroxyl radical, the most cytotoxic of reactive oxygen species (ROS), and effectively protected cells; however, H 2 did not react with other ROS, which possess physiological roles. We used an acute rat model in which oxidative stress damage was induced in the brain by focal ischemia and reperfusion. The inhalation of H 2 gas markedly suppressed brain injury by buffering the effects of oxidative stress. Thus H 2 can be used as an effective antioxidant therapy; owing to its ability to rapidly diffuse across membranes, it can reach and react with cytotoxic ROS and thus protect against oxidative damage.

Contact electrification between water and a solid surface is crucial for physicochemical processes at water–solid interfaces. However, the nature of the involved processes remains poorly understood, especially in the initial stage of the interface formation. Here we report that H₂O₂ is spontaneously produced from the hydroxyl groups on the solid surface when contact occurred. The density of hydroxyl groups affects the H₂O₂ yield. The participation of hydroxyl groups in H₂O₂ generation is confirmed by mass spectrometric detection of 18O in the product of the reaction between 4-carboxyphenylboronic acid and 18O–labeled H₂O₂ resulting from 18O₂ plasma treatment of the surface. We propose a model for H₂O₂ generation based on recombination of the hydroxyl radicals produced from the surface hydroxyl groups in the water–solid contact process. Our observations show that the spontaneous generation of H₂O₂ is universal on the surfaces of soil and atmospheric fine particles in a humid environment.

The reaction system of hydrogen peroxide (H 2 O 2 ) catalyzed by nanozyme has a broad prospect in antibacterial treatment. However, the complex catalytic activities of nanozymes lead to multiple pathways reacting in parallel, causing uncertain antibacterial results. New approach to effectively regulate the multiple catalytic activities of nanozyme is in urgent need. Herein, Cu single site is modified on nanoceria with various catalytic activities, such as peroxidase-like activity (POD) and hydroxyl radical antioxidant capacity (HORAC). Benefiting from the interaction between coordinated Cu and CeO 2 substrate, POD is enhanced while HORAC is inhibited, which is further confirmed by density functional theory (DFT) calculations. Cu-CeO 2  + H 2 O 2 system shows good antibacterial properties both in vitro and in vivo. In this work, the strategy based on the interaction between coordinated metal and carrier provides a general clue for optimizing the complex activities of nanozymes. Nanozymes used for antibacterial therapy conventionally have complex catalytic activities that cause multiple pathways in parallel and unwanted outcome. Here, the authors report a Cu-CeO 2 single site nanozyme in which Cu single site modification can enhance the peroxidase-like activity and inhibit the hydroxyl radical antioxidant capacity of CeO 2 to optimise the antibacterial effects.

Caffeic acid (CA) is a phenolic compound widely found in coffee beans with known beneficial effects in vivo. Many studies showed that CA has anti-inflammatory, anti-mutagenic, antibacterial and anti-carcinogenic properties, which could be linked to its antioxidant activity. Taking in consideration the reported in vitro antioxidant mechanism of other polyphenols, our working hypothesis was that the CA antioxidant activity could be related to its metal-chelating property. With that in mind, we sought to investigate the chemical antioxidant mechanism of CA against in vitro iron-induced oxidative damage under different assay conditions. CA was able to prevent hydroxyl radical formation promoted by the classical Fenton reaction, as determined by 2-deoxyribose (2-DR) oxidative degradation and DMPO hydroxylation. In addition to its ability to prevent hydroxyl radical formation, CA had a great inhibition of membrane lipid peroxidation. In the lipid peroxidation assays CA acted as both metal-chelator and as hydrogen donor, preventing the deleterious action promoted by lipid-derived peroxyl and alkoxyl radicals. Our results indicate that the observed antioxidant effects were mostly due to the formation of iron-CA complexes, which are able to prevent 2-DR oxidation and DMPO hydroxylation. Noteworthy, the formation of iron-CA complexes and prevention of oxidative damage was directly related to the pH of the medium, showing better antioxidant activity at higher pH values. Moreover, in the presence of lipid membranes the antioxidant potency of CA was much higher, indicating its enhanced effectiveness in a hydrophobic environment. Overall, our results show that CA acts as an antioxidant through an iron chelating mechanism, preventing the formation of free hydroxyl radicals and, therefore, inhibiting Fenton-induced oxidative damage. The chemical properties of CA described here--in association with its reported signaling effects--could be an explanation to its beneficial effects observed in vivo.

Electro-Fenton processes aim at producing oxidizing radicals with fewer added chemicals and residues but are still unable to completely eliminate both. This study demonstrates that a reagent-free electro-Fenton process that runs solely on oxygen and electricity can be achieved by sequential dual-cathode electrocatalysis. H₂O₂ is produced on an electrodeposited PEDOT on carbon cloth (PEDOT/CC) cathode and subsequently converted to hydroxyl radicals on a stainless-steel–mesh cathode. The dual-cathode system demonstrates efficient decolorization and total organic carbon (TOC) removal toward organic dyes at optimized cathodic potentials of −0.9 V for PEDOT/CC and −0.8 V for the stainless-steel mesh. The sequential dual-cathode process also displays high reusability, no iron leaching, high removal efficiency using air instead of oxygen, and low installation and operation costs. This work demonstrates a preeminent and commercially viable example of pollution control rendered by the “catalysis instead of chemical reagent” philosophy of green chemistry.

The toxic potential of H 2 O 2 is limited, even if intracellular concentrations of H 2 O 2 under conditions of oxidative stress increase to the micromolar concentration range. Its toxicity is mostly restricted to the oxidation of highly reactive thiol groups, some of which are functionally very important. Subsequently, the HO · radical is generated spontaneously from H 2 O 2 in the Fenton reaction. The HO · radical is extremely toxic and destroys any biological structure. Due to the high reactivity, its action is limited to a locally restricted site of its generation. On the other hand, H 2 O 2 with its stability and long half-life can reach virtually any site and distribute its toxic effect all over the cell. Thereby HO · , in spite of its ultra-short half-life (10 –9  s), can execute its extraordinary toxic action at any target of the cell. In this oxidative stress scenario, H 2 O 2 is the pro-radical, that spreads the toxic action of the HO · radical. It is the longevity of the H 2 O 2 molecule allowing it to distribute its toxic action from the site of origin all over the cell and may even mediate intercellular communication. Thus, H 2 O 2 acts as a spreader by transporting it to sites where the extremely short-lived toxic HO · radical can arise in the presence of “free iron”. H 2 O 2 and HO · act in concert due to their different complementary chemical properties. They are dependent upon each other while executing the toxic effects in oxidative stress under diabetic metabolic conditions in particular in the highly vulnerable pancreatic beta cell, which in contrast to many other cell types is so badly protected against oxidative stress due to its extremely low H 2 O 2 inactivating enzyme capacity.

Targeting subcellular organelle with multilevel damage has shown great promise for antitumor therapy. Here, we report a core-shell type of nanoagent with iron (III) carboxylate metal-organic frameworks (MOFs) as shell while upconversion nanoparticles (UCNPs) as core, which enables near-infrared (NIR) light-triggered synergistically reinforced oxidative stress and calcium overload to mitochondria. The folate decoration on MOFs shells enables efficient cellular uptake of nanoagents. Based on the upconversion ability of UCNPs, NIR light mediates Fe 3+ -to-Fe 2+ reduction and simultaneously activates the photoacid generator (pHP) encapsulated in MOFs cavities, which enables release of free Fe 2+ and acidification of intracellular microenvironment, respectively. The overexpressed H 2 O 2 in mitochondria, highly reactive Fe 2+ and acidic milieu synergistically reinforce Fenton reactions for producing lethal hydroxyl radicals (•OH) while plasma photoacidification inducing calcium influx, leading to mitochondria calcium overload. The dual-mitochondria-damage-based therapeutic potency of the nanoagent has been unequivocally confirmed in cell- and patient-derived tumor xenograft models in vivo. Targeting damage to mitochondria has become an effective strategy antitumor therapies. Here, the authors report on nanoagents with upconversion nanoparticles as cores and photoacid-loaded MOFs as shells for NIR triggered Fenton reaction, acidification and calcium overload to provide synergistic mitochondrial damage.

Hydrogen sulfide is a highly toxic gas—second only to carbon monoxide as a cause of inhalational deaths. Its mechanism of toxicity is only partially known and no specific therapy exists for sulfide poisoning. We show in several cell types, including human inducible pluripotent stem cell (hiPSC)-derived neurons, that sulfide inhibited complex IV of the mitochondrial respiratory chain and induced apoptosis. Sulfide increased hydroxyl radical production in isolated mouse heart mitochondria and F 2 -isoprostanes in brains and hearts of mice. The vitamin B 12 analog cobinamide reversed the cellular toxicity of sulfide and rescued Drosophila melanogaster and mice from lethal exposures of hydrogen sulfide gas. Cobinamide worked through two distinct mechanisms: direct reversal of complex IV inhibition and neutralization of sulfide-generated reactive oxygen species. We conclude that sulfide produces a high degree of oxidative stress in cells and tissues and that cobinamide has promise as a first specific treatment for sulfide poisoning.

Limited substrates content is a major hurdle dampening the antitumor effect of catalytic therapy. Herein, a two-dimensional interplanar heterojunction (FeOCl/FeOOH NSs) with ·OH generation under ultrasound irradiation is fabricated and utilized for catalytic cancer therapy. This interplanar heterojunction is prepared through replacing chlorine from iron oxychloride with hydroxyl. Benefiting from the longer hydroxyl bond length and enhanced affinity with water, the alkali replacement treatment integrates interplanar heterojunction synthesis and exfoliation in one step. In particular, a build-in electric field facilitated Z-scheme interplanar heterojunction is formed due to the aligning Fermi levels. The holes on the valence band of FeOCl have great ability to catalyze O 2 evolution from H 2 O, meanwhile, the generated O 2 is immediately and directly reduced to H 2 O 2 by the electrons on the conductive band of FeOOH. The self-supplying H 2 O 2 ability guarantees efficient ·OH generation via the Fenton-like reaction catalyzed by FeOCl/FeOOH NSs, which exhibits excellent anti-tumor performance. Chemodynamic therapy relies on Fenton or Fenton-like reactions to produce hydroxyl radical in the tumor region. Here the authors design a two-dimensional interplanar heterojunction with in situ hydroxyl radical generation under ultrasound irradiation, showing anti-cancer activity in preclinical models.

Large variations in the growth of atmospheric methane, a prominent greenhouse gas, are driven by a diverse range of anthropogenic and natural emissions and by loss from oxidation by the hydroxyl radical. We used a decade-long dataset (2010–2019) of satellite observations of methane to show that tropical terrestrial emissions explain more than 80% of the observed changes in the global atmospheric methane growth rate over this period. Using correlative meteorological analyses, we show strong seasonal correlations ( r  = 0.6–0.8) between large-scale changes in sea surface temperature over the tropical oceans and regional variations in methane emissions (via changes in rainfall and temperature) over tropical South America and tropical Africa. Existing predictive skill for sea surface temperature variations could therefore be used to help forecast variations in global atmospheric methane. Methane is a powerful greenhouse gas with emissions that are challenging to constrain. Here the authors use 10 years of satellite observations and show tropical terrestrial emissions account for 80% of observed global methane increases.