Nitric oxide (NO) has been firmly established as a key signaling molecule in plants, playing a significant role in regulating growth, development and stress responses. Given the imperative of sustainable agriculture and the urgent need to meet the escalating global demand for food, it is imperative to safeguard crop plants from the effects of climate fluctuations. Plants respond to environmental challenges by producing redox molecules, including reactive oxygen species (ROS) and reactive nitrogen species (RNS), which regulate cellular, physiological, and molecular processes. Nitric oxide (NO) plays a crucial role in plant stress tolerance, acting as a signaling molecule or free radical. NO is involved in various developmental processes in plants through diverse mechanisms. Exogenous NO supplementation can alleviate the toxicity of abiotic stresses and enhance plant resistance. In this review we summarize the studies regarding the production of NO in peroxisomes, and how its molecule and its derived products, (ONOO-) and S-nitrosoglutathione (GSNO) affect ROS metabolism in peroxisomes. Peroxisomal antioxidant enzymes including catalase (CAT), are key targets of NO-mediated post-translational modification (PTM) highlighting the dynamic metabolism of ROS and RNS in peroxisomes.

Eight previously undescribed diterpenoids, caesamins A-H (1-8), were separated and identified from the seeds of Caesalpinia minax Hance. Their structures were characterized by extensive spectroscopic data and X-ray crystallographic analysis. Structurally, caesamin A (1) is the first cassane-type diterpenoid with a C23 carbon skeleton containing an unusual isopropyl. Caesamin F (6) represents the first example of cleistanthane diterpenoid from the genus Caesalpinia. Caesamins B (2) and F (6) exhibited inhibitory activity against LPS-induced nitric oxide production in RAW 264.7 macrophages with IC50 values of 45.67 ± 0.92 and 42.99 ± 0.24 μM, comparable to positive control 43.69 ± 2.62 μM of NG-Monomethyl-L-arginine. Furthermore, the chemotaxonomic significance of the isolates was discussed.

The objective of this study was to investigate the mechanism underlying LW-1-induced resistance to TMV in wild-type and salicylic acid (SA)-deficient NahG transgenic tobacco plants. Our findings revealed that LW-1 failed to induce antivirus infection activity and increase SA content in NahG tobacco, indicating the crucial role of SA in these processes. Meanwhile, LW-1 triggered defense-related early-signaling nitric oxide (NO) generation, as evidenced by the emergence of NO fluorescence in both types of tobacco upon treatment with LW-1, however, NO fluorescence was stronger in NahG compared to wild-type tobacco. Notably, both of them were eliminated by the NO scavenger cPTIO, which also reversed LW-1-induced antivirus activity and the increase of SA content, suggesting that NO participates in LW-1-induced resistance to TMV, and may act upstream of the SA pathway. Defense-related enzymes and genes were detected in tobacco with or without TMV inoculation, and the results showed that LW-1 regulated both enzyme activity (β-1,3-glucanase [GLU], catalase [CAT] and phenylalanine ammonia-lyase [PAL]) and gene expression (PR1, PAL, WYKY4) through NO signaling in both SA-dependent and SA-independent pathways.

While mild hyperthermia holds great potential in the treatment of solid tumors, the thermal stress-triggered self-repairing autophagy significantly compromises its efficacy. To circumvent this obstacle, an injectable hydrogel (NO-Gel) composed of thermosensitive poly(ethylene glycol)-polypeptide copolymers modified with abundant NO donors on their side chains is developed. Meanwhile, ferrimagnetic Zn0.5Fe2.5O4 magnetic nanoparticles (MNPs) with high magnetic-heat conversion efficiency are synthesized and loaded into NO-Gel to obtain MNPs@NO-Gel. The MNPs@NO-Gel system exhibits a sol-gel transition upon heating, and has the ability to perform multiple magnetic hyperthermia therapy (MHT) after only one administration due to the even distribution and strong immobilization of MNPs in NO-Gel. NO can be continuously liberated from NO-Gel and this process is markedly accelerated by MHT. Additionally, MNPs@NO-Gel maintains its integrity in vivo for over one month and the released MNPs are metabolized by the spleen. After a single administration of MNPs@NO-Gel at the tumor site, three mild MHT treatments with similar effects are fulfilled, and the sufficient supply of NO effectively inhibits MHT-induced autophagic flux via blocking the formation of autophagosomes and synchronously destroying lysosomes, thereby substantially boosting the efficacy of mild MHT. As a consequence, CT-26 colon tumors are completely eliminated without causing severe side-effects.

The electrocatalytic conversion of nitric oxide (NORR) to ammonia (NH3) represents a pivotal approach for sustainable energy transformation and efficient waste utilization. Designing highly effective catalysts to facilitate the conversion of NO into NH3 remains a formidable challenge. In this work, the density functional theory (DFT) is used to design NORR catalysts based on single and double transition metal (TM:Fe, Co, Ni and Cu) atoms supported by graphdiyne (TM@GDY). Among eight catalysts, the Cu2@GDY is selected as a the most stable NORR catalyst with high NH3 activity and selectivity. A pivotal discovery underscores that the NORR mechanism is thermodynamically constrained on single atom catalysts (SACs), while being governed by electrochemical processes on double atom catalysts (DACs), a distinction arising from the different d-band centers of these catalysts. Therefore, this work not only introduces an efficient NORR catalyst but also provides crucial insights into the fundamental parameters influencing NORR performance.

Ischemic stroke (IS) is a life-threatening disease worldwide. Nitric oxide (NO) derived from l-arginine catalyzed by NO synthase (NOS) is closely associated with IS. Three isomers of NOS (nNOS, eNOS and iNOS) produce different concentrations of NO, resulting in quite unlike effects during IS. Of them, n/iNOSs generate high levels of NO, detrimental to brain by causing nerve cell apoptosis and/or necrosis, whereas eNOS releases small amounts of NO, beneficial to the brain via increasing cerebral blood flow and improving nerve function. As a result, a large variety of NO regulators (NO donors or n/iNOS inhibitors) have been developed for fighting IS. Regrettably, up to now, no review systematically introduces the progresses in this area. This article first outlines dynamic variation rule of NOS/NO in IS, subsequently highlights advances in NO regulators against IS, and finally presents perspectives based on concentration-, site- and timing-effects of NO production to promote this field forward.

Although auxin has been linked to plants\' responses to cadmium (Cd) stress, the exact mechanism is yet elusive. The objective of the current investigation was to determine the role and the mechanism of auxin in controlling rice\'s Cd accumulation. Rice roots with Cd stress have higher endogenous auxin levels, and exogenous auxin combined Cd treatment could reduce root cell wall\'s hemicellulose content when compared with Cd treatment alone, which in turn reduced its fixation of Cd, as well as decreased the expression of OsCd1 (a major facilitator superfamily gene), OsNRAMP1/5 (Natural Resistance-Associated Macrophage Protein 1/5), OsZIP5/9 (Zinc Transporter 5/9), and OsHMA2 (Heavy Metal ATPase 2) that participated in Cd uptake and root to shoot translocation. Furthermore, less Cd accumulated in the shoots as a result of auxin\'s impact in increasing the expression of OsCAL1 (Cadmium accumulation in Leaf 1), OsABCG36/OsPDR9 (G-type ATP-binding cassette transporter/Pleiotropic drug resistance 9), and OsHMA3, which were in charge of Cd efflux and sequestering into vacuoles, respectively. Additionally, auxin decreased endogenous nitric oxide (NO) levels and antioxidant enzyme activity, while treatment of a NO scavenger-cPTIO-reduced auxin\'s alleviatory effects. In conclusion, the rice\'s ability to tolerate Cd toxicity was likely increased by the auxin-accelerated cell wall Cd exclusion mechanism, a pathway that controlled by the buildup of NO.

Melatonin (MT) is participated in plants\' response to cadmium (Cd) tolerance, although its work model remains elusive. Here, the function of MT in adjusting Cd accumulation in rice was investigated. \'Nipponbare\' (Nip) was cultured in the -Cd (1/2 Kimura B), -Cd + MT (1/2 Kimura B with 1 μM MT), +Cd (1/2 Kimura B plus 1 μM Cd) and +Cd + MT (1/2 Kimura B with 1 μM Cd and 1 μM MT) nutrient solutions for 7 d. Cd markedly induced the endogenous MT accumulation in rice roots and shoots, even within 1 h. MT applied exogenously elevated the hemicelluloses level, which in turn increased the cell wall\'s binding capacity to Cd. Furthermore, MT applied exogenously down-regulated the transcription level of Natural Resistance-Associated Macrophage Protein 1 (OsNRAMP1), OsNRAMP5, a major facilitator superfamily gene (OsCd1), and IRON-REGULATED TRANSPORTER 1 (OsIRT1), all of which were responsible for Cd intake, thus less Cd was entered into roots. Moreover, MT applied exogenously also up-regulated transcription level of Cadmium accumulation in Leaf 1 (OsCAL1) and Heavy Metal ATPase 3 (OsHMA3), two genes both attributed to the decreased Cd accumulation in shoots through expelling Cd out of cells and chelating Cd in the vacuoles, respectively. In addition, MT applied exogenously further aggravated the production of nitric oxide (NO) that induced by Cd, while application of a NO donor-SNP mimicked this alleviatory effect of the MT, indicating MT decreased rice Cd accumulation relied on the accumulation of NO.

Inflammation is connected with a variety of diseases and there is still a need to develop more effective and safer anti-inflammatory drugs. Herein, we synthesized, resolved, and characterized eight enantiopure isomers of yaequinolone J1 (1), yaequinolone J2 (2), 4\'-desmethoxyyaequinolone J1 (3), and 4\'-desmethoxyyaequinolone J2 (4). The key synthetic steps were extended and 34 racemic analogues modified at the 4-aryl, the N-position, and the pyran ring were designed and synthesized. All the synthesized compounds were evaluated for their anti-inflammatory activities in RAW 264.7 cells of which 13 compounds showed significant inhibition of nitric oxide (NO) production at a concentration of 0.1 μM, which was more potent than that of indomethacin. Furthermore, compounds (-)-3, (-)-4, 5h, and 6g reduced the production of IL-6 in LPS-stimulated RAW 264.7 cells at a concentration of 50 nM. A preliminary SAR indicated that 3\'-Br (5h), 4\'-NO2 (6g) on 4-phenyl and 3-bromobenzyl (7f) on the N-position were the most effective substituents. This is the first report of the anti-inflammatory yaequinolone alkaloids and the present study provided evidence for exploiting this series of highly efficacious derivatives for new anti-inflammatory agents.

The disorganized vasculatures in tumors represent a substantial challenge of intratumor nanomedicine delivery to exert the anticancer effects. Herein, we rationally designed a glutathione (GSH)-activated nitric oxide (NO) donor loaded bioinspired lipoprotein system (NO-BLP) to normalize tumor vessels and then promote the delivery efficiency of sequential albumin-bound paclitaxel nanoparticles (PAN) in tumors. NO-BLP exhibited higher tumor accumulation and deeper penetration versus the counterpart liposomal formulation (NO-Lipo) in 4T1 breast cancer tumors, thus producing notable vascular normalization efficacy and causing a 2.33-fold increase of PAN accumulation. The sequential strategy of NO-BLP plus PAN resulted in an 81.03% inhibition of tumor growth in 4T1 tumors, which was better than the NO-BLP monotherapy, PAN monotherapy, and the counterpart NO-Lipo plus PAN treatment. Therefore, the bioinspired lipoprotein of NO-BLP provides an encouraging platform to normalize tumor vessels and promote intratumor delivery of nanomedicines for effective cancer treatment.