Overexpression of 2-Cys Peroxiredoxin alleviates the NaHCO3 stress-induced photoinhibition and reactive oxygen species damage of tobacco.

Plant 2-cysteine peroxiredoxin (2-Cys Prx) is a mercaptan peroxidase localized in chloroplasts and has unique catalytic properties. To explore the salt stress tolerance mechanisms of 2-Cys Prx in plants, we analyzed the effects of overexpressing the 2-CysPrx gene on the physiological and biochemical metabolic processes of tobacco under NaHCO3 stress through joint physiological and transcriptomic analysis. These parameters included growth phenotype, chlorophyll, photosynthesis, and antioxidant system. After NaHCO3 stress treatment, a total of 5360 differentially expressed genes (DEGs) were identified in 2-Cysprx overexpressed (OE) plants, and the number of DEGs was significantly lower than 14558 in wild-type (WT) plants. KEGG enrichment analysis showed that DEGs were mainly enriched in photosynthetic pathways, photosynthetic antenna proteins, and porphyrin and chlorophyll metabolism. Overexpressing 2-CysPrx significantly reduced the growth inhibition of tobacco induced by NaHCO3 stress, alleviating the down-regulation of the DEGs related to chlorophyll synthesis, photosynthetic electron transport and the Calvin cycle and the up-regulation of those related to chlorophyll degradation. In addition, it also interacted with other redox systems such as thioredoxins (Trxs) and the NADPH-dependent Trx reductase C (NTRC), and mediated the positive regulation of the activities of antioxidant enzymes such as peroxidase (POD) and catalase (CAT) and the expression of related genes, thereby reducing the accumulation of superoxide anion (O2·-), hydrogen peroxide (H2O2) and malondialdehyde (MDA). In conclusion, 2-CysPrx overexpression could alleviate the NaHCO3 stress-induced photoinhibition and oxidative damage by regulating chlorophyll metabolism, promoting photosynthesis and participating in the regulation of antioxidant enzymes, and thus improve the ability of plants to resist salt stress damage.

Hollow mesoporous organosilica nanoparticles reduced graphene oxide based nanosystem for multimodal image-guided photothermal/photodynamic/chemo combinational therapy triggered by near-infrared.

Developing a nanosystem that can perform multimodal imaging-guided combination therapy is highly desirable but challenging. In this study, we introduced multifunctional nanoparticles (NPs) consisting of graphene oxide-grafted hollow mesoporous organosilica loaded with the drug doxorubicin (DOX) and photosensitizers tetraphenylporphyrin (TPP). These NPs were encapsulated by thermosensitive liposomes that release their contents once the temperature exceeds a certain threshold. Metal oxide NPs grown on the graphene oxide (GO) surface served multiple roles, including enhancing photothermal efficiency, acting as contrast agents to improve magnetic resonance imaging, increasing the sensitivity and specificity of photoacoustic imaging, and catalysing hydrogen peroxide for the generation of reactive oxygen species (ROS). When locally injected, the HMONs-rNGO@Fe3 O4 /MnOx@FA/DOX/TPP NPs effectively enriched in subcutaneous Hela cell tumour of mice. The photothermal/photodynamic/chemo combination therapy triggered by near-infrared (NIR) successfully suppressed the tumour without noticeable side effects. This study presented a unique approach to develop multimodal imaging-guided combination therapy for cancer.

Trx CDSP32-overexpressing tobacco plants improves cadmium tolerance by modulating antioxidant mechanism.

The effects of overexpression of the thioredoxin-like protein CDSP32 (Trx CDSP32) on reactive oxygen species (ROS) metabolism in tobacco leaves exposed to cadmium (Cd) were studied by combining physiological measures and proteomics technology. Thus, the number of differentially expressed proteins (DEPs) in plants overexpressing the Trx CDSP32 gene in tobacco (OE) was observed to be evidently lower than that in wild-type (WT) tobacco under Cd exposure, especially the number of down-regulated DEPs. Cd exposure induced disordered ROS metabolism in tobacco leaves. Although Cd exposure inhibited the activities of superoxide dismutase (SOD), catalase (CAT), and l-ascorbate peroxidase (APX) and the expression of proteins related to the thioredoxin-peroxiredoxin (Trx-Prx) pathway, the increase in the activities of peroxidase (POD), monodehydroascorbate reductase (MDHAR), dehydroascorbate reductase (DHAR), glutathione reductase (GR), glutathione peroxidase (GPX), and glutathione S-transferase (GST) and their protein expression levels played an important role in the physiological response to Cd exposure. Notably, Trx CDSP32 was observed to alleviate the decrease in the expression and activities of SOD and CAT caused by Cd exposure and enhance the function of POD. Trx CDSP32 was observed to increase the H2O2 scavenging capacity of the ascorbic acid-glutathione (AsA-GSH) cycle and Trx-Prx pathway under Cd exposure, and it can especially regulate 2-Cys peroxiredoxin (2-Cys Prx) protein expression and thioredoxin peroxidase (TPX) activity. Thus, overexpression of the Trx CDSP32 gene can alleviate the oxidative damage that occurs in tobacco leaves under Cd exposure by modulating antioxidant defense systems.

Exogenous melatonin alleviates NO2 damage in tobacco leaves by promoting antioxidant defense, modulating redox homeostasis, and signal transduction.

Nitrogen dioxide (NO2) is a common outdoor air pollutant, which has adverse effects on the environment and human health. Herein, NO2 inhibited photosynthesis and antioxidant capacity in plants. Melatonin (Mel) is a neurohormone found in the pineal gland. Exogenous Mel alleviated chlorophyll degradation and increased the expression of key proteins and genes in the process of chlorophyll synthesis in tobacco leaves exposed to NO2. Additionally, the activities of photosystem II (PSII) and photosystem I (PSI) were enhanced. PSII and PSI reaction center proteins and genes were upregulated. Mel pre-treatment enhanced enzyme activities and expression of proteins related to the ascorbic acid-glutathione cycle and thioredoxin-peroxiredoxin pathway in leaves exposed to NO2, thus regulating their redox balance. Furthermore, exogenous Mel mediated the polyamine synthesis pathway and increased the expression of the key enzyme proteins SAMS1, SAMS2, and SAMS3 in the polyamine synthesis pathway in leaves under NO2 stress. Mel regulated ABA signal transduction and calmodulin binding transcription factors CAMTA12 and NtCaM calmodulin NtCaM2 in Ca2+ signal transduction. Collectively, these results elucidate that Mel can alleviate high-concentration NO2, thus suitable for agricultural application.

The phytotoxicity of exposure to two polybrominated diphenyl ethers (BDE47 and BDE209) on photosynthesis and the response of the hormone signaling and ROS scavenging system in tobacco leaves.

To reveal the response and adaptative mechanism of plants to the organic pollutants PBDEs, physiological and transcriptomic techniques were used to study the effects of exposure to BDE47 and BDE209 on tobacco (Nicotiana tabacum L.) plant growth, physiological function and response of key genes. Exposure to both BDE47 and BDE209 inhibited the growth of tobacco plants. The number of down-regulated DEGs following exposure to BDE47 was significantly higher than that following exposure to BDE209. Enrichment analysis using the KEGG showed that BDE47 and BDE209 primarily affected tobacco leaf photosynthesis-antenna proteins, photosynthesis, plant hormone signal transduction and α-linolenic acid metabolism. BDE47 primarily inhibits the synthesis of Chl a, and BDE209 has a more significant impact on Chl b. Most photosynthesis-related DEGs were concentrated in PSII and PSI; the number of down-regulated DEGs in PSI was significantly higher than that in PSII, and the range in which the PSI activity was reduced was also higher than that of PSII, i.e., PSII and PSI (particularly PSI) were sensitive to the effects of exposure to BDE47 and BDE209 on photosynthesis. The increase of the ratio of regulatory energy dissipation played an important protective role in alleviating the photoinhibition of PSII. Exposure to BDE47 and BDE209 can lead to the accumulation of ROS in tobacco leaves, but correspondingly, the activities of antioxidant enzymes SOD, POD, CAT, APX and GPX and the up-regulated expression of their coding genes play an important role in preventing excessive oxidative damage. Exposure to BDE47 and BDE209 promoted the up-regulation of gene expression related to Pro synthesis. In particular, the Pro synthetic process of the Orn pathway was promoted. Exposure to BDE47 and BDE209 induced the up-regulated expression of genes related to the synthesis of ABA and JA, promoted the synthesis of ABA and JA, and activated ABA and JA signal transduction pathways. In conclusion, both BDE47 and BDE209 inhibit the synthesis of chlorophyll and hinder the process of light energy capture and electron transfer in tobacco leaves. BDE47 was more toxic than BDE209. However, tobacco leaves can also adapt to BDE47 and BDE209 by regulating the antioxidant system, accumulating Pro and initiating the hormone signal transduction process. The results of this study provide a theoretical basis for the phytotoxicity mechanism of PBDEs.

New Insights Into Cancer Chronotherapies.

Circadian clocks participate in the coordination of various metabolic and biological activities to maintain homeostasis. Disturbances in the circadian rhythm and cancers are closely related. Circadian clock genes are differentially expressed in many tumors, and accelerate the development and progression of tumors. In addition, tumor tissues exert varying biological activities compared to normal tissues due to resetting of altered rhythms. Thus, chronotherapeutics used for cancer treatment should exploit the timing of circadian rhythms to achieve higher efficacy and mild toxicity. Due to interpatient differences in circadian functions, our findings advocate an individualized precision approach to chronotherapy. Herein, we review the specific association between circadian clocks and cancers. In addition, we focus on chronotherapies in cancers and personalized biomarkers for the development of precision chronotherapy. The understanding of circadian clocks in cancer will provide a rationale for more effective clinical treatment of tumors.

Thioredoxin-like protein CDSP32 alleviates Cd-induced photosynthetic inhibition in tobacco leaves by regulating cyclic electron flow and excess energy dissipation.

Thioredoxin-like protein CDSP32 (Trx CDSP32), a thioredoxin-like (Trx-like) protein located in the chloroplast, can regulate photosynthesis and the redox state of plants under stress. In order to examine the role of Trx CDSP32 in the photosynthetic apparatus of plants exposed to cadmium (Cd), the effects of Trx CDSP32 on photosynthetic function and photoprotection in tobacco leaves under Cd exposure were studied using a proteomics approach with wild-type (WT) and Trx CDSP32 overexpression (OE) tobacco plants. Cd exposure reduced stomatal conductance, blocked PSII photosynthetic electron transport, and inhibited carbon assimilation. Increased water use efficiency (WUE), cyclic electron flow (CEF) of the proton gradient regulation 5 pathway (PGR5-CEF), and regulated energy dissipation [Y(NPQ)] are important mechanisms of Cd adaptation. However, CEF of the NAD(P)H dehydrogenase pathway (NDH-CEF) was inhibited by Cd exposure. Relative to control conditions, the expression levels of violaxanthin de-epoxidase (VDE) and photosystem II 22 kDa protein (PsbS) in OE leaves were significantly increased under Cd exposure, but those in WT leaves did not change significantly. Moreover, the expression of zeaxanthin epoxidase (ZE) under Cd exposure was significantly higher than that in WT leaves. Thus, Trx CDSP32 increased Y(NPQ) and alleviated PSII photoinhibition under Cd exposure. Trx CDSP32 not only increased PGR5-like protein 1A and 1B expression, but also alleviated the down-regulation of NAD(P)H-quinone oxidoreductase subunits induced by Cd exposure. Thus, Trx CDSP32 promotes CEF in Cd-exposed tobacco leaves. Thus, Trx CDSP32 alleviates the Cd-induced photoinhibition in tobacco leaves by regulating two photoprotective mechanisms: CEF and xanthophyll cycle-dependent energy dissipation.