-
1.
Improving oxidative stress resilience in plants.
Kerchev, PI, Van Breusegem, F
The Plant journal : for cell and molecular biology. 2022;(2):359-372
-
-
Free full text
-
Abstract
Originally conceived as harmful metabolic byproducts, reactive oxygen species (ROS) are now recognized as an integral part of numerous cellular programs. Thanks to their diverse physicochemical properties, compartmentalized production, and tight control exerted by the antioxidant machinery they activate signaling pathways that govern plant growth, development, and defense. Excessive ROS levels are often driven by adverse changes in environmental conditions, ultimately causing oxidative stress. The associated negative impact on cellular constituents have been a major focus of decade-long research efforts to improve the oxidative stress resilience by boosting the antioxidant machinery in model and crop species. We highlight the role of enzymatic and non-enzymatic antioxidants as integral factors of multiple signaling cascades beyond their mere function to prevent oxidative damage under adverse abiotic stress conditions.
-
2.
Role of ROS-Induced NLRP3 Inflammasome Activation in the Formation of Calcium Oxalate Nephrolithiasis.
Liu, Y, Sun, Y, Kang, J, He, Z, Liu, Q, Wu, J, Li, D, Wang, X, Tao, Z, Guan, X, et al
Frontiers in immunology. 2022;:818625
Abstract
Calcium oxalate nephrolithiasis is a common and highly recurrent disease in urology; however, its precise pathogenesis is still unknown. Recent research has shown that renal inflammatory injury as a result of the cell-crystal reaction plays a crucial role in the development of calcium oxalate kidney stones. An increasing amount of research have confirmed that inflammation mediated by the cell-crystal reaction can lead to inflammatory injury of renal cells, promote the intracellular expression of NADPH oxidase, induce extensive production of reactive oxygen species, activate NLRP3 inflammasome, discharge a great number of inflammatory factors, trigger inflammatory cascading reactions, promote the aggregation, nucleation and growth process of calcium salt crystals, and ultimately lead to the development of intrarenal crystals and even stones. The renal tubular epithelial cells (RTECs)-crystal reaction, macrophage-crystal reaction, calcifying nanoparticles, endoplasmic reticulum stress, autophagy activation, and other regulatory factors and mechanisms are involved in this process.
-
3.
Therapeutic potential of flavonoids in cancer: ROS-mediated mechanisms.
Slika, H, Mansour, H, Wehbe, N, Nasser, SA, Iratni, R, Nasrallah, G, Shaito, A, Ghaddar, T, Kobeissy, F, Eid, AH
Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie. 2022;:112442
Abstract
Cancer is a leading cause of morbidity and mortality around the globe. Reactive oxygen species (ROS) play contradicting roles in cancer incidence and progression. Antioxidants have attracted attention as emerging therapeutic agents. Among these are flavonoids, which are natural polyphenols with established anticancer and antioxidant capacities. Increasing evidence shows that flavonoids can inhibit carcinogenesis via suppressing ROS levels. Surprisingly, flavonoids can also trigger excessive oxidative stress, but this can also induce death of malignant cells. In this review, we explore the inherent characteristics that contribute to the antioxidant capacity of flavonoids, and we dissect the scenarios in which they play the contrasting role as pro-oxidants. Furthermore, we elaborate on the pathways that link flavonoid-mediated modulation of ROS to the prevention and treatment of cancer. Special attention is given to the ROS-mediated anticancer functions that (-)-epigallocatechin gallate (EGCG), hesperetin, naringenin, quercetin, luteolin, and apigenin evoke in various cancers. We also delve into the structure-function relations that make flavonoids potent antioxidants. This review provides a detailed perspective that can be utilized in future experiments or trials that aim at utilizing flavonoids or verifying their efficacy for developing new pharmacologic agents. We support the argument that flavonoids are attractive candidates for cancer therapy.
-
4.
Hydrogen peroxide-induced stress acclimation in plants.
Qureshi, MK, Gawroński, P, Munir, S, Jindal, S, Kerchev, P
Cellular and molecular life sciences : CMLS. 2022;(2):129
Abstract
Among all reactive oxygen species (ROS), hydrogen peroxide (H2O2) takes a central role in regulating plant development and responses to the environment. The diverse role of H2O2 is achieved through its compartmentalized synthesis, temporal control exerted by the antioxidant machinery, and ability to oxidize specific residues of target proteins. Here, we examine the role of H2O2 in stress acclimation beyond the well-studied transcriptional reprogramming, modulation of plant hormonal networks and long-distance signalling waves by highlighting its global impact on the transcriptional regulation and translational machinery.
-
5.
Acute cytotoxicity of mineral fibres observed by time-lapse video microscopy.
Di Giuseppe, D, Scarfì, S, Alessandrini, A, Bassi, AM, Mirata, S, Almonti, V, Ragazzini, G, Mescola, A, Filaferro, M, Avallone, R, et al
Toxicology. 2022;:153081
Abstract
Inhalation of mineral fibres is associated with the onset of an inflammatory activity in the lungs and the pleura responsible for the development of fatal malignancies. It is known that cell damage is a necessary step for triggering the inflammatory response. However, the mechanisms by which mineral fibres exert cytotoxic activity are not fully understood. In this work, the kinetics of the early cytotoxicity mechanisms of three mineral fibres (i.e., chrysotile, crocidolite and fibrous erionite) classified as carcinogenic by the International Agency for Research on Cancer, was determined for the first time in a comparative manner using time-lapse video microscopy coupled with in vitro assays. All tests were performed using the THP-1 cell line, differentiated into M0 macrophages (M0-THP-1) and exposed for short times (8 h) to 25 μg/mL aliquots of chrysotile, crocidolite and fibrous erionite. The toxic action of fibrous erionite on M0-THP-1 cells is manifested since the early steps (2 h) of the experiment while the cytotoxicity of crocidolite and chrysotile gradually increases during the time span of the experiment. Chrysotile and crocidolite prompt cell death mainly via apoptosis, while erionite exposure is also probably associated to a necrotic-like effect. The potential mechanisms underlying these different toxicity behaviours are discussed in the light of the different morphological, and chemical-physical properties of the three fibres.
-
6.
Empagliflozin reduces oxidative stress through inhibition of the novel inflammation/NHE/[Na+]c/ROS-pathway in human endothelial cells.
Uthman, L, Li, X, Baartscheer, A, Schumacher, CA, Baumgart, P, Hermanides, J, Preckel, B, Hollmann, MW, Coronel, R, Zuurbier, CJ, et al
Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie. 2022;:112515
Abstract
Inflammation causing oxidative stress in endothelial cells contributes to heart failure development. Sodium/glucose cotransporter 2 inhibitors (SGLT2i's) were shown to reduce heart failure hospitalization and oxidative stress. However, how inflammation causes oxidative stress in endothelial cells, and how SGLT2i's can reduce this is unknown. Here we hypothesized that 1) TNF-α activates the Na+/H+ exchanger (NHE) and raises cytoplasmatic Na+ ([Na+]c), 2) increased [Na+]c causes reactive oxygen species (ROS) production, and 3) empagliflozin (EMPA) reduces inflammation-induced ROS through NHE inhibition and lowering of [Na+]c in human endothelial cells. Human umbilical vein endothelial cells (HUVECs) and human coronary artery endothelial cells (HCAECs) were incubated with vehicle (V), 10 ng/ml TNF-α, 1 µM EMPA or the NHE inhibitor Cariporide (CARI, 10 µM) and NHE activity, intracellular [Na+]c and ROS were analyzed. TNF-α enhanced NHE activity in HCAECs and HUVECs by 92% (p < 0.01) and 51% (p < 0.05), respectively, and increased [Na+]c from 8.2 ± 1.6 to 11.2 ± 0.1 mM (p < 0.05) in HCAECs. Increasing [Na+]c by ouabain elevated ROS generation in both HCAECs and HUVECs. EMPA inhibited NHE activity in HCAECs and in HUVECs. EMPA concomitantly lowered [Na+]c in both cell types. In both cell types, TNF α-induced ROS was lowered by EMPA or CARI, with no further ROS lowering by EMPA in the presence of CARI, indicating EMPA attenuated ROS through NHE inhibition. In conclusion, inflammation induces oxidative stress in human endothelial cells through NHE activation causing elevations in [Na+]c, a process that is inhibited by EMPA through NHE inhibition.
-
7.
Use of Thiols in the Treatment of COVID-19: Current Evidence.
Cazzola, M, Rogliani, P, Salvi, SS, Ora, J, Matera, MG
Lung. 2021;(4):335-343
-
-
Free full text
-
Abstract
There is a possible role for oxidative stress, a state characterized by an altered balance between the production of free radicals or reactive oxygen species (ROS) and antioxidant defences, in coronavirus disease 2019 (COVID-19), the genesis of which is quite complex. Excessive oxidative stress could be responsible for the alveolar damage, thrombosis, and red blood cell dysregulation observed in COVID-19. Apparently, deficiency of glutathione (GSH), a low-molecular-weight thiol that is the most important non-enzymatic antioxidant molecule and has the potential to keep the cytokine storm in check, is a plausible explanation for the severe manifestations and death in COVID-19 patients. Thiol drugs, which are considered mucolytic, also possess potent antioxidant and anti-inflammatory properties. They exhibit antibacterial activity against a variety of medically important bacteria and may be an effective strategy against influenza virus infection. The importance of oxidative stress during COVID-19 and the various pharmacological characteristics of thiol-based drugs suggest a possible role of thiols in the treatment of COVID-19. Oral and intravenous GSH, as well as GSH precursors such as N-acetylcysteine (NAC), or drugs containing the thiol moiety (erdosteine) may represent a novel therapeutic approach to block NF-kB and address the cytokine storm syndrome and respiratory distress observed in COVID-19 pneumonia patients.
-
8.
Oxygen and reactive oxygen species-dependent regulation of plant growth and development.
Considine, MJ, Foyer, CH
Plant physiology. 2021;(1):79-92
-
-
Free full text
-
Abstract
Oxygen and reactive oxygen species (ROS) have been co-opted during evolution into the regulation of plant growth, development, and differentiation. ROS and oxidative signals arising from metabolism or phytohormone-mediated processes control almost every aspect of plant development from seed and bud dormancy, liberation of meristematic cells from the quiescent state, root and shoot growth, and architecture, to flowering and seed production. Moreover, the phytochrome and phytohormone-dependent transmissions of ROS waves are central to the systemic whole plant signaling pathways that integrate root and shoot growth. The sensing of oxygen availability through the PROTEOLYSIS 6 (PRT6) N-degron pathway functions alongside ROS production and signaling but how these pathways interact in developing organs remains poorly understood. Considerable progress has been made in our understanding of the nature of hydrogen peroxide sensors and the role of thiol-dependent signaling networks in the transmission of ROS signals. Reduction/oxidation (redox) changes in the glutathione (GSH) pool, glutaredoxins (GRXs), and thioredoxins (TRXs) are important in the control of growth mediated by phytohormone pathways. Although, it is clear that the redox states of proteins involved in plant growth and development are controlled by the NAD(P)H thioredoxin reductase (NTR)/TRX and reduced GSH/GRX systems of the cytosol, chloroplasts, mitochondria, and nucleus, we have only scratched the surface of this multilayered control and how redox-regulated processes interact with other cell signaling systems.
-
9.
Deterioration of orthodox seeds during ageing: Influencing factors, physiological alterations and the role of reactive oxygen species.
Zhang, K, Zhang, Y, Sun, J, Meng, J, Tao, J
Plant physiology and biochemistry : PPB. 2021;:475-485
Abstract
Seed viability is an important trait in agriculture which directly influences seedling emergence and crop yield. However, even when stored under optimal conditions, all seeds will eventually lose their viability. Our primary aims were to describe factors influencing seed deterioration, determine the morphological, physiological, and biochemical changes that occur during the process of seed ageing, and explore the mechanisms involved in seed deterioration. High relative humidity and high temperature are two factors that accelerate seed deterioration. As seeds age, frequently observed changes include membrane damage and the destruction of organelle structure, an increase in the loss of seed leachate, decreases of respiratory rates and ATP production, and a loss of enzymatic activity. These phenomena could be inter-related and reflect the general breakdown in cellular organization. Many processes can result in seed ageing; it is likely that oxidative damage caused by free radicals and reactive oxygen species (ROS) is primarily responsible. ROS can have vital interactions with any macromolecule of biological interest that result in damage to various cellular components caused by protein damage, lipid peroxidation, chromosomal abnormalities, and DNA lesions. Further, ROS may also cause programmed cell death by inducing the opening of mitochondrial permeability transition pores and the release of cytochrome C. Some repairs can occur in the early stages of imbibition, but repair processes fail if sufficient damage has been caused to critical functional components. As a result, a given seed will lose its viability and eventually fail to germinate in a relatively short time period.
-
10.
Atorvastatin and pravastatin stimulate nitric oxide and reactive oxygen species generation, affect mitochondrial network architecture and elevate nicotinamide N-methyltransferase level in endothelial cells.
Dymkowska, D, Wrzosek, A, Zabłocki, K
Journal of applied toxicology : JAT. 2021;(7):1076-1088
Abstract
Statins belong to the most often prescribed medications, which efficiently normalise hyperlipidaemia and prevent cardiovascular complications in obese and diabetic patients. However, beside expected therapeutic results based on the inhibition of 3-hydroxyl-3-methylglutaryl-CoA reductase, these drugs exert multiple side effects of poorly understood characteristic. In this study, side effects of pravastatin and atorvastatin on EA.hy926 endothelial cell line were investigated. It was found that both statins activate proinflammatory response, elevate nitric oxide and reactive oxygen species (ROS) generation and stimulate antioxidative response in these cells. Moreover, only slight stimulation of the mitochondrial biogenesis and significant changes in the mitochondrial network organisation have been noted. Although biochemical bases behind these effects are not clear, they may partially be explained as an elevation of AMP-activated protein kinase (AMPK) activity and an increased activating phosphorylation of sirtuin 1 (Sirt1), which were observed in statins-treated cells. In addition, both statins increased nicotinamide N-methyltransferase (NNMT) protein level that may explain a reduced fraction of methylated histone H3. Interestingly, a substantial reduction of the total level of histone H3 in cells treated with pravastatin but not atorvastatin was also observed. These results indicate a potential additional biochemical target for statins related to reduced histone H3 methylation due to increased NNMT protein level. Thus, NNMT may directly modify gene activity.