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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.
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Pre-diagnostic derivatives of reactive oxygen metabolites and the occurrence of lung, colorectal, breast and prostate cancer: An individual participant data meta-analysis of two large population-based studies.
Gào, X, Wilsgaard, T, Jansen, EH, Holleczek, B, Zhang, Y, Xuan, Y, Anusruti, A, Brenner, H, Schöttker, B
International journal of cancer. 2019;(1):49-57
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Abstract
Oxidative stress may be involved in carcinogenesis and biomarkers of oxidative stress like derivatives of reactive oxygen metabolites (d-ROM) may be useful for cancer prediction. However, no previous study assessed the association of pre-diagnostic d-ROM measurements with cancer incidence. We measured serum d-ROM levels in a cohort sample of n = 4,345 participants of the German ESTHER study and in a case-cohort sample of the Norwegian Tromsø study (cancer cases: n = 941; subcohort: n = 1,000). Moreover, d-ROM was repeatedly measured at follow-ups of both studies. Hazard ratios (HRs) and 95% confidence intervals (95% CIs) were derived by (weighted) multivariable-adjusted Cox regression with time-dependent modeling of d-ROM levels for incident lung, colorectal, breast and prostate cancer. Individual study results were pooled by random effects meta-analysis. The HRs (95% CI) for comparison of top and bottom d-ROM tertile were statistically significant for lung (1.90 [1.25-2.89]), colorectal (1.70 [1.15-2.51]) and breast cancer incidence (1.45 [1.01-2.09]) but not for prostate cancer incidence (1.20 [0.84-1.72]). In conclusion, this individual participant data meta-analysis of two large population-based cohort studies with repeated d-ROM measurements yielded evidence for an involvement of high oxidative stress in carcinogenesis. Given the observed associations of pre-diagnostic d-ROM measurements with lung, colorectal and breast cancer incidence, subjects with increased serum d-ROM levels should be recommended to reduce these levels by lifestyle changes including smoking cessation, a healthy diet and an increase in physical activity.
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2-D08 as a SUMOylation inhibitor induced ROS accumulation mediates apoptosis of acute myeloid leukemia cells possibly through the deSUMOylation of NOX2.
Zhou, P, Chen, X, Li, M, Tan, J, Zhang, Y, Yuan, W, Zhou, J, Wang, G
Biochemical and biophysical research communications. 2019;(4):1063-1069
Abstract
Acute myeloid leukemia (AML) is a heterogeneous clonal hematopoietic malignancy with poor survival and frequent relapse. Recently, a posttranslational modification of proteins with small ubiquitin-like modifiers (SUMO) has been notably implicated in a wide spectrum of diseases, especially cancers. Ubc9, as the sole E2-conjugating enzyme in SUMOylation cascade, particularly has been associated with adverse clinical outcomes. 2-D08, a small molecular agent, functions by blocking the transfer of SUMO from the Ubc9 thioester to SUMO substrates without any effects on other individual steps in this process. However, both the effects and mechanisms of 2-D08 on AML cells are still unknown. In this study, we found that 2-D08 significantly suppressed cell viability and colony formation ability. Additionally, it induced mitochondrial-mediated apoptosis with dramatic accumulation of the reactive oxygen species (ROS), which could be almost completely rescued by the ROS scavenger N-acetylcysteine (NAC). Furthermore, we confirmed that the fatal accumulation of ROS was due to its aberrant generation instead of defective scavenging. In summary, our results suggest that 2-D08, as a specific SUMOylation inhibitor, induces ROS accumulation-mediated intrinsic apoptosis of AML cells possibly through deSUMOylation of NOX2. Therefore, 2-D08 might be a promising therapeutic agent for the treatment of AML in the future.
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Individual Amino Acid Supplementation Can Improve Energy Metabolism and Decrease ROS Production in Neuronal Cells Overexpressing Alpha-Synuclein.
Delic, V, Griffin, JWD, Zivkovic, S, Zhang, Y, Phan, TA, Gong, H, Chaput, D, Reynes, C, Dinh, VB, Cruz, J, et al
Neuromolecular medicine. 2017;(2-3):322-344
Abstract
Parkinson's disease (PD) is a neurodegenerative disorder characterized by alpha-synuclein accumulation and loss of dopaminergic neurons in the substantia nigra (SN) region of the brain. Increased levels of alpha-synuclein have been shown to result in loss of mitochondrial electron transport chain complex I activity leading to increased reactive oxygen species (ROS) production. WT alpha-synuclein was stably overexpressed in human BE(2)-M17 neuroblastoma cells resulting in increased levels of an alpha-synuclein multimer, but no increase in alpha-synuclein monomer levels. Oxygen consumption was decreased by alpha-synuclein overexpression, but ATP levels did not decrease and ROS levels did not increase. Treatment with ferrous sulfate, a ROS generator, resulted in decreased oxygen consumption in both control and alpha-synuclein overexpressing cells. However, this treatment only decreased ATP levels and increased ROS production in the cells overexpressing alpha-synuclein. Similarly, paraquat, another ROS generator, decreased ATP levels in the alpha-synuclein overexpressing cells, but not in the control cells, further demonstrating how alpha-synuclein sensitized the cells to oxidative insult. Proteomic analysis yielded molecular insights into the cellular adaptations to alpha-synuclein overexpression, such as the increased abundance of many mitochondrial proteins. Many amino acids and citric acid cycle intermediates and their ester forms were individually supplemented to the cells with L-serine, L-proline, L-aspartate, or L-glutamine decreasing ROS production in oxidatively stressed alpha-synuclein overexpressing cells, while diethyl oxaloacetate or L-valine supplementation increased ATP levels. These results suggest that dietary supplementation with individual metabolites could yield bioenergetic improvements in PD patients to delay loss of dopaminergic neurons.
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Reactive Oxygen Species Regulate T Cell Immune Response in the Tumor Microenvironment.
Chen, X, Song, M, Zhang, B, Zhang, Y
Oxidative medicine and cellular longevity. 2016;:1580967
Abstract
Reactive oxygen species (ROS) produced by cellular metabolism play an important role as signaling messengers in immune system. ROS elevated in the tumor microenvironment are associated with tumor-induced immunosuppression. T cell-based therapy has been recently approved to be effective for cancer treatment. However, T cells often become dysfunctional after reaching the tumor site. It has been reported that ROS participate extensively in T cells activation, apoptosis, and hyporesponsiveness. The sensitivity of T cells to ROS varies among different subsets. ROS can be regulated by cytokines, amino acid metabolism, and enzymatic activity. Immunosuppressive cells accumulate in the tumor microenvironment and induce apoptosis and functional suppression of T cells by producing ROS. Thus, modulating the level of ROS may be important to prolong survival of T cells and enhance their antitumor function. Combining T cell-based therapy with antioxidant treatment such as administration of ROS scavenger should be considered as a promising strategy in cancer treatment, aiming to improve antitumor T cells immunity.
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Piperlongumine Blocks JAK2-STAT3 to Inhibit Collagen-Induced Platelet Reactivity Independent of Reactive Oxygen Species.
Yuan, H, Houck, KL, Tian, Y, Bharadwaj, U, Hull, K, Zhou, Z, Zhu, M, Wu, X, Tweardy, DJ, Romo, D, et al
PloS one. 2015;(12):e0143964
Abstract
BACKGROUND Piperlongumine (PL) is a compound isolated from the piper longum plant. It possesses anti-cancer activities through blocking the transcription factor STAT3 and by inducing reactive oxygen species (ROS) in cancer, but not normal cells. It also inhibits platelet aggregation induced by collagen, but the underlying mechanism is not known. OBJECTIVE We conducted in vitro experiments to test the hypothesis that PL regulates a non-transcriptional activity of STAT3 to specifically reduce the reactivity of human platelets to collagen. RESULTS PL dose-dependently blocked collagen-induced platelet aggregation, calcium influx, CD62p expression and thrombus formation on collagen with a maximal inhibition at 100 μM. It reduced platelet microvesiculation induced by collagen. PL blocked the activation of JAK2 and STAT3 in collagen-stimulated platelets. This inhibitory effect was significantly reduced in platelets pretreated with a STAT3 inhibitor. Although PL induced ROS production in platelets; quenching ROS using excessive reducing agents: 20 μM GSH and 0.5 mM L-Cysteine, did not block the inhibitory effects. The NADPH oxidase inhibitor Apocynin also had no effect. CONCLUSIONS PL inhibited collagen-induced platelet reactivity by targeting the JAK2-STAT3 pathway. We also provide experimental evidence that PL and collagen induce different oxidants that have differential effects on platelets. Studying these differential effects may uncover new mechanisms of regulating platelet functions by oxidants in redox signals.
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Redox proteins and radiotherapy.
Zhang, Y, Martin, SG
Clinical oncology (Royal College of Radiologists (Great Britain)). 2014;(5):289-300
Abstract
Although conventional radiotherapy can directly damage DNA and other organic molecules within cells, most of the damage and the cytotoxicity of such ionising radiation, comes from the production of ions and free radicals produced via interactions with water. This 'indirect effect', a form of oxidative stress, can be modulated by a variety of systems within cells that are in place to, in normal situations, maintain homeostasis and redox balance. If cancer cells express high levels of antioxidant redox proteins, they may be more resistant to radiation and so targeting such systems may be a profitable strategy to increase therapeutic efficacy of conventional radiotherapy. An overview, with exemplars, of the main systems regulating redox homeostasis is supplied and discussed in relation to their use as prognostic and predictive biomarkers, and how targeting such proteins and systems may increase radiosensitivity and, potentially, improve the radiotherapeutic response.