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1.
Mechanism of freeze-thaw injury and recovery: A cool retrospective and warming up to new ideas.
Arora, R
Plant science : an international journal of experimental plant biology. 2018;:301-313
Abstract
Understanding cellular mechanism(s) of freeze-thaw injury (FTI) is key to the efforts for improving plant freeze-tolerance by cultural methods or molecular/genetic approaches. However, not much work has been done in the last 25+ years to advance our understanding of the nature and cellular loci of FTI. Currently, two FTI lesions are predominantly implicated: 1) structural and functional perturbations in plasma membrane; 2) ROS-induced oxidative damage. While both have stood the test of time, many questions remain unresolved and other potentially significant lesions need to be investigated. Additionally, molecular mechanism of post-thaw recovery (PTR), a critical component of frost-survival, has not been well investigated. Mechanistic understanding of repair after reversible injury could expand the options for strategies to improve frost-hardiness. In this review, without claiming to be exhaustive, I have attempted to synthesize major discoveries from last several decades on the mechanisms of FTI and the relatively little research conducted thus far on PTR mechanisms. It is followed by proposing of hypotheses for mechanism(s) for irreversible FTI or PTR involving cytosolic calcium and ROS signaling. Perspective is presented on some unresolved questions and research on new ideas to fill the knowledge gaps and advance the field.
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2.
Reduction of oxidative stress a key for enhanced postoperative recovery with fewer complications in esophageal surgery patients: Randomized control trial to investigate therapeutic impact of anesthesia management and usefulness of simple blood test for prediction of high-risk patients.
Tsuchiya, M, Shiomoto, K, Mizutani, K, Fujioka, K, Suehiro, K, Yamada, T, Sato, EF, Nishikawa, K
Medicine. 2018;(47):e12845
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Abstract
BACKGROUND Oxidative stress may be an integral determinant of surgical stress severity. We examined whether the preoperative level of derivatives of reactive oxygen metabolites (d-ROMs), an oxidative stress biomarker based on total hydroperoxides in circulating blood, is predictive of increased risk of delayed recovery and complications after surgery, as well as the effects of anesthesia management on postoperative recovery in light of oxidative stress. METHODS Patients (American Society of Anesthesiologists physical status I-II) scheduled for a radical esophagectomy (n = 186) were randomly selected to receive inhalational sevoflurane (n = 94) or intravenous propofol (n = 92) anesthesia. Preoperative blood d-ROMs level, as well as pre-and postoperative plasma ferric-reducing ability, were analyzed to assess oxidative stress, with white blood cell (WBC) count, C-reactive protein (CRP) level, incidence of severe postoperative complications, and postoperative recovery process within 30 days after surgery also examined in a double-blind fashion. RESULTS Postoperative normalization of WBC and CRP was extended in patients with elevated preoperative d-ROMs [WBC versus d-ROMs: correlation coefficient (r) = 0.58 P < .001; CRP versus d-ROMs: r = 0.46 P < .001]. Receiver operating characteristics analysis of d-ROMs in relation to incidence of severe postoperative complications revealed an optimum d-ROMs threshold value of 410 UCarr and that patients with ≥410 UCarr had a greater risk of complications as compared to those with lower values (odds ratio = 4.7). Plasma ferric-reducing ability was decreased by 61 ± 185 mmol·l (P < .001) after surgery, demonstrating development of surgery-related oxidative stress, the magnitude of which was positively correlated with preoperative d-ROMs level (r = 0.16, P = .043). A comparison of the 2 anesthesia management protocols showed that patients who received propofol, an antioxidant anesthetic, had no postoperative decrease in ferric-reducing ability, lower incidence of severe postoperative complications (7 of 92 versus 18 of 94, P = .030, odds ratio = 0.35), and faster uneventful recovery time (WBC normalization days 7.1 ± 5.2 versus 13.6 ± 10.2, P < .001) as compared to those who received sevoflurane. CONCLUSIONS Elevated preoperative blood d-ROMs predicts greater intraoperative oxidative stress and increased postoperative complications with prolonged recovery, thus is useful for identifying high-risk patients for delayed and complicated surgical recovery. Reduction of oxidative stress is vital for enhanced recovery, with control by antioxidants such as propofol a possible solution.
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Cytotoxic Drugs Activate KSHV Lytic Cycle in Latently Infected PEL Cells by Inducing a Moderate ROS Increase Controlled by HSF1, NRF2 and p62/SQSTM1.
Granato, M, Gilardini Montani, MS, Angiolillo, C, D'Orazi, G, Faggioni, A, Cirone, M
Viruses. 2018;(1)
Abstract
Previous studies have indicated that cytotoxic treatments may induce or not activate viral lytic cycle activation in cancer cells latently infected by Kaposi's sarcoma-associated herpesvirus (KSHV). To investigate the molecular mechanisms responsible for such an effect, we compared two cytotoxic treatments able to induce the viral lytic cycle, named 12-O-tetradecanoylphorbol 13-acetate (TPA) (T) in combination with sodium butyrate (B) and bortezomib (BZ), with two cytotoxic treatments that did not activate this process, named metformin (MET) and quercetin (Q). Our results indicated that TB and bortezomib increased levels of oxygen reactive species (ROS) while metformin and quercetin reduced them. The finding that N-acetylcysteine (NAC), a reactive oxigen species (ROS) scavenger, counteracted K-bZIP expression induced by TB or bortezomib, confirmed that an ROS increase played a role in KSHV lytic cycle activation. Moreover, we found that TB and bortezomib up-regulated p62/Sequestosome1(p62/SQSTM1) protein, while metformin and quercetin down-regulated it. p62/SQSTM1 silencing or the inhibition of NF-E2-related factor 2 (NRF2) or Heat Shock Factor 1 (HSF1), that mediate p62/SQSTM1 transcription, also reduced KSHV lytic antigen expression induced by TB or bortezomib. Interestingly, such combination treatments further increased intracellular ROS and cytotoxicity induced by the single TB or bortezomib treatment, suggesting that NRF2, HSF1 and p62/SQSTM1 keep the ROS level under control, allowing primary effusion lymphoma (PEL) cells to continue to survive and KSHV to replicate.
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Alternative hypotheses related to Alzheimer's disease.
Cubinkova, V, Valachova, B, Uhrinova, I, Brezovakova, V, Smolek, T, Jadhav, S, Zilka, N
Bratislavske lekarske listy. 2018;(4):210-216
Abstract
Alzheimer's disease represents the most common form of dementia and belongs to the group of neurodegenerative disorders characterized by progressive loss of neurons in the central nervous system. In the pathogenesis of Alzheimer's disease several etiologic and pathogenic factors exist, which lead to the dysfunction of neurotransmitter systems and consequent cognitive decline. Last three decades have delivered a crucial progress leading to better understanding of Alzheimer's disease, however, the exact mechanisms of pathology remain unclear. In this review, we summarize some hypotheses such as amyloid and tau hypotheses, inflammatory processes, prion-like hypothesis, the hypothesis of oxidative stress, vascular and cholesterol hypothesis, the hypothesis of metal accumulation in the brain, cell cycle hypothesis, the hypothesis of impaired insulin signalization and another, which were proposed to explain the pathogenesis of this severe disorder (Ref. 115).
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Reactive oxygen species and redox regulation in mesophyll and bundle sheath cells of C4 plants.
Turkan, I, Uzilday, B, Dietz, KJ, Bräutigam, A, Ozgur, R
Journal of experimental botany. 2018;(14):3321-3331
Abstract
Redox regulation, antioxidant defence, and reactive oxygen species (ROS) signalling are critical in performing and tuning metabolic activities. However, our concepts have mostly been developed for C3 plants since Arabidopsis thaliana has been the major model for research. Efforts to convert C3 plants to C4 to increase yield (such as IRRI's C4 Rice Project) entail a better understanding of these processes in C4 plants. Various photosynthetic enzymes that take part in light reactions and carbon reactions are regulated via redox components, such as thioredoxins as redox transmitters and peroxiredoxins. Hence, understanding redox regulation in the mesophyll and bundle sheath chloroplasts of C4 plants is of paramount importance: it appears impossible to utilize efficient C4 photosynthesis without understanding its exact redox needs and the regulation mechanisms used during light reactions. In this review, we discuss current knowledge on redox regulation in C3 and C4 plants, with special emphasis on the mesophyll and bundle sheath differences that are found in C4. In these two cell types in C4 plants, linear and cyclic electron transport in the chloroplasts operate differentially when compared to C3 chloroplasts, changing the redox needs of the cell. Therefore, our focus is on photosynthetic light reactions, ROS production dynamics, antioxidant defence, and thiol-based redox regulation, with the aim of providing an overview of our current knowledge.
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Human dihydrolipoamide dehydrogenase (E3) deficiency: Novel insights into the structural basis and molecular pathomechanism.
Ambrus, A, Adam-Vizi, V
Neurochemistry international. 2018;:5-14
Abstract
This review summarizes our present view on the molecular pathogenesis of human (h) E3-deficiency caused by a variety of genetic alterations with a special emphasis on the moonlighting biochemical phenomena related to the affected (dihydro)lipoamide dehydrogenase (LADH, E3, gene: dld), in particular the generation of reactive oxygen species (ROS). E3-deficiency is a rare autosomal recessive genetic disorder frequently presenting with a neonatal onset and premature death; the highest carrier rate of a single pathogenic dld mutation (1:94-1:110) was found among Ashkenazi Jews. Patients usually die during acute episodes that generally involve severe metabolic decompensation and lactic acidosis leading to neurological, cardiological, and/or hepatological manifestations. The disease owes its severity to the fact that LADH is the common E3 subunit of the alpha-ketoglutarate (KGDHc), pyruvate (PDHc), and branched-chain α-keto acid dehydrogenase complexes and is also part of the glycine cleavage system, hence the malfunctioning of LADH simultaneously incapacitates several central metabolic pathways. Nevertheless, the clinical pictures are usually not unequivocally portrayed through the loss of LADH activities and imply auxiliary mechanisms that exacerbate the symptoms and outcomes of this disorder. Enhanced ROS generation by disease-causing hE3 variants as well as by the E1-E2 subcomplex of the hKGDHc likely contributes to selected pathogeneses of E3-deficiency, which could be targeted by specific drugs or antioxidants; lipoic acid was demonstrated to be a potent inhibitor of ROS generation by hE3 in vitro. Flavin supplementation might prove to be beneficial for those mutations triggering FAD loss in the hE3 component. Selected pathogenic hE3 variants lose their affinity for the E2 component of the hPDHc, a mechanism which warrants scrutiny also for other E3-haboring complexes.
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Differential antibacterial control by neutrophil subsets.
Leliefeld, PHC, Pillay, J, Vrisekoop, N, Heeres, M, Tak, T, Kox, M, Rooijakkers, SHM, Kuijpers, TW, Pickkers, P, Leenen, LPH, et al
Blood advances. 2018;(11):1344-1355
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Abstract
Neutrophils comprise a heterogeneous population of cells essential for bacterial eradication, and defects in neutrophil function are associated with increased susceptibility to infection. In this study, neutrophils from healthy controls were shown to prevent bacterial proliferation for at least 48 hours when cocultured with methicillin-resistant Staphylococcus aureus (MRSA) in tissue-like scaffolds by establishing a bacteriostatic environment inside their phagolysosome. This intracellular bacterial containment is independent of reactive oxygen species because neutrophils that lack a functional nicotinamide adenine dinucleotide phosphate-oxidase complex displayed no defect in intracellular bacterial containment, whereas killing of the pathogen was impaired. During acute inflammation, a subset of CD16bright/CD62Ldim hypersegmented neutrophils displayed normal phagocytosis associated with a remarkably poor capacity to contain bacteria intracellularly. Conversely, CD16dim-banded neutrophils were the only neutrophil subset that adequately contained MRSA. These findings demonstrate a clear neutrophil heterogeneity in their antimicrobial capacity and the appearance of neutrophil subsets with a clear differentiation in functionality during acute inflammation. Furthermore, this study provides an evolutionary basis for the rapid release of banded neutrophils into the circulation during acute inflammation.
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Plasmodesmal regulation during plant-pathogen interactions.
Cheval, C, Faulkner, C
The New phytologist. 2018;(1):62-67
Abstract
Contents Summary 62 I. Introduction 62 II. Plasmodesmal regulation is an innate defence response 63 III. Reactive oxygen species regulate plasmodesmal function 63 IV. Plasmodesmal regulation by and of defence-associated small molecules 64 V. Plasmodesmata facilitate systemic defence signalling 64 VI. Virulent pathogens exploit plasmodesmata 66 VII. Outlook 66 Acknowledgements 66 References 66 SUMMARY Plasmodesmata (PD) are plasma membrane-lined pores that connect neighbouring plant cells, bridging the cell wall and establishing cytoplasmic and membrane continuity between cells. PD are dynamic structures regulated by callose deposition in a variety of stress and developmental contexts. This process crudely controls the aperture of the pore and thus the flux of molecules between cells. During pathogen infection, plant cells initiate a range of immune responses and it was recently identified that, following perception of fungal and bacterial pathogens, plant cells initially close their PD. Systemic defence responses depend on the spread of signals between cells, raising questions about whether PD are in different functional states during different immune responses. It is well established that viral pathogens exploit PD to spread between cells, but it has more recently been identified that protein effectors secreted by fungal pathogens can spread between host cells via PD. It is possible that many classes of pathogens specifically target PD to aid infection, which would infer antagonistic regulation of PD by host and pathogen. How PD regulation benefits both host immune responses and pathogen infection is an important question and demands that we examine the multicellular nature of plant-pathogen interactions.
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Exogenous pentraxin-3 inhibits the reactive oxygen species-mitochondrial and apoptosis pathway in acute kidney injury.
Lee, HH, Kim, SY, Na, JC, Yoon, YE, Han, WK
PloS one. 2018;(4):e0195758
Abstract
Pentraxin-3 (PTX3) is a long-form member of the pentraxin family of proteins that has been studied in inflammatory diseases and in various organs. We found that PTX3 protects kidney cells during ischemia and proinflammatory acute kidney injury. The aim of this study was to develop an in vitro experimental model of acute kidney injury and to analyze the protective mechanism of exogenous recombinant PTX3. In this study, cells of the HK-2 renal tubular cell line were treated with a calcium ionophore (A23187), which induced injury by increasing intracellular calcium concentrations and inducing calpain activity and the generation of reactive oxygen species. Exposure of cells to PTX3 significantly attenuated these effects. In addition, the activity of caspase-3 and PARP-1 were decreased in ischemic cells exposed to exogenous recombinant PTX3. PTX3 stabilized the mitochondrial membrane potential and suppressed apoptosis, resulting in the protection of renal tubular cells from ischemic injury.
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Mechanical wounding promotes local and long distance response in the halophyte Cakile maritima through the involvement of the ROS and RNS metabolism.
Houmani, H, Rodríguez-Ruiz, M, Palma, JM, Corpas, FJ
Nitric oxide : biology and chemistry. 2018;:93-101
Abstract
Mechanical wounding in plants, which are capable of generating defense responses possibly associated with nitro-oxidative stress, can be caused by (a)biotic factors such as rain, wind, herbivores and insects. Sea rocket (Cakile maritima L.), a halophyte plant belonging to the mustard family Brassicaceae, is commonly found on sandy coasts throughout Europe. Using 7-day-old Cakile maritima L. seedlings, mechanical wounding was induced in hypocotyls by pinching with a striped-tip forceps; after 3 h, several biochemical parameters were analyzed in both the damaged and unwounded organs (green cotyledons and roots). We thus determined NO production, H2O2 content, lipid oxidation as well as protein nitration patterns; we also identified several antioxidant enzymes including catalase, superoxide dismutase (SOD) isozymes, peroxidases, ascorbate-glutathione cycle enzymes and NADP-dehydrogenases. All these parameters were differentially modulated in the damaged (hypocotyls) and unwounded organs, which clearly indicated an induction of CuZnSOD V in the three organs, an increase in protein nitration in green cotyledons and an induction of NADP-isocitrate dehydrogenase activity in roots. On the whole, our results indicate that the wounding of hypocotyls, which showed an active ROS metabolism and oxidative stress, causes long-distance signals that also trigger responses in unwounded tissues with a more active RNS metabolism. These data therefore confirm the existence of local and long-distance responses which counteract negative effects and provide appropriate responses, enabling the wounded seedlings to survive.