Myotubularins, PtdIns5P, and ROS in ABA-mediated stomatal movements in dehydrated Arabidopsis seedlings

2018 ◽  
Vol 45 (2) ◽  
pp. 259 ◽  
Author(s):  
Akanksha Nagpal ◽  
Ammar Hassan ◽  
Ivan Ndamukong ◽  
Zoya Avramova ◽  
František Baluška
Keyword(s):  
Cell Signalling ◽  
Membrane Dynamics ◽  
Dehydration Stress ◽  
Oxygen Species ◽  
Secondary Messenger ◽  
Signalling Molecule ◽  
Ros Accumulation ◽  
Evolutionarily Conserved ◽  
Stomatal Movements

Myotubularins (MTMs) are lipid phosphoinositide 3-phosphate phosphatases and the product of their enzyme activity – phosphoinositide 5-phosphate (PtdIns5P) – functions as a signalling molecule in pathways involved in membrane dynamics and cell signalling. Two Arabidopsis genes, AtMTM1 and AtMTM2, encode enzymatically active phosphatases but although AtMTM1 deficiency results in increased tolerance to dehydration stress and a decrease in cellular PtdIns5P, the role of AtMTM2 is less clear, as it does not contribute to the PtdIns5P pool upon dehydration stress. Here we analysed the involvement of AtMTM1, AtMTM2 and PtdIns5P in the response of Arabidopsis seedlings to dehydration stress/ABA, and found that both AtMTM1 and AtMTM2 were involved but affected oppositely stomata movement and the accumulation of reactive oxygen species (ROS, e.g. H2O2). Acting as a secondary messenger in the ABA-induced ROS production in guard cells, PtdIns5P emerges as an evolutionarily conserved signalling molecule that calibrates cellular ROS under stress. We propose the biological relevance of the counteracting AtMTM1 and AtMTM2 activities is to balance the ABA-induced ROS accumulation and cellular homeostasis under dehydration stress.

scholarly journals The Double-Edged Sword in Pathogenic Trypanosomatids: The Pivotal Role of Mitochondria in Oxidative Stress and Bioenergetics

2014 ◽  
Vol 2014 ◽  
pp. 1-14 ◽  
Author(s):  
Rubem Figueiredo Sadok Menna-Barreto ◽  
Solange Lisboa de Castro
Keyword(s):  
Trypanosoma Brucei ◽  
Cell Signalling ◽  
Oxygen Species ◽  
Kinetoplast Dna ◽  
Excellent Candidate ◽  
Causative Agents ◽  
Parasite Biology ◽  
Oxidative Regulation ◽  
Single Mitochondrion

The pathogenic trypanosomatidsTrypanosoma brucei,Trypanosoma cruzi, andLeishmaniaspp. are the causative agents of African trypanosomiasis, Chagas disease, and leishmaniasis, respectively. These diseases are considered to be neglected tropical illnesses that persist under conditions of poverty and are concentrated in impoverished populations in the developing world. Novel efficient and nontoxic drugs are urgently needed as substitutes for the currently limited chemotherapy. Trypanosomatids display a single mitochondrion with several peculiar features, such as the presence of different energetic and antioxidant enzymes and a specific arrangement of mitochondrial DNA (kinetoplast DNA). Due to mitochondrial differences between mammals and trypanosomatids, this organelle is an excellent candidate for drug intervention. Additionally, during trypanosomatids’ life cycle, the shape and functional plasticity of their single mitochondrion undergo profound alterations, reflecting adaptation to different environments. In an uncoupling situation, the organelle produces high amounts of reactive oxygen species. However, these species role in parasite biology is still controversial, involving parasite death, cell signalling, or even proliferation. Novel perspectives on trypanosomatid-targeting chemotherapy could be developed based on better comprehension of mitochondrial oxidative regulation processes.

scholarly journals Oxidative stress in marathon runners: interest of antioxidant supplementation

2006 ◽  
Vol 96 (S1) ◽  
pp. S31-S33 ◽  
Author(s):  
Mari-Carmen Gomez-Cabrera ◽  
Agustín Martínez ◽  
Gustavo Santangelo ◽  
Federico V. Pallardó ◽  
Juan Sastre ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Xanthine Oxidase ◽  
Cell Signalling ◽  
Reactive Oxygen ◽  
Peripheral Blood Lymphocytes ◽  
Signalling Pathways ◽  
Marathon Running ◽  
Oxygen Species ◽  
Marathon Runners

We have recently reported that xanthine oxidase is involved in the generation of free radicals in exhaustive exercise. Allopurinol, an inhibitor of xanthine oxidase, prevents it. The aim of the present work was to elucidate the role of exercise-derived reactive oxygen species in the cell signalling pathways involved in the adaptation to exercise in man. We have found that exercise causes an increase in the activity of plasma xanthine oxidase and an activation of NF-κB in peripheral blood lymphocytes after marathon running. This activation is dependent on free radical formation in exercise: treatment with allopurinol completely prevents it. In animal models, we previously showed that NF-κB activation induced by exhaustive physical exercise leads to an increase in the expression of superoxide dismutase, an enzyme involved in antioxidant defence. We report evidence in man that reactive oxygen species act as signals in exercise as decreasing their formation prevents activation of important signalling pathways which can cause useful adaptations in cells.

scholarly journals Drosophila SLC22 Orthologs Related to OATs, OCTs, and OCTNs Regulate Development and Responsiveness to Oxidative Stress

2020 ◽  
Vol 21 (6) ◽  
pp. 2002 ◽  
Author(s):  
Darcy C. Engelhart ◽  
Priti Azad ◽  
Suwayda Ali ◽  
Jeffry C. Granados ◽  
Gabriel G. Haddad ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Drosophila Melanogaster ◽  
Organic Molecules ◽  
Fruit Fly ◽  
Evolutionary Analysis ◽  
Oxygen Species ◽  
Small Organic Molecules ◽  
Evolutionarily Conserved

The SLC22 family of transporters is widely expressed, evolutionarily conserved, and plays a major role in regulating homeostasis by transporting small organic molecules such as metabolites, signaling molecules, and antioxidants. Analysis of transporters in fruit flies provides a simple yet orthologous platform to study the endogenous function of drug transporters in vivo. Evolutionary analysis of Drosophila melanogaster putative SLC22 orthologs reveals that, while many of the 25 SLC22 fruit fly orthologs do not fall within previously established SLC22 subclades, at least four members appear orthologous to mammalian SLC22 members (SLC22A16:CG6356, SLC22A15:CG7458, CG7442 and SLC22A18:CG3168). We functionally evaluated the role of SLC22 transporters in Drosophila melanogaster by knocking down 14 of these genes. Three putative SLC22 ortholog knockdowns—CG3168, CG6356, and CG7442/SLC22A—did not undergo eclosion and were lethal at the pupa stage, indicating the developmental importance of these genes. Additionally, knocking down four SLC22 members increased resistance to oxidative stress via paraquat testing (CG4630: p < 0.05, CG6006: p < 0.05, CG6126: p < 0.01 and CG16727: p < 0.05). Consistent with recent evidence that SLC22 is central to a Remote Sensing and Signaling Network (RSSN) involved in signaling and metabolism, these phenotypes support a key role for SLC22 in handling reactive oxygen species.

The role of ferroptosis in organ toxicity

2021 ◽  
pp. 096032712110529
Author(s):  
Fatemeh Yarmohammadi ◽  
A Wallace Hayes ◽  
Gholamreza Karimi
Keyword(s):  
Reactive Oxygen Species ◽  
Iron Overload ◽  
Iron Chelators ◽  
Ros Generation ◽  
Oxygen Species ◽  
Organ Toxicity ◽  
Ros Accumulation ◽  
Dependent Form ◽  
Novel Therapeutic

Ferroptosis, an iron-dependent form of programmed cell death, is characterized by iron overload, increased reactive oxygen species (ROS) generation, and depletion of glutathione (GSH) and lipid peroxidation. Lipophilic antioxidants and iron chelators can prevent ferroptosis. GSH-dependent glutathione peroxidase 4 (GPX4) prevents lipid ROS accumulation. Ferroptosis is thought to be initiated through GPX4 inactivation. Moreover, mitochondrial iron overload derived from the degradation of ferritin is involved in increasing ROS generation. Ferroptosis has been suggested to explain the mechanism of action of organ toxicity induced by several drugs and chemicals. Inhibition of ferroptosis may provide novel therapeutic opportunities for treatment and even prevention of such organ toxicities.

Analysis of radicals and radical reaction products in cell signalling and biomolecular damage: the long hard road to gold-standard measures

2011 ◽  
Vol 39 (5) ◽  
pp. 1217-1220 ◽  
Author(s):  
Paul G. Winyard ◽  
Corinne M. Spickett ◽  
Helen R. Griffiths
Keyword(s):  
Free Radical ◽  
Cell Signalling ◽  
Radical Reaction ◽  
Research Area ◽  
Oxygen Species ◽  
Reaction Products ◽  
Research Areas ◽  
Key Factor ◽  
Topical Interest

The field of free radical biology and medicine continues to move at a tremendous pace, with a constant flow of ground-breaking discoveries. The following collection of papers in this issue of Biochemical Society Transactions highlights several key areas of topical interest, including the crucial role of validated measurements of radicals and reactive oxygen species in underpinning nearly all research in the field, the important advances being made as a result of the overlap of free radical research with the reinvigorated field of lipidomics (driven in part by innovations in MS-based analysis), the acceleration of new insights into the role of oxidative protein modifications (particularly to cysteine residues) in modulating cell signalling, and the effects of free radicals on the functions of mitochondria, extracellular matrix and the immune system. In the present article, we provide a brief overview of these research areas, but, throughout this discussion, it must be remembered that it is the availability of reliable analytical methodologies that will be a key factor in facilitating continuing developments in this exciting research area.

scholarly journals The 29-Kilodalton Thiol-Dependent Peroxidase of Entamoeba histolytica Is a Factor Involved in Pathogenesis and Survival of the Parasite during Oxidative Stress

2007 ◽  
Vol 6 (4) ◽  
pp. 664-673 ◽  
Author(s):  
Abhik Sen ◽  
Nabendu Sekhar Chatterjee ◽  
M. Ali Akbar ◽  
Nilay Nandi ◽  
Pradeep Das
Keyword(s):  
Oxidative Stress ◽  
Entamoeba Histolytica ◽  
Antisense Rna ◽  
Antioxidant Activities ◽  
Cytotoxic Activities ◽  
Oxygen Species ◽  
Tissue Invasion ◽  
Ros Accumulation ◽  
Parasite Survival

ABSTRACT The 29-kDa surface antigen (thiol-dependent peroxidase; Eh29) of Entamoeba histolytica exhibits peroxidative and protective antioxidant activities. During tissue invasion, the trophozoites are exposed to oxidative stress and need to deal with highly toxic reactive oxygen species (ROS). In this investigation, attempts have been made to understand the role of the 29-kDa peroxidase gene in parasite survival and pathogenesis. Inhibition of eh29 gene expression by antisense RNA technology has shown approximately 55% inhibition in eh29 expression, maximum ROS accumulation, and significantly lower viability in 29-kDa downregulated trophozoites during oxidative stress. The cytopathic and cytotoxic activities were also found to decrease effectively in the 29-kDa downregulated trophozoites. Size of liver abscesses was substantially lower in hamsters inoculated with 29-kDa downregulated trophozoites compared to the normal HM1:IMSS. These findings clearly suggest that the 29-kDa protein of E. histolytica has a role in both survival of trophozoites in the presence of ROS and pathogenesis of amoebiasis.

scholarly journals Coral-associated micro-organisms and their roles in promoting coral health and thwarting diseases

2013 ◽  
Vol 280 (1755) ◽  
pp. 20122328 ◽  
Author(s):  
Cory J. Krediet ◽  
Kim B. Ritchie ◽  
Valerie J. Paul ◽  
Max Teplitski
Keyword(s):  
Cell Signalling ◽  
Taxonomic Diversity ◽  
Microbial Interactions ◽  
Opportunistic Pathogens ◽  
Functional Capabilities ◽  
Evolutionarily Conserved ◽  
Coral Health ◽  
Micro Organisms

Over the last decade, significant advances have been made in characterization of the coral microbiota. Shifts in its composition often correlate with the appearance of signs of diseases and/or bleaching, thus suggesting a link between microbes, coral health and stability of reef ecosystems. The understanding of interactions in coral-associated microbiota is informed by the on-going characterization of other microbiomes, which suggest that metabolic pathways and functional capabilities define the ‘core’ microbiota more accurately than the taxonomic diversity of its members. Consistent with this hypothesis, there does not appear to be a consensus on the specificity in the interactions of corals with microbial commensals, even though recent studies report potentially beneficial functions of the coral-associated bacteria. They cycle sulphur, fix nitrogen, produce antimicrobial compounds, inhibit cell-to-cell signalling and disrupt virulence in opportunistic pathogens. While their beneficial functions have been documented, it is not certain whether or how these microbes are selected by the hosts. Therefore, understanding the role of innate immunity, signal and nutrient exchange in the establishment of coral microbiota and in controlling its functions will probably reveal ancient, evolutionarily conserved mechanisms that dictate the outcomes of host–microbial interactions, and impact the resilience of the host.

scholarly journals Reactive Oxygen Species: A Promising Therapeutic Target for SDHx-Mutated Pheochromocytoma and Paraganglioma

Cancers ◽  
2021 ◽  
Vol 13 (15) ◽  
pp. 3769
Author(s):  
Katerina Hadrava Hadrava Vanova ◽  
Chunzhang Yang ◽  
Leah Meuter ◽  
Jiri Neuzil ◽  
Karel Pacak
Keyword(s):  
Reactive Oxygen Species ◽  
Tumor Cells ◽  
Reactive Oxygen ◽  
Ros Production ◽  
Oxygen Species ◽  
Ros Scavenging ◽  
Promising Therapeutic Target ◽  
Ros Accumulation ◽  
Intracellular Ros

Pheochromocytoma (PHEO) and paraganglioma (PGL) are rare neuroendocrine tumors derived from neural crest cells. Germline variants in approximately 20 PHEO/PGL susceptibility genes are found in about 40% of patients, half of which are found in the genes that encode succinate dehydrogenase (SDH). Patients with SDH subunit B (SDHB)-mutated PHEO/PGL exhibit a higher likelihood of developing metastatic disease, which can be partially explained by the metabolic cell reprogramming and redox imbalance caused by the mutation. Reactive oxygen species (ROS) are highly reactive molecules involved in a multitude of important signaling pathways. A moderate level of ROS production can help regulate cellular physiology; however, an excessive level of oxidative stress can lead to tumorigenic processes including stimulation of growth factor-dependent pathways and the induction of genetic instability. Tumor cells effectively exploit antioxidant enzymes in order to protect themselves against harmful intracellular ROS accumulation, which highlights the essential balance between ROS production and scavenging. Exploiting ROS accumulation can be used as a possible therapeutic strategy in ROS-scavenging tumor cells. Here, we focus on the role of ROS production in PHEO and PGL, predominantly in SDHB-mutated cases. We discuss potential strategies and approaches to anticancer therapies by enhancing ROS production in these difficult-to-treat tumors.

scholarly journals Mitochondrial localization of SESN2

2019 ◽  
Author(s):  
Irina E. Kovaleva ◽  
Artem V. Tokarchuk ◽  
Andrei O. Zeltukhin ◽  
Grigoriy Safronov ◽  
Aleksandra G. Evstafieva ◽  
...  
Keyword(s):  
Protein Complex ◽  
Inhibitory Effect ◽  
Small Gtpase ◽  
Stress Factors ◽  
Mitochondrial Localization ◽  
Mitochondrial Functions ◽  
Ros Accumulation ◽  
Evolutionarily Conserved ◽  
Established Role

SESN2 is a member of evolutionarily conserved sestrin protein family found in most of Metazoa species. SESN2 is transcriptionally activated by many stress factors including metabolic derangements, oxidants and DNA-damage. As a result, SESN2 controls ROS accumulation, metabolism and cell viability. The best known function of SESN2 is the regulation of mechanistic target of rapamycin complex 1 kinase (mTORC1) that plays the central role in the stimulation of cell growth and suppression of autophagy. SESN2 inhibits mTORC1 activity through interaction with the GATOR2 protein complex that suppresses an inhibitory effect of GATOR2 on the GATOR1 protein complex. GATOR1 inhibits mTORC1 through its GAP activity toward the small GTPase RagA/B which in complex with RagC/D proteins stimulate mTORC1 translocation to the lysosomes where this kinase is activated by small GTPase Rheb. Despite the well-established role of SESN2 in mTORC1 inhibition, the other SESN2 activities are not well characterised. We recently showed that SESN2 can control mitochondrial function and cell death via mTORC1-independent mechanisms and these activities might be explained by direct effects of SESN2 on mitochondria. In this work we examined mitochondrial localization of SESN2 and demonstrated that SESN2 is located on mitochondria and can be directly involved in the regulation of mitochondrial functions.

scholarly journals Cell signalling by oxidized lipids and the role of reactive oxygen species in the endothelium

2005 ◽  
Vol 33 (6) ◽  
pp. 1385 ◽  
Author(s):  
A. Landar ◽  
J.W. Zmijewski ◽  
N. Watanabe ◽  
D.A. Dickinson ◽  
N. Noguchi ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Cell Signalling ◽  
Reactive Oxygen ◽  
Oxidized Lipids ◽  
Oxygen Species
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