scholarly journals Roles of bicarbonate ion in the deterministic Z-scheme and the stochastic murburn model for the light reaction of oxygenic photosynthesis

2021 ◽  
Author(s):  
Kelath Murali Manoj ◽  
Nikolai Bazhin ◽  
Afsal Manekkathodi ◽  
Yanyou Wu
Keyword(s):  
Reactive Oxygen Species ◽  
Theoretical Analysis ◽  
Oxygenic Photosynthesis ◽  
Oxygen Species ◽  
Bimolecular Reactions ◽  
Light Reaction ◽  
Potential Source ◽  
Oxygen Gas ◽  
Neutral Water ◽  
Positively Charged

Bicarbonate ion has been proposed as a potential source for electrons/O-atom in the light reaction of oxygenic photosynthesis, both in the pre-Zscheme era and in recent times. In the light of murburn concept being mooted as a viable explanation for photophosphorylation, we present substantial theoretical analysis which supports the proposal that: (i) Bicarbonate ion can serve as a viable source of electrons to electron-discharged photosystems or other positively-charged intermediates (formed after photo-activation) in thylakoids. This is because electron abstraction from bicarbonate anion [(a). HCO3- → CO2 + *OH + e-; ° ≈ 491 kJ/mol] is more viable with respect to the classical alternative/available option like the neutral water molecule [(b). H2O → H+ + *OH + e-; ° ≈ 527 kJ/mol]. (ii) The hydroxyl radical directly produced in reaction (a) in conjunction with other diffusible reactive oxygen species (DROS) sponsor murburn phosphorylation cycles and/or dismutations/cross-reactions. Spontaneous involvement/formation of molecular oxygen in several such discretized bimolecular reactions is also a kinetically viable process. Therefore, the incorporation of an O-atom from bicarbonate into the oxygen gas evolved in the light reaction is a tenable outcome of the stochastic/statistical murburn model. We provide the pertinent equations and abrogate the bioenergetic calculations.

Mitochondrial Dysfunction As a Potential Source of Reactive Oxygen Species in Cellular Models of Shwachman-Diamond Syndrome

Blood ◽  
2011 ◽  
Vol 118 (21) ◽  
pp. 1343-1343
Author(s):  
Adrianna Henson ◽  
Joseph B Moore ◽  
Johnson M. Liu ◽  
Steven Ellis
Keyword(s):  
Reactive Oxygen Species ◽  
Mitochondrial Function ◽  
Molecular Mechanisms ◽  
Reactive Oxygen ◽  
Yeast Cells ◽  
Oxygen Species ◽  
Ribosome Synthesis ◽  
Potential Source ◽  
Shwachman Diamond Syndrome ◽  
Respiratory Deficient

Abstract Abstract 1343 Shwachman-Diamond Syndrome (SDS) is an inherited bone marrow failure syndrome linked to defects in ribosome synthesis. The heterogeneous array of clinical findings associated with this disease state most commonly includes exocrine pancreas insufficiency, neutropenia, and metaphyseal chondroplasia. Patients also show a predisposition for progression to myelodysplastic syndromes and acute myelogenous leukemia. Mutations in the gene SBDS are known to be responsible for most cases of SDS. Initial studies of the yeast ortholog of SBDS, Sdo1, revealed that this family of proteins is involved in the maturation of 60S subunits. Other studies have suggested that SBDS is a multifunctional protein affecting processes other than ribosome synthesis. Most recently it has been shown that reactive oxygen species are dysregulated in TF-1 erythroleukemic cells depleted of SBDS leading to increased cell death (Pediatr Blood Cancer. 2010 Dec 1;55(6): 1138–44). In an effort to elucidate potential sources of increased reactive oxygen species we investigated mitochondrial function in yeast and human models of SDS. Yeast cells lacking Sdo1 fail to grow on media containing only respiratory carbon sources, indicative of a defect in mitochondrial energy metabolism. Related studies in human TF-1 cells revealed that cells depleted of SBDS exhibit reduced oxygen consumption relative to controls. Given that the largest producer of reactive oxygen species is the mitochondrial electron transport chain, perturbation of respiratory function in cells depleted of SBDS family members could be a potential source of elevated reactive oxygen species. To investigate the potential molecular mechanisms underlying these respiratory deficient phenotypes we carried out a proteomic analysis comparing yeast cells depleted of Sdo1 with controls. Our data reveal that cells lacking Sdo1 overexpress Por1, an ortholog of human VDAC1. VDAC1 is a voltage dependent anion channel of the mitochondrial outer membrane that is thought to be an essential component of the mitochondrial permeability pore. Both over and under expression of VDAC1 have been shown to disrupt mitochondrial function and lead to enhanced apoptosis. Current efforts are focused on possible changes in VDAC1 expression and the role they play in the respiratory deficient phenotype in human SDS models. These studies continue to shed further insight into the molecular mechanisms underlying SDS pathophysiology. Disclosures: No relevant conflicts of interest to declare.

scholarly journals Molecular genetics of xanthophyll–dependent photoprotection in green algae and plants

2000 ◽  
Vol 355 (1402) ◽  
pp. 1385-1394 ◽  
Author(s):  
Irene Baroli ◽  
Krishna K. Niyogi
Keyword(s):  
Reactive Oxygen Species ◽  
Photosynthetic Apparatus ◽  
Reactive Oxygen ◽  
High Light ◽  
Multiple Roles ◽  
Oxygenic Photosynthesis ◽  
Photochemical Quenching ◽  
Oxygen Species ◽  
Non Photochemical Quenching ◽  
Extragenic Suppressors

The involvement of excited and highly reactive intermediates in oxygenic photosynthesis inevitably results in the generation of reactive oxygen species. To protect the photosynthetic apparatus from oxidative damage, xanthophyll pigments are involved in the quenching of excited chlorophyll and reactive oxygen species, namely 1 Chl*, 3 Chl*, and 1 1O 2 *. Quenching of 1 Chl* results in harmless dissipation of excitation energy as heat and is measured as non–photochemical quenching (NPQ) of chlorophyll fluorescence. The multiple roles of xanthophylls in photoprotection are being addressed by characterizing mutants of Chlamydomonas reinhardtii and Arabidopsis thaliana . Analysis of Arabidopsis mutants that are defective in 1 Chl* quenching has shown that, in addition to specific xanthophylls, the psbS gene is necessary for NPQ. Double mutants of Chlamydomonas and Arabidopsis that are deficient in zeaxanthin, lutein and NPQ undergo photo–oxidative bleaching in high light. Extragenic suppressors of the Chlamydomonas npq1 lor1 double mutant identify new mutations that restore varying levels of zeaxanthin accumulation and allow survival in high light.

scholarly journals A study of free radical chemistry: their role and pathophysiological significance.

2013 ◽  
Vol 60 (1) ◽  
Author(s):  
Mariusz Gutowski ◽  
Sławomir Kowalczyk
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Redox Homeostasis ◽  
Reactive Oxygen ◽  
Oxygenic Photosynthesis ◽  
Oxygen Species ◽  
Ischaemia Reperfusion Injury ◽  
Ischaemia Reperfusion ◽  
Obstructive Sleep ◽  
Free Radical Chemistry

Oxygen is one of the most important molecules on Earth mainly because of the biochemical symmetry of oxygenic photosynthesis and aerobic respiration that can maintain homeostasis within our planet's biosphere. Oxygen can also produce toxic molecules, reactive oxygen species (ROS). ROS play a dual role in biological systems, since they can be either harmful or beneficial to living systems. They can be considered a double-edged sword because at moderate concentrations, nitric oxide (NO•), superoxide anion, and related reactive oxygen species play an important role as regulatory mediators in signalling processes. Many of the ROS-mediated responses actually protect the cells against oxidative stress and re-establish "redox homeostasis". On the other hand, overproduction of ROS has the potential to cause damage. In the recent decades, ROS has become a focus of interest in most biomedical disciplines and many types of clinical research. Increasing evidence from research on several diseases shows that oxidative stress is associated with the pathogenesis of diabetes mellitus, obesity, cancer, cardiovascular diseases, inflammation, ischaemia/reperfusion injury, obstructive sleep apnea, neurodegenerative disorders, hypertension and ageing.

Mitochondria as a source of reactive oxygen species

2009 ◽  
pp. c3 ◽  
Author(s):  
Helena M. Cochemé ◽  
Michael P. Murphy
Keyword(s):  
Reactive Oxygen Species ◽  
Reactive Oxygen ◽  
Oxygen Species

Clinical aspects of reactive oxygen and nitrogen species

2004 ◽  
Vol 71 ◽  
pp. 121-133 ◽  
Author(s):  
Ascan Warnholtz ◽  
Maria Wendt ◽  
Michael August ◽  
Thomas Münzel
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Risk Factor ◽  
Endothelial Dysfunction ◽  
Vascular Tissue ◽  
Rapid Development ◽  
Reactive Oxygen ◽  
Clinical Aspects ◽  
No Production ◽  
Oxygen Species

Endothelial dysfunction in the setting of cardiovascular risk factors, such as hypercholesterolaemia, hypertension, diabetes mellitus and chronic smoking, as well as in the setting of heart failure, has been shown to be at least partly dependent on the production of reactive oxygen species in endothelial and/or smooth muscle cells and the adventitia, and the subsequent decrease in vascular bioavailability of NO. Superoxide-producing enzymes involved in increased oxidative stress within vascular tissue include NAD(P)H-oxidase, xanthine oxidase and endothelial nitric oxide synthase in an uncoupled state. Recent studies indicate that endothelial dysfunction of peripheral and coronary resistance and conductance vessels represents a strong and independent risk factor for future cardiovascular events. Ways to reduce endothelial dysfunction include risk-factor modification and treatment with substances that have been shown to reduce oxidative stress and, simultaneously, to stimulate endothelial NO production, such as inhibitors of angiotensin-converting enzyme or the statins. In contrast, in conditions where increased production of reactive oxygen species, such as superoxide, in vascular tissue is established, treatment with NO, e.g. via administration of nitroglycerin, results in a rapid development of endothelial dysfunction, which may worsen the prognosis in patients with established coronary artery disease.

Fas ligand expression in rat kupffer cells in response to lipopolysaccharide is mediated by reactive oxygen species

2001 ◽  
Vol 120 (5) ◽  
pp. A361-A361
Author(s):  
K UCHIKURA ◽  
T WADA ◽  
Z SUN ◽  
S HOSHINO ◽  
G BULKLEY ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Kupffer Cells ◽  
Fas Ligand ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Ligand Expression
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