scholarly journals Leaf Rolling and Stem Fasciation in Grass Pea (Lathyrus sativusL.) Mutant Are Mediated through Glutathione-Dependent Cellular and Metabolic Changes and Associated with a Metabolic Diversion through Cysteine during Phenotypic Reversal

2014 ◽  
Vol 2014 ◽  
pp. 1-21 ◽  
Author(s):  
Dibyendu Talukdar ◽  
Tulika Talukdar
Keyword(s):  
Antioxidant Defense ◽  
Imaging Study ◽  
Buthionine Sulfoximine ◽  
Mitotic Cell ◽  
Glycolate Oxidase ◽  
Leaf Rolling ◽  
Proliferating Cells ◽  
Glutathione Synthesis ◽  
Phenotypic Reversal ◽  
Rolled Leaf

ALathyrus sativusL. mutant isolated in ethylmethane sulfonate-treated M2progeny of mother variety BioL-212 and designated asrlfL-1was characterized by inwardly rolled-leaf and stem and bud fasciations. The mutant exhibited karyomorphological peculiarities in both mitosis and meiosis with origin of aneuploidy. The mitosis was vigorous with high frequency of divisional cells and their quick turnover presumably steered cell proliferations. Significant transcriptional upregulations of cysteine and glutathione synthesis and concomitant stimulations of glutathione-mediated antioxidant defense helpedrlfL-1mutant to maintain balanced reactive oxygen species (ROS) metabolisms, as deduced by ROS-imaging study. Glutathione synthesis was shut down in buthionine sulfoximine- (BSO-) treated mother plant and mutant, and leaf-rolling and stems/buds fasciations in the mutant were reversed, accompanied by normalization of mitotic cell division process. Antioxidant defense was downregulated under low glutathione-redox but cysteine-desulfurations and photorespiratory glycolate oxidase transcripts were markedly overexpressed, preventing cysteine overaccumulation but resulted in excess H2O2in BSO-treated mutant. This led to oxidative damage in proliferating cells, manifested by severe necrosis in rolled-leaf and fasciated stems. Results indicated vital role of glutathione in maintaining abnormal proliferations in plant organs, and its deficiency triggered phenotypic reversal through metabolic diversions of cysteine and concomitant cellular and metabolic modulations.

An analysis of the mitotic cell cycle in the root meristem of Zea mays

1973 ◽  
Vol 183 (1073) ◽  
pp. 385-398 ◽  
Keyword(s):  
Cell Cycle ◽  
Zea Mays ◽  
Root Meristem ◽  
Mitotic Cell ◽  
Mitotic Cell Cycle ◽  
Pulse Labelling ◽  
Quiescent Centre ◽  
Proliferating Cells ◽  
Average Delay ◽  
The Mean

A pulse labelling experiment was used to study the mitotic cell cycle of proliferating cells throughout the root meristem of Zea mays . Seventeen different regions were identified within the area of proliferative activity, extending from the initial cells of the cap columella up to the stele, cortex and epidermis 1000 μm from the cap-quiescent centre junction, and the data were analysed for each region separately. The analyses were made in terms of a mathematical model for cell proliferation and yield statistically efficient estimates of the cell-cycle parameters. The validity of the model is discussed in some detail. It appears that the main difference between the regions studied is in the mean duration of G 1 , that is, the average delay a newborn cell experiences before it begins to synthesize DNA. The mean durations of S and G 2 , the DNA-synthetic and post-DNA-synthetic phases of the mitotic cycle, are relatively constant. The one exception to this pattern is the quiescent centre; this region includes a relatively high proportion of slowly dividing and non-proliferating cells.

Antioxidant defense mechanisms of endothelial cells: glutathione redox cycle versus catalase

1986 ◽  
Vol 251 (5) ◽  
pp. C671-C680 ◽  
Author(s):  
N. Suttorp ◽  
W. Toepfer ◽  
L. Roka
Keyword(s):  
Endothelial Cells ◽  
Defense Mechanisms ◽  
Antioxidant Defense ◽  
Buthionine Sulfoximine ◽  
Alpha Tocopherol ◽  
Target Cells ◽  
Redox Cycle ◽  
Extracellular Flux ◽  
Glutathione Redox Cycle ◽  
Antioxidant Defense Systems

The importance of the glutathione (GSH) redox cycle and of catalase as intracellular antioxidant defense systems in cultured endothelial cells against an extracellular flux of H2O2, a critical mediator of polymorphonuclear leukocyte-induced oxidant injury of endothelial cells, was examined. The activities of different parts of the GSH redox cycle were impaired by 1,3-bis(2-chloroethyl)-1-nitrosourea, buthionine sulfoximine, diethyl maleate and 2-cyclohexene-1-one. Catalase activity was inhibited by 3-amino-1,2,4-triazole. After an impairment of the GSH redox cycle, but not of catalase, the susceptibility of pulmonary artery endothelial cells to an attack by H2O2 was dramatically increased independent of the source of extracellularly generated hydrogen peroxide (i.e., glucose oxidase or stimulated polymorphonuclear leukocytes). Exogenous catalase, d-alpha-tocopherol, and particularly Trolox, the chroman compound of tocopherol, but not phytol, the fatty acid side chain of tocopherol, provided almost complete protection of the endothelial cells against a H2O2-mediated attack. Additional fluorometric studies suggested that H2O2 is scavenged by the antioxidants before it hits the target cells.

Interactions of nitroglycerin and sulfhydryl-donating compounds in coronary microvessels

1994 ◽  
Vol 266 (1) ◽  
pp. H291-H297 ◽  
Author(s):  
R. M. Wheatley ◽  
S. P. Dockery ◽  
M. A. Kurz ◽  
H. S. Sayegh ◽  
D. G. Harrison
Keyword(s):  
Redox Potential ◽  
Potent Inhibitor ◽  
Buthionine Sulfoximine ◽  
Glutathione Synthesis ◽  
Endothelin 1 ◽  
Intracellular Glutathione ◽  
Enzymatic Bioconversion

Previous studies have shown the effect of nitroglycerin on coronary microvessels < 100 microns in diameter is markedly enhanced by L-cysteine. These studies were performed to examine the mechanisms responsible for this effect. Under control conditions, nitroglycerin caused potent dilations of large (> 200 microns diam) coronary microvessels while having minimal effects on small (< 100 microns diam) coronary microvessels [peak relaxations 85 +/- 4 vs. 23 +/- 3% (mean +/- SE) of endothelin-1-constricted vessels, respectively]. L-Cysteine (100 microM) and N-acetylcysteine (100 microM) markedly enhanced nitroglycerin-induced relaxations of small coronary microvessels (peak relaxation 84 +/- 6 and 87 +/- 12%, respectively) while having no effect on relaxations of vessels > 100 microns. In contrast, neither L-methionine (100 microM) nor glutathione (100 microM) enhanced nitroglycerin's vasodilation of small coronary microvessels. The effects of L-cysteine and N-acetylcysteine on the augmentation of nitroglycerin vasodilatation in smaller coronary microvessels was abolished in the presence of buthionine sulfoximine (100 microM), a potent inhibitor of intracellular glutathione synthesis. Buthionine sulfoximine had no effect on the vasodilatation produced by nitroprusside. These data demonstrate that, in smaller coronary microvessels, L-cysteine and N-acetylcysteine enhance nitroglycerin-induced vasodilatation by increasing intracellular glutathione concentrations. Intracellular glutathione, formed from either L-cysteine or N-acetylcysteine, may participate in the formation of an intermediate of nitroglycerin biotransformation or may maintain a redox potential within coronary microvessels that favors enzymatic bioconversion of nitroglycerin.

scholarly journals Exogenous thiourea modulates antioxidant defence and glyoxalase systems in lentil genotypes under arsenic stress

2016 ◽  
Vol 2 ◽  
pp. 9 ◽  
Author(s):  
Dibyendu Talukdar
Keyword(s):  
Oxidative Damage ◽  
Antioxidant Defense ◽  
Imaging Study ◽  
Dry Weight ◽  
Crop Productivity ◽  
Mitigation Strategies ◽  
Grain Legume ◽  
Glutathione S Transferase ◽  
Study Results ◽  
Antioxidant Defense Enzymes

<p>Arsenic (As) is a wide-spread toxic and carcinogenic metalloid, affecting crop productivity worldwide. Lentil, an edible grain legume, is increasingly exposed to soil arsenic contamination. However, our understandings regarding mechanistic details and mitigation strategies against arsenic toxicity in edible legume are extremely poor. Main purpose of the present study was to investigate the As-effects and its mitigation by thiourea (TU), a sulfhydryl bioregulator, in lentil. Four widely grown lentil genotypes were grown in nutrient media, supplemented with 30 μM sodium arsenate (As), As + 6.5 mM TU and As + 13 mM TU, keeping an untreated control for 10 d. As severely affected plant dry weight by accumulating in shoots and roots. However, TU application sequestered As in crop roots and prevented up-ward translocation of As. TU coordinately modulated glyoxalase system I and II (Gly I and II) and ascorbate (AsA)-glutathione (GSH) redox, and antioxidant defense enzymes in both leaves and roots of four genotypes. Elevation of Gly system prevented toxic methyl glyoxal overaccumulation whereas stimulated AsA-GSH cycle enzymes and Glutathione s-transferase and catalase effectively scavenged H<sub>2</sub>O<sub>2</sub> and prevented reactive oxygen species (ROS) -mediated onset of oxidative damage in four genotypes, as was evident from ROS-imaging study. Results suggested exogenous TU stimulated the Gly and antioxidant defense in fine tune against As-induced oxidative damage in lentil genotypes.</p>

Glutathione modulates toxic oxygen metabolite injury of canine chief cell monolayers in primary culture

1988 ◽  
Vol 254 (1) ◽  
pp. G49-G56 ◽  
Author(s):  
C. E. Olson
Keyword(s):  
Oxidant Stress ◽  
Buthionine Sulfoximine ◽  
Cell Lysis ◽  
Glutathione Depletion ◽  
Glutathione Synthesis ◽  
Chief Cells ◽  
Cell Monolayers ◽  
Lactate Dehydrogenase Release ◽  
Endogenous Antioxidant ◽  
Generating System

Cultured canine gastric chief cells exposed to a toxic oxygen metabolite-generating system (xanthine plus xanthine oxidase) demonstrated minimal cytolysis, suggesting that these cells have important endogenous antioxidant mechanisms. We have quantified the role of glutathione for protection against toxic oxygen metabolites by measuring cell lysis by lactate dehydrogenase release after variable depletion and repletion of cellular glutathione content. In the absence of exogenous oxidant stress, the glutathione content of chief cells can be depleted to less than 0.2 nmol total glutathione/micrograms DNA or 22% of control without cell lysis over 5 h. However, when challenged with the oxygen metabolite-generating system, cytolysis was greatly enhanced by glutathione depletion. Oxygen metabolite-mediated cytolysis after glutathione depletion was inhibited by exogenous catalase, thiourea, and deferoximine, but not superoxide dismutase or mannitol. These data suggested that hydrogen peroxide and hydroxyl radical mediated cytolysis in glutathione-depleted chief cells. If a substrate for glutathione synthesis, N-acetyl-L-cysteine, was provided to the depleted cells for 1 h before challenge with the oxygen radical-generating system, cell lysis was markedly decreased. However, if glutathione synthesis was blocked during the repletion period by buthionine sulfoximine, protection was not restored. The data supported an important role for glutathione as an endogenous antioxidant, which modulated the sensitivity of cultured chief cells to toxic oxygen metabolite injury.

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