Effect of oxidative stress during imbibition of soybean embryonic axes

1994 ◽  
Vol 102 ◽  
pp. 279-286 ◽  
Author(s):  
Susana Puntarulo
Keyword(s):  
Oxidative Stress ◽  
Steady State ◽  
External Medium ◽  
Tocopherol Content ◽  
Active Species ◽  
Oxygen Species ◽  
Steady State Concentration ◽  
Embryonic Axes ◽  
State Concentration

SynopsisBoth respiration and generation by soybean embryonic axes showed a sharp increase upon germination, leading to a significant increase in the steady-state concentration of and H2O2 after 6 h of imbibition. An assay was developed to assess in vivo generation of reactive oxygen species, based upon DCFH-DA oxidation. Fluorescence of the external medium was dependent on reaction time and axes number and was inhibited by catalase.α-Tocopherol content declined significantly after 24 h of incubation, as compared to the content at the onset of germination. Incubation in the presence of redox cycling agent paraquat (4 mM) for 24 h increased α-tocopherol content to 1.9±0.2 nmol per axis from 1.0 ± 0.1 nmol per axis in the absence of paraquat. Supplementation of the incubation medium with 500 μM Fe-EDTA increased α-tocopherol content to 1.8±0.1 nmol/axis and DCFH-DA oxidation by two-fold.The data presented here showed that active metabolism at the onset of germination increased steady-state concentration of oxygen active species and suggest that cellular content of α-tocopherol is physiologically adjusted as a response to conditions of oxidative stress.

Apoptosis induced by exposure to a low steady-state concentration of H2O2 is a consequence of lysosomal rupture

2001 ◽  
Vol 356 (2) ◽  
pp. 549-555 ◽  
Author(s):  
Fernando ANTUNES ◽  
Enrique CADENAS ◽  
Ulf T. BRUNK
Keyword(s):  
Oxidative Stress ◽  
Steady State ◽  
Culture Conditions ◽  
Bolus Administration ◽  
Apoptotic Cells ◽  
Steady State Concentration ◽  
Continuous Increase ◽  
Induced Apoptosis ◽  
State Concentration

We have re-examined the lysosomal hypothesis of oxidative-stress-induced apoptosis using a new technique for exposing cells in culture to a low steady-state concentration of H2O2. This steady-state technique mimics the situation in vivo better than the bolus-administration method. A key aspect of H2O2-induced apoptosis is that the apoptosis is evident only after several hours, although cells may become committed within a few minutes of exposure to this particular reactive oxygen species. In the present work, we were able to show, for the first time, several correlative links between the triggering effect of H2O2 and the later onset of apoptosis: (i) a short (15min) exposure to H2O2 caused almost immediate, albeit limited, lysosomal rupture; (ii) early lysosomal damage, and later apoptosis, showed a similar dose-related response to H2O2; (iii) both events were inhibited by pre-treatment with iron chelators, including desferrioxamine. This compound is known to be taken up by endocytosis only and thus to become localized in the lysosomal compartment. After exposure to oxidative stress, when cells were again in standard culture conditions, a time-dependent continuous increase in lysosomal rupture was observed, resulting in a considerably lowered number of intact lysosomes in apoptotic cells, whereas non-apoptotic cells from the same batch of oxidative-stress-exposed cells showed mainly intact lysosomes. Taken together, our results reinforce earlier findings and strongly suggest that lysosomal rupture is an early upstream initiating event, and a consequence of intralysosomal iron-catalysed oxidative processes, when apoptosis is induced by oxidative stress.

Divergent effects of intravenous GSH and cysteine on renal and hepatic GSH

1992 ◽  
Vol 263 (2) ◽  
pp. R348-R352 ◽  
Author(s):  
S. Aebi ◽  
B. H. Lauterburg
Keyword(s):  
Steady State ◽  
De Novo ◽  
Feedback Inhibition ◽  
Therapeutic Use ◽  
Steady State Concentration ◽  
De Novo Synthesis ◽  
State Concentration ◽  
Cellular Thiol

There is a growing interest in the therapeutic use of sulfhydryls. To assess the effect of glutathione (GSH) and cysteine on the cellular thiol status, thiols were administered intravenously to rats in doses ranging from 1.67 to 8.35 mmol/kg with and without pretreatment with 4 mmol/kg buthionine-[S,R]-sulfoximine (BSO), an inhibitor of GSH synthesis. One hour after administration of 1.67 mmol/kg GSH, the concentration of GSH rose from 5.2 +/- 1.0 to 8.4 +/- 0.9 mumol/g and from 2.5 +/- 0.5 to 3.7 +/- 0.7 mumol/g in liver and kidneys, respectively. After 8.35 mmol/kg, hepatic GSH did not increase further, but renal GSH rose to 6.7 +/- 1.8 mumol/g. Infusion of cysteine increased hepatic GSH to the same extent as intravenous GSH, but renal GSH did not increase after 1.67 mmol/kg and even significantly decreased to 0.6 +/- 0.2 mumol/g after 8.35 mmol/kg. In the presence of BSO, GSH resulted in a significant increase in renal but not hepatic GSH, suggesting that the kidneys take up intact GSH and indicating that the increment in hepatic GSH was due to de novo synthesis. The present data show that hepatic GSH can be markedly increased in vivo by increasing the supply of cysteine. Measurements of hepatic cysteine indicate that up to a concentration of approximately 0.5 mumol/g cysteine is a key determinant of hepatic GSH, such that the physiological steady-state concentration of GSH in the liver appears to be mainly determined by the availability of cysteine. At higher concentrations GSH does not increase further, possibly due to feedback inhibition of GSH synthesis or increased efflux.(ABSTRACT TRUNCATED AT 250 WORDS)

The independent regulation of and tRNAAsn synthesis during Friend cell erythroid differentiation

1988 ◽  
Vol 66 (7) ◽  
pp. 772-779
Author(s):  
Lawrence Kleiman ◽  
Erich Schmedt ◽  
Harvey Miller
Keyword(s):  
Steady State ◽  
Relative Concentration ◽  
Erythroid Differentiation ◽  
Trna Genes ◽  
Steady State Concentration ◽  
Nuclear Rna ◽  
Erythroleukemia Cell ◽  
Regulation Of Synthesis ◽  
State Concentration

In this report, we have compared the changes in the production of [Formula: see text] (initiator tRNAMet) and tRNAAsn, which occur during erythroid differentiation in the Friend erythroleukemia cell. The relative steady-state concentration of these two tRNAs (relative to the total tRNA population) was measured by aminoacylation. The results show that while the relative steady-state concentration of [Formula: see text] changes very little in the cytoplasmic tRNA population, the relative concentration of tRNAAsn decreases during the first two days of differentiation and then undergoes an increase. This difference in the behavior of these two tRNAs is also seen when their relative concentrations in newly synthesized tRNA is examined. When tRNA is labeled with tritiated uridine for 24 h in vivo prior to isolation, the hybridization of this labeled tRNA to filter-bound tRNA genes shows that the relative concentration of [Formula: see text] in newly synthesized tRNA changes very little, while the relative concentration of newly synthesized tRNAAsn again decreases through the first 2 days of differentiation, and then undergoes a smaller increase. Thus, the production of these two tRNAs appears to be independently regulated. Independent regulation of synthesis is also observed when examining the production of these two tRNAs in isolated nuclei. During erythroid differentiation, the relative synthesis of [Formula: see text] (relative to total nuclear RNA synthesis) remains constant, while the relative synthesis of tRNAAsn undergoes periodic increases and decreases in value.

Testosterone transport in brain: primary role of plasma protein-bound hormone

1985 ◽  
Vol 249 (5) ◽  
pp. E534-E542 ◽  
Author(s):  
W. M. Pardridge ◽  
E. M. Landaw
Keyword(s):  
Steady State ◽  
Plasma Protein ◽  
Kinetic Studies ◽  
Primary Role ◽  
Steady State Concentration ◽  
Tracer Kinetic ◽  
Blood Transport ◽  
State Concentration

Physiologically based mathematical modeling is used to predict the steady-state concentration of intracellular free and bound testosterone in brain. On the basis of previous in vivo tracer kinetic studies of blood-to-brain and brain-to-blood transport of testosterone in the rat, values are assigned to various physiological parameters (hormone association and dissociation reactions with plasma and cytosolic binding proteins, capillary transit time, and membrane transport). The model does not adhere to the restrictions of the free hormone hypothesis and allows for the enhanced transport of hormone from the plasma protein-bound pool into the tissue extravascular space. This process is believed to occur via an endothelial inhibition of ligand binding to the plasma protein without the protein crossing the endothelial wall. The model predicts that the steady-state concentration of intracellular free hormone changes in parallel more closely to changes in the concentration of plasma protein-bound hormone as measured in vitro and not the free hormone as measured in vitro.

Cerebrospinal fluid iodide

1961 ◽  
Vol 201 (6) ◽  
pp. 1149-1151 ◽  
Author(s):  
Bernard Becker
Keyword(s):  
Cerebrospinal Fluid ◽  
Steady State ◽  
Metabolic Inhibitors ◽  
Steady State Concentration ◽  
Temperature Dependent ◽  
Ocular Fluids ◽  
The Media ◽  
State Concentration

In vitro preparations of rabbit choroid plexus accumulated I131 to a concentration 20–30 times the media. The accumulation was temperature dependent and was blocked by metabolic inhibitors. It could also be saturated with iodide, and was inhibited by perchlorate, fluoroborate, and related anions. In vivo the low 4-hr steady state concentration (1.6% of plasma) of trace doses of I131 in the rabbit cerebrospinal fluid was increased (to 40% of plasma) by the systemic administration of iodide or perchlorate. The results resembled qualitatively those obtained in the vitreous and aqueous humors of the same animals and suggested an active transport of iodide out of the cerebrospinal fluid, much as postulated previously for ocular fluids.

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