scholarly journals The effect of 2,4-D and ABA on respiration of isolated mitochondria from maize coleoptiles

2014 ◽  
Vol 53 (3) ◽  
pp. 363-376
Author(s):  
Ewa Raczek
Keyword(s):  
Oxidative Phosphorylation ◽  
Growth Regulators ◽  
Growth Inhibitor ◽  
Inhibitory Effect ◽  
Similar Response ◽  
Mitochondrial Membranes ◽  
Oxidative Potential ◽  
Succinate Oxidation ◽  
Uncoupling Of Oxidative Phosphorylation ◽  
2,4 Dichlorophenoxyacetic Acid

The susceptibility of isolated maize mitochondria to the growth regulators: 2,4-dichlorophenoxyacetic acid (2,4-D) and abscisic acid (ABA) was studied. It was found that 2,4-D (a herbicide) inhibits respiration in mitochondria, as do other herbicides or phenoxy-acids. In the entire range of concentrations used (10<sup>-3</sup>-10<sup>-9</sup> M), 2,4-D introduced into the medium before the respiration reaction was begun, or during it, limited the intensity of succinate oxidation. It did not, however, markedly change phosphorylation properties. Uncoupling of oxidative phosphorylation took place only after preincubation of mitochondria with 2,4-D and was the result of the destruction of mitochondrial membranes. ABA (a growth inhibitor of plants) caused a similar response in maize mitochondria. Preincubation of mitochondria with ABA lead to the uncoupling of oxidative phosphorylation. Whereas ABA introduced during respiration (state 4 respiration) or before its onset, lowered the oxidative potential of mitochondria, it also changed the pattern of state 4-3-4 transition after addition of ADP (it was especially visible at high concentrations), which indicates that the coupling of oxidative phosphorylation with the respiratory chain has faltered. It seems that this negative effect of 2,4-D and ABA on respiration of isolated maize mitochondria is connected with the inhibitory effect of these growth regulators on the growth of maize coleoptiles. Interference in the organization mitochondrial membranes results in a lowered supply of ATP - a source of energy needed in elongation processes.

THE UNCOUPLING OF OXIDATIVE PHOSPHORYLATION BY IONIZING RADIATION

1962 ◽  
Vol 40 (8) ◽  
pp. 1025-1042 ◽  
Author(s):  
J. F. Scaife ◽  
B. Hill
Keyword(s):  
Oxidative Phosphorylation ◽  
Liver Mitochondria ◽  
Cell Suspensions ◽  
Whole Body ◽  
X Rays ◽  
Succinate Oxidation ◽  
Mouse Ascites ◽  
Uncoupling Of Oxidative Phosphorylation

Whole body irradiation of rabbits or rats with X-rays or Co60γ-rays causes uncoupling of oxidative phosphorylation in thymus mitochondria, which is not prevented by the prior administration of AET. Whole body irradiation was not found to affect oxidative phosphorylation in liver or mouse ascites cell mitochondria. The radiation lesion can be repaired in vitro by the addition of cytochrome c, bovine serum albumin, or vitamin K1to mitochondria. Vitamin E and coenzyme Q10 were without effect. Both phosphorylating steps in the electron transport chain associated with succinate oxidation are affected by irradiation. The diphosphopyridine nucleotide dependent steps in the oxidation of α-ketoglutarate by thymus mitochondria are damaged by in vivo irradiation. Diphosphopyridine nucleotide levels of thymus and spleen but not liver or ascites cells are reduced by in vivo irradiation. No effect of in vitro irradiation on oxidative phosphorylation could be found for thymocyte cell suspensions, isolated thymus or liver mitochondria, or ascites or HeLa cell suspensions. Respiration of ascites or thymocyte cells was unaffected by in vitro irradiation.

scholarly journals Inhibitory effect of t-butyl hydroperoxide on mitochondrial oxidative phosphorylation in isolated rat hepatocytes

2007 ◽  
pp. 137-140
Author(s):  
P Křiváková ◽  
A Lábajová ◽  
Z Červinková ◽  
Z Drahota
Keyword(s):  
Oxidative Phosphorylation ◽  
Rat Hepatocytes ◽  
Inhibitory Effect ◽  
Experimental Conditions ◽  
Isolated Rat Hepatocytes ◽  
Butyl Hydroperoxide ◽  
Peroxidative Damage ◽  
Cell Energy ◽  
Uncoupling Of Oxidative Phosphorylation ◽  
Low Activity

Using high-resolution oxygraphy, we tested the changes of various parameters characterizing the mitochondrial energy provision system that were induced by peroxidative damage. In the presence of succinate as respiratory substrate, 3 mM t-butyl hydroperoxide increased respiration in the absence of ADP, which indicated partial uncoupling of oxidative phosphorylation. Low activity of coupled respiration was still maintained as indicated by the ADP-activated and oligomycin-inhibited respiration. However, during the incubation the phosphorylative capacity decreased as indicated by the continuous decrease of the mitochondrial membrane potential. Under these experimental conditions the maximum capacity of the succinate oxidase system was inhibited by 50% in comparison with values obtained in the absence of t-butyl hydroperoxide. Our data thus indicate that the oxygraphic evaluation of mitochondrial function represents a useful tool for evaluation of changes participating in peroxidative damage of cell energy metabolism.

Effect of Growth Regulators on Stomatal Structure and Development in the Cotyledons of Lagenaria leucantha (Duch.) Rusby

1975 ◽  
Vol 23 (1) ◽  
pp. 13 ◽  
Author(s):  
JA Inamdar ◽  
M Gangadhara
Keyword(s):  
Growth Regulators ◽  
Growth Inhibitor ◽  
Guard Cells ◽  
Inhibitory Effect ◽  
Subsidiary Cell ◽  
Growth Promoter ◽  
Stomatal Index ◽  
Stomatal Frequency ◽  
Growth Promoters ◽  
High Concentration

In untreated cotyledons (controls) anomocytic stomata and stomata with a single subsidiary cell were observed. In cotyledons treated with growth regulators, anisocytic, paracytic, cyclocytic and several abnormal stomatal types were observed in addition to those found in the controls. Gibberellic acid, though a growth promoter, acted as an inhibitor at high concentration. Ascorbic acid at 25 p.p.m. increased the stomatal index and the size of guard cells, while the stomatal frequency decreased. Sucrose at 2000 p.p.m. increased the stomatal index and the length of guard cells. 2,3,5-Tri-iodobenzoic acid caused degeneration of guard cells and acted as a growth inhibitor at higher concentrations. As the concentration of kinetin increased, decreases in the stomatal frequency, index and size of guard cells were noted. Kinetin also induced the formation of contiguous stomata and the division of guard cells. Sulphanilamide could act either as an inhibitor or as a promoter as its concentration increased. Coumarin at 50 p.p.m. reduced the size of guard cells and the stomatal frequency, and commonly induced persistent stomatal initials, while at 100 p.p.m. only the radicle emerged and the cotyledons failed to emerge from the seed-coat. Increased concentrations of colchicine promoted more induction of persistent stomatal initials, and inhibited stomatal formation as was evidenced by a reduced stomatal frequency and index. Colchicine at 50 p.p.m. induced formation of double pores in a stoma, abnormally large pore sizes, and increases in the size of guard cells and their nuclei. With maleic hydrazide the sizes of guard and epidermal cells were reduced and persistent stomatal initials occasionally formed. Growth promoters could sometimes interact with inhibitors to overcome their inhibitory effect, depending on the substances used in combination and their concentrations.

scholarly journals Influence of ubiquinone on the inhibitory effect of adriamycin on mitochondrial oxidative phosphorylation

1984 ◽  
Vol 217 (2) ◽  
pp. 493-498 ◽  
Author(s):  
H Muhammed ◽  
C K R Kurup
Keyword(s):  
Oxidative Phosphorylation ◽  
Rat Heart ◽  
Liver Mitochondria ◽  
Inhibitory Effect ◽  
Oxidative Activity ◽  
Mitochondrial Oxidative Phosphorylation ◽  
Succinate Oxidation ◽  
Exogenous Addition

The inhibition of succinate oxidation in both heart and liver mitochondria by the cardiotoxic anticancer antibiotic adriamycin in vitro was reversed to a large extent by exogenous ubiquinone-45. Inhibition of the oxidation of NAD+-linked substrates in heart and liver mitochondria responded differently to ubiquinone, the inhibition being reversed only in liver organelles. Administration of adriamycin inhibited oxidative phosphorylation in rat heart, kidney and liver mitochondria, the inhibition being highest in the heart organelles (about 50% for both NAD+-linked substrates and succinate). Exogenous addition of ubiquinone to mitochondria isolated from drug-treated animals did not reverse the inhibition. Administration of ubiquinone along with adriamycin did not change effectively the pattern of drug-mediated decrease in oxidative activity of the organelles, particularly in the heart.

THE UNCOUPLING OF OXIDATIVE PHOSPHORYLATION BY IONIZING RADIATION

1962 ◽  
Vol 40 (1) ◽  
pp. 1025-1042 ◽  
Author(s):  
J. F. Scaife ◽  
B. Hill
Keyword(s):  
Oxidative Phosphorylation ◽  
Liver Mitochondria ◽  
Cell Suspensions ◽  
Whole Body ◽  
X Rays ◽  
Succinate Oxidation ◽  
Mouse Ascites ◽  
Uncoupling Of Oxidative Phosphorylation

Whole body irradiation of rabbits or rats with X-rays or Co60γ-rays causes uncoupling of oxidative phosphorylation in thymus mitochondria, which is not prevented by the prior administration of AET. Whole body irradiation was not found to affect oxidative phosphorylation in liver or mouse ascites cell mitochondria. The radiation lesion can be repaired in vitro by the addition of cytochrome c, bovine serum albumin, or vitamin K1to mitochondria. Vitamin E and coenzyme Q10 were without effect. Both phosphorylating steps in the electron transport chain associated with succinate oxidation are affected by irradiation. The diphosphopyridine nucleotide dependent steps in the oxidation of α-ketoglutarate by thymus mitochondria are damaged by in vivo irradiation. Diphosphopyridine nucleotide levels of thymus and spleen but not liver or ascites cells are reduced by in vivo irradiation. No effect of in vitro irradiation on oxidative phosphorylation could be found for thymocyte cell suspensions, isolated thymus or liver mitochondria, or ascites or HeLa cell suspensions. Respiration of ascites or thymocyte cells was unaffected by in vitro irradiation.

Effect of Growth Regulators on Rooting of Magnolia grandifloraCultivars

HortScience ◽  
1998 ◽  
Vol 33 (3) ◽  
pp. 503d-503
Author(s):  
Ning Jiang ◽  
Donglin Zhang ◽  
Michael A. Dirr
Keyword(s):  
Growth Regulators ◽  
Combination Treatment ◽  
Similar Response ◽  
Combination Treatments ◽  
Rooting Of Cuttings ◽  
Root Quality

Cuttings from three southern magnolia cultivars, `Claudia Wannamaker', `Greenback™', and `Little Gem', were treated with KIBA, KNAA, and Hormodin #3, separately and in combination, at varying concentrations. The rooting of cuttings was cultivar-dependent, with `Greenback™' responding significantly to all the treatments. Only the high KNAA and combination treatments were effective with `Little Gem' and `Claudia Wannamaker'. The effect of KNAA on rooting with increasing concentration was significant. No similar response was observed with KIBA. The combination treatment with quick dip plus the talc formation produced the greatest rooting and root quality with the three cultivars. With this treatment, the average rooting rate of three cultivars was 67.4%, whereas the rooting rate of control plants was only 11.8%.

Two Enzyme Immunoassays to Screen for 2,4-Dichlorophenoxyacetic Acid in Water

1987 ◽  
Vol 70 (5) ◽  
pp. 874-878 ◽  
Author(s):  
James Fleeker
Keyword(s):  
Limit Of Detection ◽  
Solid Phase ◽  
Dichlorophenoxyacetic Acid ◽  
Carrier Protein ◽  
Similar Response ◽  
Enzyme Immunoassays ◽  
Concentration Step ◽  
Chlorophenoxyacetic Acid ◽  
Phenoxy Herbicides ◽  
2,4 Dichlorophenoxyacetic Acid

Abstract Two solid-phase enzyme immunoassays were developed to measure 2,4-dichlorophenoxyacetic acid (2,4-D), using 2 sets of structurally distinct immunogens and enzyme ligands. The 2,4-D analog, 2-methyl- 4-chlorophenoxyacetic acid (MCPA), gave a similar response with both methods, whereas other phenoxy herbicides cross-reacted differently. In method A, the aromatic moiety of 2,4-D was distal from the carrier protein and labeled enzyme, whereas in method B, the acetic acid portion of the herbicide was distal. The use of both methods to screen for this herbicide in ground water and municipal and river water reduced the number of false-positive responses. Water sources having a low background response could be monitored with either method alone. When a concentration step, with disposable C18 extraction columns, was used, the limit of sensitivity was 5 ng/L,. Method A was the more sensitive of the 2 methods with a limit of detection of 10 j*g/L without the concentration step

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