Effects of Triazines on Energy Relations of Mitochondria and Chloroplasts

The effects of eights-triazines on respiration of (Phaseolus vulgarisL. ‘Black Valentine’) bean and rat liver mitochondria and on cyclic photophosphorylation of pea (Pisum sativumL. ‘Thomas Laxton’) chloroplasts were determined. All triazines inhibited state 3 respiration and cyclic photophosphorylation. The degree of inhibition was similar in both rat liver and bean mitochondria. Prometryne [2,4-bis-(isopropylamino)-6-(methylthio)-s-triazine] was the most potent inhibitor of both respiration and cyclic photophosphorylation. Triazines with the methylthio group showed the most activity, followed by those with the methoxy and chloro substituents in that order.

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Mitochondrial Swelling Induced by Glutathione

The Journal of Cell Biology ◽

10.1083/jcb.5.1.109 ◽

1959 ◽

Vol 5 (1) ◽

pp. 109-116 ◽

Cited By ~ 78

Author(s):

Albert L. Lehninger ◽

Marion Schneider

Keyword(s):

Rat Liver ◽

Potent Inhibitor ◽

Reduced Glutathione ◽

Liver Mitochondria ◽

Rat Liver Mitochondria ◽

Respiratory Inhibitors ◽

Oxidation Reduction ◽

Optimum Ph ◽

High Concentrations

Reduced glutathione, in concentrations approximating those occurring in intact rat liver, causes swelling of rat liver mitochondria in vitro which is different in kinetics and extent from that yielded by L-thyroxine. The effect is also given by cysteine, which is more active, and reduced coenzyme A, but not by L-ascorbate, cystine, or oxidized glutathione. The optimum pH is 6.5, whereas thyroxine-induced swelling is optimal at pH 7.5. The GSH-induced swelling is not inhibited by DNP or dicumarol, nor by high concentrations of sucrose, serum albumin, or polyvinylpyrrolidone, in contrast to thyroxine-induced swelling. ATP inhibits the GSH swelling, but ADP and AMP are ineffective. Mn-+ is a very potent inhibitor, but Mg++ is ineffective. Ethylenediaminetetraacetate is also an effective inhibitor of GSH-induced swelling. The respiratory inhibitors amytal and antimycin A do not inhibit the swelling action of GSH, but cyanide does; these findings are consistent with the view that the oxidation-reduction state of the respiratory chain between cytochrome c and oxygen is a determinant of GSH-induced swelling. Reversal of GSH-induced swelling by osmotic means or by ATP in KCl media could not be observed. Large losses of nucleotides and protein occur during the swelling by GSH, suggesting that the action is irreversible. The characteristically drastic swelling action of GSH could be prevented if L-thyroxine was also present in the medium.

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The inhibition by fluorocitrate of rat liver mitochondrial and extramitochondrial aconitate hydratase

Biochemical Journal ◽

10.1042/bj1130853 ◽

1969 ◽

Vol 113 (5) ◽

pp. 853-860 ◽

Cited By ~ 27

Author(s):

Valentina Guarriera-Bobyleva ◽

P. Buffa

Keyword(s):

Rat Liver ◽

Liver Cell ◽

Potent Inhibitor ◽

Liver Mitochondria ◽

Rat Liver Mitochondria ◽

Aconitate Hydratase ◽

Weak Inhibitor ◽

Respiratory State

1. The effects of synthetic fluorocitrate were studied on: (a) the oxidation of citrate and cis-aconitate by rat liver mitochondria; (b) the activity of the aconitate hydratase found in the liver cell sap; (c) the activity of the aconitate hydratase solubilized from liver mitochondria. 2. Fluorocitrate was found to be a potent inhibitor of oxidation of citrate but only a weak inhibitor of oxidation of cis-aconitate: 6·7μm-fluorocitrate (containing 4% of the inhibitory isomer) caused 94% inhibition of the oxidation of citrate (2mm) whereas 1·0mm-fluorocitrate was necessary to provoke the same inhibition when cis-aconitate (2mm) was the substrate. The degree of inhibition varied in relation to the respiratory state of mitochondria when fluorocitrate was added. The inhibition could be partially reversed by cis-aconitate. 3. The aconitate hydratase extracted from the mitochondria was much less inhibited by fluorocitrate than was the mitochondria-bound enzyme, and the aconitate hydratase found in the cell sap was even less sensitive. 0·3mm-Fluorocitrate was required to cause 50% inhibition of the reaction citrate→cis-aconitate, catalysed by the aconitate hydratase extracted from the mitochondria, and 1·2m-fluorocitrate for the extramitochondrial enzyme. For both enzymes the reaction citrate→cis-aconitate was 2–3 times more sensitive to fluorocitrate than was the reaction isocitrate→cis-aconitate. The inhibition was of the competitive type for both reactions.

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Effects of 5-5'-Diphenyl-2-thiohydantoin (DPTH) and Thyroxine on the Ultrastructure and Chemical Composition of Rat Liver

Proceedings, annual meeting, Electron Microscopy Society of America ◽

10.1017/s0424820100066917 ◽

1971 ◽

Vol 29 ◽

pp. 570-571

Author(s):

E. A. Elfont ◽

R. B. Tobin ◽

D. G. Colton ◽

M. A. Mehlman

Keyword(s):

Chemical Composition ◽

Rat Liver ◽

Future Study ◽

Mode Of Action ◽

Liver Mitochondria ◽

Rat Liver Mitochondria ◽

Effective Inhibitor ◽

Biochemical Effects ◽

Glycerophosphate Dehydrogenase ◽

Stimulation Of

Summary5,-5'-diphenyl-2-thiohydantoin (DPTH) is an effective inhibitor of thyroxine (T4) stimulation of α-glycerophosphate dehydrogenase in rat liver mitochondria. Because this finding indicated a possible tool for future study of the mode of action of thyroxine, the ultrastructural and biochemical effects of DPTH and/or thyroxine on rat liver mere investigated.Rats were fed either standard or DPTH (0.06%) diet for 30 days before T4 (250 ug/kg/day) was injected. Injection of T4 occurred daily for 10 days prior to sacrifice. After removal of the liver and kidneys, part of the tissue was frozen at -50°C for later biocheailcal analyses, while the rest was prefixed in buffered 3.5X glutaraldehyde (390 mOs) and post-fixed in buffered 1Z OsO4 (376 mOs). Tissues were embedded in Araldlte 502 and the sections examined in a Zeiss EM 9S.Hepatocytes from hyperthyroid rats (Fig. 2) demonstrated enlarged and more numerous mitochondria than those of controls (Fig. 1). Glycogen was almost totally absent from the cytoplasm of the T4-treated rats.

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