Multiple monoamine oxidases in rat liver mitochondria

1970 ◽  
Vol 48 (6) ◽  
pp. 659-663 ◽  
Author(s):  
L. Sierens ◽  
A. D'Iorio

Indirect evidence from the kinetics of oxidative deamination is presented for the existence of two different monoamine oxidases in rat liver mitochondria. The enzymes can be differentiated on the basis of their affinities for benzylamine and serotonin. Electrophoretic separation yielded two fractions, each with the characteristics predicted from the kinetic experiments.

1973 ◽  
Vol 134 (4) ◽  
pp. 1023-1029 ◽  
Author(s):  
Norah M. Bradford ◽  
J. D. McGivan

1. The kinetics of glutamate transport into mitochondria were determined by using Bromocresol Purple to terminate the transport process. 2. Glutamate transport was found to have a Vmax. of 9.1nmol/min per mg of protein at pH6.9 and 20°C; the Km for glutamate was 4mm. 3. The rate of glutamate deamination in intact mitochondria was tenfold slower than in disrupted mitochondria. 4. These results suggest that glutamate deamination may be controlled by the rate of glutamate transport. Possible consequences of these findings are discussed.


Biochemistry ◽  
1979 ◽  
Vol 18 (26) ◽  
pp. 5972-5978 ◽  
Author(s):  
Marco Bragadin ◽  
Tullio Pozzan ◽  
Giovanni Felice Azzone

Biochemistry ◽  
1979 ◽  
Vol 18 (12) ◽  
pp. 2590-2595 ◽  
Author(s):  
Joyce Johnson Diwan ◽  
Michel Daze ◽  
Ronald Richardson ◽  
David Aronson

FEBS Letters ◽  
1971 ◽  
Vol 13 (2) ◽  
pp. 92-94 ◽  
Author(s):  
H. Bugany ◽  
L. Flohe ◽  
U. Weser

1972 ◽  
Vol 129 (1) ◽  
pp. 39-54 ◽  
Author(s):  
P. C. Holland ◽  
H. S. A. Sherratt

1. The hypoglycaemic compound diphenyleneiodonium causes rapid and extensive swelling of rat liver mitochondria suspended in 150mm-NH4Cl, and in 150mm-KCl in the presence of 2,4-dinitrophenol and valinomycin. This indicates that diphenyleneiodonium catalyses a compulsory exchange of OH-for Cl-across the mitochondrial inner membrane. Br-and SCN-were the only other anions found whose exchange for OH-is catalysed by diphenyleneiodonium. 2. Diphenyleneiodonium inhibited state 3 respiration of mitochondria and slightly stimulated state 4 respiration with succinate or glutamate as substrate in a standard Cl--containing medium. 3. Diphenyleneiodonium did not inhibit state 3 respiration significantly in two Cl--free media (based on glycerol 2-phosphate or sucrose) but caused some stimulation of state 4. 4. In Cl--containing medium diphenyleneiodonium only slightly inhibited the 2,4-dinitrophenol-stimulated adenosine triphosphatase and it had little effect in the absence of Cl-. 5. The inhibition of respiration in the presence of Cl-is dependent on the Cl-–OH-exchange. 2,4-Dichlorodiphenyleneiodonium is ten times as active as diphenyleneiodonium both in causing swelling of mitochondria suspended in 150mm-NH4Cl and in inhibiting state 3 respiration in Cl--containing medium. Indirect evidence suggests that the Cl-–OH-exchange impairs the rate of uptake of substrate anions. 6. It is proposed that stimulation of state 4 respiration in the absence of Cl-depends, at least in part, on an electrogenic uptake of diphenyleneiodonium cations. 7. Tripropyl-lead acetate, methylmercuric iodide and nine substituted diphenyleneiodonium derivatives also catalyse Cl-–OH-exchange across the mitochondrial membrane. 8. Diphenyleneiodonium is compared with the trialkyltin compounds, which are also known to mediate Cl-–OH-exchange and which have in addition strong oligomycin-like effects on respiration. It is concluded that diphenyleneiodonium is specific for catalysing anion–OH-exchange and will be a useful reagent for investigating membrane-dependent systems.


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