The Structural Specificity of the Nucleotide-Binding Site and the Reversible Nature of the Inhibition of Proton Conductance Induced by Bound Nucleotides in Brown-Adipose-Tissue Mitochondria

1977 ◽  
Vol 5 (1) ◽  
pp. 210-212 ◽  
Author(s):  
G. M. HEATON ◽  
D. G. NICHOLLS
Keyword(s):  
Adipose Tissue ◽  
Brown Adipose Tissue ◽  
Binding Site ◽  
Nucleotide Binding ◽  
Nucleotide Binding Site ◽  
Proton Conductance ◽  
Structural Specificity ◽  
Brown Adipose ◽  
Reversible Nature

Increased purine nucleotide binding, altered polypeptide composition, and thermogenesis in brown adipose tissue mitochondria of cold-acclimated rats

1978 ◽  
Vol 56 (6) ◽  
pp. 378-383 ◽  
Author(s):  
M. Desautels ◽  
G. Zaror-Behrens ◽  
J. Himms-Hagen
Keyword(s):  
Adipose Tissue ◽  
Brown Adipose Tissue ◽  
Nucleotide Binding ◽  
Proton Conductance ◽  
Purine Nucleotide ◽  
Polypeptide Composition ◽  
Purine Nucleotides ◽  
Brown Adipose ◽  
Simultaneous Decrease ◽  
Thermogenic Capacity

Rapid increases in atractyloside-insensitive binding of purine nucleotides (ADP or GDP) and in a polypeptide of 32 000 occur in brown adipose tissue mitochondria of the rat during acclimation to cold. The increased binding is apparent within 1 h and reaches a maximum after 3–7 days of exposure to 4 °C. The increase in the 32 000 peptide occurs more slowly and reaches a maximum after 2–3 weeks. There is a simultaneous decrease in a polypeptide of 96 000, apparent after 1 day and reaching a maximum after 1–2 weeks. Results are interpreted in terms of the appearance of an increased amount of the purine nucleotide-sensitive proton conductance pathway in association with the development of an enhanced thermogenic capacity of brown adipose tissue mitochondria during acclimation of the rat to cold.

Roles of noradrenaline and protein synthesis in the cold-induced increase in purine nucleotide binding by rat brown adipose tissue mitochondria

1979 ◽  
Vol 57 (6) ◽  
pp. 968-976 ◽  
Author(s):  
Michel Desautels ◽  
Jean Himms-Hagen
Keyword(s):  
Protein Synthesis ◽  
Adipose Tissue ◽  
Cold Stress ◽  
Brown Adipose Tissue ◽  
Cold Exposure ◽  
Intravenous Infusion ◽  
Nucleotide Binding ◽  
Proton Conductance ◽  
Purine Nucleotide ◽  
Brown Adipose

Exposure of a rat to cold (4 °C) is known to induce a biphasic change in brown adipose tissue mitochondria, believed to reflect alterations in the thermogenic, purine nucleotide sensitive proton conductance pathway; an initial rapid and large increase in purine nucleotide binding, unaccompanied by any marked change in the 32 000 polypeptide which is the binding site for these nucleotides, is followed by a slower increase in concentration of the 32 000 polypeptide accompanied by a further increase in purine nucleotide binding. The initial rapid effect of cold stress was mimicked by intravenous infusion of noradrenaline; neither the effect of cold exposure for 24 h nor the effect of intravenous infusion of noradrenaline was prevented by cycloheximide. In contrast, the slow adaptive changes in the mitochondria did not occur in response to prolonged (2 weeks) treatment with noradrenaline, although such treatment did induce the expected tissue hypertrophy accompanied by mitochondrial proliferation. Cold-induced (1 week) increases in purine nucleotide binding and 32 000 polypeptide were not prevented by oxytetracycline. The increase in purine nucleotide binding during the 2nd day of cold exposure was prevented by cycloheximide. The effect of cycloheximide on the increase in the 32 000 polypeptide could not be assessed because sufficiently long-term experiments could not be done with this compound. Thus, the initial response to cold stress appears to involve unmasking of mitochondrial proton conductance pathway sites, most probably mediated by noradrenaline. The slower adaptive response occurs in parallel with tissue hypertrophy, which itself may be mediated by noradrenaline, and appears to require cytosolic but not mitochondrial protein synthesis. However, the changes in mitochondrial composition which result in an increased concentration of proton conductance pathway sites are not mediated by noradrenaline.

scholarly journals Oxidative phosphorylation. The specific binding of trimethyltin and triethyltin to rat liver mitochondria

1970 ◽  
Vol 118 (1) ◽  
pp. 171-179 ◽  
Author(s):  
W. N. Aldridge ◽  
B. W. Street
Keyword(s):  
Adipose Tissue ◽  
Oxidative Phosphorylation ◽  
Brown Adipose Tissue ◽  
Binding Site ◽  
Rat Liver ◽  
Specific Binding ◽  
Liver Mitochondria ◽  
Rat Liver Mitochondria ◽  
Affinity Constants ◽  
Brown Adipose

1. The binding of trimethyltin and triethyltin to rat liver mitochondria was determined and the results were analysed by the method of Scatchard (1949). 2. One binding site (site 1) has the correct characteristics for the site to which trimethyltin and triethyltin are attached when they inhibit oxidative phosphorylation. For each compound the concentration of site 1 is 0.8nmol/mg of protein and the ratios of their affinity constants are the same as the ratio of the concentrations inhibiting oxidative phosphorylation. 3. Binding site 1 is present in a fraction derived from mitochondria containing only 15% of the original protein. In this preparation ultrasonication rapidly destroyed site 1. 4. Dimethyltin and diethyltin do not prevent binding of triethyltin to rat liver mitochondria, whereas triethyl-lead does. 5. Trimethyltin and triethyltin bind to mitochondria from brown adipose tissue and the results indicate a binding site 1 similar to that in rat liver mitochondria. 6. The advantages and limitations of this approach to the study of inhibitors are discussed.

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