Mechanism of the formation of megamitochondria by copper-chelating agents. V. Further studies on isolated megamitochondria.
Effect of cuprizone has been studied on some biochemical properties of megamitochondria obtained from the mouse liver. (1) Contents of Ca2+, Mg2+ and Cu2+ in the blood or the liver homogenates were not altered by cuprizone intoxication, whereas those in liver mitochondria were significantly altered: after 3-4 days' intoxication, content of Ca2+ was decreased and was remarkably increased after 14-15 days' intoxication. Content of Mg2+ behaved contrarily. (2) Both cytochrome oxidase and ATPase activities were unchanged in the liver megamitochondria, but monoamine oxidase (MAO) activity was significantly decreased. Value of I50 (50% inhibition) for MAO was determined to be 0.33 mM using the control liver mitochondria. Cuprizone had almost no effect on MAO activity of kidney or heart mitochondria both in vivo and in vitro. (3) The amount of lysolecithin was increased in the liver megamitochondria. These results were discussed in the light of membrane fusion phenomenon which plays a key role in the mechanism of megamitochondrial formation.
D000251:Adenosine Triphosphatases / Q000032:analysis; D000818:Animals; D003471:Cuprizone / Q000494:pharmacology*; D003510:Cyclohexanes / Q000494:pharmacology*; D003576:Electron Transport Complex IV / Q000032:analysis; D066298:In Vitro Techniques; D008297:Male; D008670:Metals / Q000032:analysis; D051379:Mice; D008930:Mitochondria, Liver / Q000032:analysis / Q000187:drug effects / Q000648:ultrastructure*; D010743:Phospholipids / Q000032:analysis
D003510:Cyclohexanes; D008670:Metals; D010743:Phospholipids; D003471:Cuprizone; D003576:Electron Transport Complex IV; D000251:Adenosine Triphosphatases