Membrane lipid environment of carp brain and liver mitochondrial monoamine oxidase.
Delipidation of carp liver mitochondria by treatment with methyl ethyl ketone (MEK) or Triton X-100 and then perchlorate greatly reduced MAO activities. Treatment with only Triton X-100 resulted in less reduction in activity. The Km values of the remaining activities were similar regardless of these treatments. The sensitivities towards clorgyline and l-deprenyl of the remaining activity in the Triton X-100-treated residue and the phospholipase C-treated carp brain mitochondria were found to be unchanged, but those of the activity remaining in the MEK-treated residue were similarly decreased. No evidence was obtained suggesting conversion of carp MAO to either MAO-A or MAO-B by the modification of the mitochondrial lipid environment by the treatments employed.
Kinemuchi
H
H
Sunami
Y
Y
Sudo
M
M
Suh
Y H
YH
Arai
Y
Y
Kamijo
K
K
D000818:Animals; D001921:Brain / Q000201:enzymology; D002074:Butanones / Q000494:pharmacology; D002347:Carps / Q000378:metabolism*; D003530:Cyprinidae / Q000378:metabolism*; D007700:Kinetics; D008563:Membrane Lipids / Q000378:metabolism; D008930:Mitochondria, Liver / Q000378:metabolism; D008995:Monoamine Oxidase / Q000378:metabolism*; D008996:Monoamine Oxidase Inhibitors / Q000494:pharmacology; D011092:Polyethylene Glycols / Q000494:pharmacology; D013379:Substrate Specificity; D010738:Type C Phospholipases / Q000494:pharmacology
D002074:Butanones; D008563:Membrane Lipids; D008996:Monoamine Oxidase Inhibitors; D011092:Polyethylene Glycols; C005222:methylethyl ketone; D008995:Monoamine Oxidase; D010738:Type C Phospholipases