Kinemuchi H, Sunami Y, Sudo M, Suh Y H, Arai Y, Kamijo K
Comp Biochem Physiol C Comp Pharmacol Toxicol. 1985;80(2):245-52. doi: 10.1016/0742-8413(85)90050-7.
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.
用甲乙酮（MEK）或曲拉通X-100处理鲤鱼肝脏线粒体，然后用高氯酸盐处理使其脱脂，可大大降低单胺氧化酶（MAO）的活性。仅用曲拉通X-100处理导致活性降低较少。无论采用何种处理，剩余活性的米氏常数（Km）值相似。发现曲拉通X-100处理后的残渣和磷脂酶C处理的鲤鱼脑线粒体中剩余活性对氯吉兰和左旋丙炔苯丙胺的敏感性未发生变化，但MEK处理后的残渣中剩余活性的敏感性同样降低。未获得证据表明所采用的处理通过改变线粒体脂质环境将鲤鱼MAO转化为MAO-A或MAO-B。
