Petrov V V
Institute of Biochemistry, Moscow, USSR.
Arch Microbiol. 1990;153(6):580-4. doi: 10.1007/BF00245268.
Addition of ethanol and some other primary alcohols, except methanol, to cells and protoplasts (but not membrane particles) considerably stimulated the rate of oxygen consumption. This additional respiration was strongly inhibited by 0.1 mM KCN. The cyanide inhibition curve of endogenous substrate oxidation was slightly biphasic while in the presence of ethanol it became clearly biphasic having Ki values of approx. 0.1 and 0.5 mM. Based on the steady-state cytochrome spectra in the presence of 0.1 mM KCN, we attributed the lower Ki to cytochrome a602. Proteolysis of protoplasts external membrane proteins did not change the rate of endogeneous substrate oxidation but prevented the inhibition of this respiration by low concentrations of KCN and stimulation of oxygen consumption by ethanol. The activity of NAD(+)-dependent ethanol dehydrogenase in the cytoplasm was found to be 520 nmol NADH- x min-1 x mg-1 protein. Proteolysis of external membrane proteins apparently inhibits the operation of the cytochrome a602-containing electron transport branch inducing the suppression of electron flow from NADH to oxygen.
向细胞和原生质体(而非膜颗粒)中添加乙醇及除甲醇外的其他一些伯醇,可显著刺激耗氧速率。这种额外的呼吸作用受到0.1 mM KCN的强烈抑制。内源性底物氧化的氰化物抑制曲线略显双相,而在乙醇存在时则明显呈双相,其Ki值约为0.1和0.5 mM。基于在0.1 mM KCN存在下的稳态细胞色素光谱,我们将较低的Ki归因于细胞色素a602。原生质体外膜蛋白的蛋白水解并未改变内源性底物氧化的速率,但可防止低浓度KCN对这种呼吸作用的抑制以及乙醇对耗氧的刺激。发现细胞质中依赖NAD(+)的乙醇脱氢酶活性为520 nmol NADH·min⁻¹·mg⁻¹蛋白。外膜蛋白的蛋白水解显然抑制了含细胞色素a602的电子传递分支的运作,从而导致从NADH到氧的电子流受到抑制。