The entry of glycerol molecules in unphosphorylated form into mitochondria was studied. The effective binding of glycerol with membranes of rat liver mitochondria was demonstrated using spectrofluorimetry and FTIR spectroscopy. It was shown using polarography and turbidimetry that glycerol at low concentrations ​​(0.1–0.4 mM) increased the permeability of the inner membrane for NADH and succinate, while at high concentrations it severely damaged the membranes. Glycerol at low concentrations increased oxygen consumption by intact mitochondria in an isotonic medium with NADH or succinate, while at high concentrations it inhibited oxygen consumption. In a hypotonic medium, glycerol instantly inhibited NADH dehydrogenase, while it did not inhibit succinate dehydrogenase. The data we obtained allowed us to conclude that glycerol can be transported into mitochondria not only in the form of glycerophosphate, but directly by itself (passively along the concentration gradient). It was hypothesized that glycerol interacts with lipids and proteins and forms channels in the inner membrane for the its permeation and that of the substrates.

研究了未磷酸化形式的甘油分子进入线粒体。使用荧光分光光度法和 FTIR 光谱法证明了甘油与大鼠肝线粒体膜的有效结合。使用极谱法和比浊法表明，低浓度（0.1-0.4 mM）的甘油增加了内膜对 NADH 和琥珀酸盐的渗透性，而在高浓度下，它严重损坏了膜。在含有 NADH 或琥珀酸盐的等渗介质中，低浓度的甘油会增加完整线粒体的耗氧量，而在高浓度时，它会抑制耗氧量。在低渗介质中，甘油立即抑制 NADH 脱氢酶，但不抑制琥珀酸脱氢酶。我们获得的数据使我们得出结论，甘油不仅可以以甘油磷酸的形式运输到线粒体中，而且可以直接运输到线粒体中（被动地沿着浓度梯度）。假设甘油与脂质和蛋白质相互作用并在内膜中形成通道以供其渗透和底物渗透。