Glycerol transport in human red cells.
The kinetics of 14C-glycerol exchange was studied in human red cells. Glycerol appeared to be transported by two mechanisms: (i) by facilitated diffusion with permeability depending on glycerol concentration, and (ii) by an unspecific pathway, presumably representing the diffusion of individual glycerol molecules through the membrane with permeability independent of glycerol concentration. The latter permeability was 8 X 10(-8) cm/s at 20 degrees C, it was independent of pH, and had an activation energy of 25 kcal/mol. The facilitated transport of glycerol was completely inhibited by Cu++, and the activation energy was low, about 10 kcal/mol. The transport system was competitively inhibited by H+, reacting with at least three hydrogen analogue, as well as dimethylsulfoxide (a hydrogen bonding molecule with no structural resemblance to glycerol), inhibited glycerol transport competitively. Steins "dimerizer hypothesis" was revised according to our findings. A kinetic scheme describing the reactions of a transport controlling site with glycerol is presented in the Appendix. It is demonstrated in the article that the scheme accounts for out experimental results.
D001692:Biological Transport / Q000187:drug effects; D002463:Cell Membrane Permeability / Q000187:drug effects; D003300:Copper / Q000494:pharmacology; D004912:Erythrocytes / Q000378:metabolism*; D005990:Glycerol / Q000097:blood*; D006801:Humans; D006863:Hydrogen-Ion Concentration; D011409:Propylene Glycols / Q000494:pharmacology; D013454:Sulfoxides / Q000494:pharmacology; D013696:Temperature
D011409:Propylene Glycols; D013454:Sulfoxides; D003300:Copper; D005990:Glycerol