The effect of ions and ionophores on cystine egress from human leucocyte lysosome-rich granular fraction.
This paper describes the stimulation of exodus of cystine from lysosome-rich granular fractions by potassium. Potassium permeability into lysosomes is low, but in the presence of an ionophore or permeable anion, the movement of K+ into lysosomes caused a large stimulation of cystine exodus. Lysosomal preparations from leucocytes of cystinotic patients, which lack carrier-mediated cystine transport, also manifested stimulation of cystine egress by valinomycin and K+. This suggests that potassium-dependent cystine egress involves a carrier different from that defective in cystinosis, or occurs through a non-carrier-mediated mechanism.
D002414:Cations, Monovalent; D002463:Cell Membrane Permeability; D003553:Cystine / Q000097:blood*; D003554:Cystinosis / Q000097:blood; D003594:Cytoplasmic Granules / Q000378:metabolism*; D006801:Humans; D007962:Leukocytes / Q000187:drug effects / Q000648:ultrastructure*; D008247:Lysosomes / Q000378:metabolism*; D009550:Nigericin / Q000494:pharmacology; D011188:Potassium / Q000378:metabolism / Q000494:pharmacology*; D014634:Valinomycin / Q000494:pharmacology
D002414:Cations, Monovalent; D014634:Valinomycin; D003553:Cystine; D009550:Nigericin; D011188:Potassium