Minocycline-induced loss of potassium from erythrocytes: identification of a family with an augmented response.
The effect of several tetracycline antibiotics of human erythrocytes was examined because of previous findings that these drugs bind to erythrocyte membranes. Minocycline and cetocycline, two highly lipid-soluble analogues, but not tetracycline, induced loss of K+ from red blood cells. Loss of K+ increased linearly with time of incubation, concentration of minocycline, and temperature. The effect of minocycline was inhibited by plasma and calcium. The cells from one volunteer consistently showed an augmented response to minocycline; similar findings for family members of the volunteer suggested a dominant autosomal mode of inheritance. The only abnormality noted in the subject was mild reticulocytosis and a slightly reduced K+ content in his red blood cells. Preliminary studies did not demonstrate alterations in protein composition of his red blood cell membranes, enhanced osmotic fragility, or defects in Ca++-dependent or ouabain-sensitive (Na+-K+)-dependent adenosine triphosphatase activity. The exact site of the minocycline effect remains to be determined.
D000251:Adenosine Triphosphatases / Q000378:metabolism; D000328:Adult; D002118:Calcium / Q000494:pharmacology; D004912:Erythrocytes / Q000187:drug effects*; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D008911:Minocycline / Q000494:pharmacology*; D011188:Potassium / Q000378:metabolism*; D012964:Sodium / Q000378:metabolism; D013696:Temperature; D013754:Tetracyclines / Q000494:pharmacology*; D013997:Time Factors
D013754:Tetracyclines; D012964:Sodium; D000251:Adenosine Triphosphatases; D008911:Minocycline; D011188:Potassium; D002118:Calcium