Erythrocytes may play a role in the blood transport of thyroid hormones. There is probably some link between changes in parameters of red blood cell uptake and depression. Thyroxin (T4) enters the erythrocyte by free diffusion, while L-T3 by facilitated diffusion through a membrane carrier - mediated system which is saturable, stereospecific, energy and Na + -independent. Red blood cells (RBC) act as a circulating pool of triiodthyronine. In erythrocytes L-tryptophan shares the same transport system for L-T3 (named the T system). L-T3 and L-tryptophan interact as competitive inhibitors. In depressive patients we suppose that impaired RBC L-T3 uptake results in RBC L-tryptophan uptake and L-tryptophan plasma availibility and thus cerebral synthesis of serotonin is impaired. Changes in kinetic parameters correlate with treatment with antidepressants and non-respondents can be distinguished from respondents. Resistance to treatment with antidepressants and changes in kinetic parameters can be due to changes of lipid structure of the RBS membrane, in case the transport protein is lipid - dependent.

        Key words: thyroid hormones, erythrocyte, transport, depression.