X. Moreau et al., Kinetics of red blood cell T3 uptake in hypothyroidism with or without hormonal replacement, in the rat, J ENDOC INV, 22(4), 1999, pp. 257-261
L-triiodothyronine (L-T3) is taken up and accumulated into red blood cells
(RBC) by means of a specific carrier-mediated system. The aim of this study
was to evaluate the reactivity of this system in relation to induced alter
ations in thyroid hormone (TH) supply. We investigated the kinetic paramete
rs (Vmax, maximal velocity and Km, Michaelis constant) of washed-RBC L-T3 u
ptake 1) in thyroidectomized (TXT)) rats, 2) in TXT rats administered with
low doses of L-T4 (15 mu g/kg/day x 14) to restore normal serum TH levels (
REPL), 3) in TXT rats administered with high doses of L-T4 (200 mu g/kg/day
x14) to achieve a large increase in serum TH levels (HIGH). Serum free T3 a
nd T4 levels were significantly decreased in TXT rats (2.4 and 8.8 fold, re
spectively), not different in REPL rats and significantly increased in HIGH
rats (2.4 and 3 fold, respectively) compared to sham-operated rats (SHAM).
Both kinetics of RBC L-T3 uptake were significantly increased in TXT rats
(Vmax+/-SE in pmol/min/10(8) cells=235.1+/-11.1, p<0.05 and Km+/-SE in nM=1
90.1+/-9.0, p<0.05), not different in REPL rats (Vmax=184.8+/-7.6 and Km=15
1.9+/-7.1) and significantly decreased in HIGH rats (Vmax=168.0+/-4.1, p<0.
01 and Km=131.9+/-4.6, p<0.01) compared to SHAM rats (Vmax=197.7+/-5.8 and
Km=160.9+/-6.1). These results show that kinetics of RBC L-T3 uptake are mo
dified in response to defect or excess in circulating TH levels. Since RBC
play likely a role of a buffer system, the changes in carrier-mediated infl
ux of L-T3 could be seen as a compensatory mechanism that counteract the di
sturbances in the TH availability for the target tissues. (J. Endocrinol. I
nvest. 22: 257-261, 1999) (C)1999, Editrice Kurtis.