Endogenous thyrocyte-produced nitric oxide inhibits iodide uptake and thyroid-specific gene expression in FRTL-5 thyroid cells

FOZZATTI L; VÉLEZ ML; LUCERO AM; NICOLA JP; MACCIÓ DR; PELLIZAS CG; ROTH GA; MASINI-REPISO AM

Society for Endocrinology

Lugar: Bristol, UK; Año: 2007 vol. 192 p. 627 - 627

font size="2" face="AdvPS800D"> Nitric oxide (NO) is a free radical that mediates a wide array of cell functions. It is generated from L-arginine by NO-synthase (NOS). Expression of NOS isoforms has been demonstrated in thyroid cells. Previous reports indicated that NO donors induce dedifferentiation in thyrocytes. However, the functional significance of endogenous thyrocyte-produced NO has not been explored. This work aimed to study the influence of endogenous NO on parameters of thyroid cell function and differentiation in FRTL-5 cells. We observed that treatment with the NOS inhibitor, Nu-nitro- L-arginine methyl ester (L-NAME), increased the TSHstimul