Sixteen Wistar rats were studied in the last week of pregnancy. Another group of 6 nonpregnant animals served as control. Eight pregnant and 6 control ratas were kept in the cold room at 4-degrees-C for 4 days, while 8 pregnant rats remained at 22-degrees-C. After blocking the thyroid gland with potassium perchlorate to prevent iodine reutilization, a dose of 4-mu-Ci of I-125-T3 was injected i.p. Thereafter, animals were placed in individual metabolic cages for separate 24 h collection of urine and feces. Heparinized blood samples were obtained at 4, 14,24 and 28 h following tracer injection. Pregnant rats exposed to cold had a significant increase in T3 fractional turnover as compared to pregnants at 22-degrees-C (p < 0.005) and to controls at 4-degrees-C (p < 0.02). No changes were observed in space of distribution, serum concentration and body pool of T3. Degradation of this hormone, however, was significantly augmented (p < 0.05) in pregnants at 4-degrees-C as compared to ps at 22-degrees-C, although not when compared to controls at 4-degrees-C. The urinary excretion of I-125 was increased in pregnants in the cold (p < 0.005) versus pregnants at 22-degrees-C. The metabolic (p < 0.005), urinary (p < 0.001) and fecal (p < 0.05) clearances in pregnants at 4-degrees-C were augmented with respect to the other two groups. The results show and acceleration of the peripheral metabolism of T3 during pregnancy and cold exposure, which may derive from changes in deiodination of T3 in maternal as well as fetal tissues in order to adapt to the increased caloric requirements at 4-degrees-C.