HYPOTHYROIDISM PREVENTS POSTNATAL CHANGES IN RAT-LIVER MITOCHONDRIAL POPULATIONS DEFINED BY RHODAMINE-123 STAINING

The effect of hypothyroidism on the percentages of low fluorescence po pulation (LFP) and high fluorescence population (HFP) rhodamine-123-st ained mitochondria, respiratory parameters, and ATPase activity were s tudied in liver mitochondria from early newborn rats. Hypothyroidism p revented the decrease in the percentage of HFP and the subsequent incr ease in LFP that occurs immediately after birth. This effect coincides with the impairment of mitochondrial respiratory function, as shown b y the low respiratory control ratio and the low activity of F0,F1-ATPa se found in hypothyroid newborns. All of these changes were reversed b y the administration of thyroid hormones. ATP in vitro promotes the co nversion of HFP into LFP and increases the respiratory control ratio i n hypothyroid newborns, although this effect was not observed after th yroid hormone treatment. The effect of thyroid hormones on both the po stnatal changes in mitochondrial populations and in F0,F1-ATPase activ ity was prevented by cycloheximide, but not by streptomycin. Thus, the observed effects of thyroid hormones on neonatal mitochondria must be ac complished by the induction of the synthesis of some nuclei-coded protein, possibly involved in F0,F1-ATPase assembly.