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Endocrinology Vol. 138, No. 2 764-770
Copyright © 1997 by The Endocrine Society

Articles

Thyroid Hormones Regulate the Onset of Osmotic Activity of Rat Liver Mitochondria after Birth1

A. Almeida2, C. Lopez-Mediavilla and J. M. Medina

Departamento de Bioquímica y Biología Molecular, Facultad de Farmacia, Universidad de Salamanca, 37007 Salamanca, Spain

Address all correspondence and requests for reprints to: J. M. Medina, Departamento de Bioquímica y Biología Molecular, Edificio Departamental, Universidad de Salamanca, Avda Campo Charro s/n, 37007 Salamanca, Spain.

The effect of thyroid hormone deprivation on the osmotic activity of liver mitochondria from early newborn rats was studied. Experimentally induced hypothyroidism prevented the increase in the osmotic activity of mitochondria observed immediately after birth. Osmotic activity was restored by T4 and T3 treatment to hypothyroid newborns but not when this treatment was supplemented with cycloheximide. Under the same circumstances, streptomycin had no effect. Hypothyroidism abolished the change in the slope of the osmotic curve (plot of inverse absorbance of mitochondrial suspensions incubated in sucrose solutions vs. inverse sucrose concentration) observed in mitochondria from euthyroid newborns at 110–120 mOsm sucrose, suggesting that hypothyroidism prevents the formation of tight physical connections between mitochondrial outer and inner membranes. Thyroid hormone deprivation increased the passive permeability of the mitochondrial inner membrane to protons, resulting in a decreased respiratory control ratio. Hypothyroidism prevented the sharp decrease in the affinity of mitochondria for ATP observed in euthyroid newborns immediately after birth. These results corroborate our previous suggestion that, during the early neonatal period, thyroid hormones control the synthesis of some nucleus-coded protein(s) involved in the assembly of F0,F1-ATPase.




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Copyright © 1997 by The Endocrine Society