The sedimentation characteristics of mitochondria from livers of mice treated with various radioprotective aminothiols were measured by techniques of density-gradient and zonal centrifugation. Treatment with cysteine, MEA, or the phosphorothioate of MEA caused the mitochondria to sediment more slowly; AET caused them to sediment more rapidly. Other compounds had no significant effect. These changes are interpreted as the result of either swelling or contraction of the mitochondrial outer membranes. None of the compounds that affected liver mitochondria had any effect on the sedimentability of mitochondria isolated from Ehrlich ascites tumor cells that had been incubated with those compounds.
When rats are transferred to a 5°C environment immediately after exposure to 400 R of x-irradiation, the rate of growth of interscapular brown fat is significantly inhibited, in comparison with that in pair-fed unirradiated cold-exposed controls. The most striking effect is on the early hyperplasia of the tissue, which in the controls is maximal after 3 days in the cold. After 3 weeks, the mass of interscapular brown fat in the irradiated animals is only slightly less than that in control rats, but the total amounts of various components of the tissue (total nitrogen, nucleic acids, phospholipids, respiratory enzymes) remain below the control level for at least 5 weeks. It seems unlikely that decreased thermogenic activity is of major importance in reducing the survival of cold-exposed irradiated rats.