Thyronamines T(0)AM and T(1)AM are naturally occurring decarboxylated thyroid 
hormone derivatives. Their in vivo administration induces effects opposite to 
those induced by thyroid hormone, including lowering of body temperature. Since 
the mitochondrial energy-transduction apparatus is known to be a potential 
target of thyroid hormone and its derivatives, we investigated the in vitro 
effects of T(0)AM and T(1)AM on the rates of O(2) consumption and H(2)O(2) 
release by rat liver mitochondria. Hypothyroid animals were used because of the 
low levels of endogenous thyronamines. We found that both compounds are able to 
reduce mitochondrial O(2) consumption and increase H(2)O(2) release. The 
observed changes could be explained by a partial block, operated by 
thyronamines, at a site located near the site of action of antimycin A. This 
hypothesis was confirmed by the observation that thyronamines reduced the 
activity of Complex III where the site of antimycin action is located. Because 
thyronamines exerted their effects at concentrations comparable to those found 
in hepatic tissue, it is conceivable that they can affect in vivo mitochondrial 
O(2) consumption and H(2)O(2) production acting as modulators of thyroid hormone 
action.