Abstract
Male rats were given daily injections of 200 μg/kg I-thyroxine, s.c., for a period of 10 days. Monoamine oxidase (MAO) activities in the heart, lung and liver mitochondria decreased rapidly to about 50% those of the control rats with 5-HT and β-phenylethylamine (β-PEA) as substrates on the first day. After that, heart MAO activity increased gradually and exceeded the control value after 10 days with 5-HT as the substrate. The level of liver MAO activity was maintained at about 50-70% during the same period of administration with 5-HT as the substrate. The thyroxine treated rats showed no marked change in brain MAO activity. In vitro, I-thyroxine and its metabolites had no discriminative actions on MAO activities in these organs of rats. The heart, lung and liver MAO have unaltered Km values for 5-HT and β-PEA, but decreases in the Vmax for both substrates were observed between the control and I-thyroxine-treated rats. Addition of the brain, heart and liver cytosol fractions from I-thyroxine treated rats caused MAO activities of heart mitochondria to decrease with 5-HT as a substrate and caused them to increase with β-PEA as a substrate. MAO activities in liver also were inhibited by adding all the cytosols when β-PEA was the substrate, but on the contrary, lung MAO activities were increased when 5-HT was the substrate. These results indicate the possible presence of multiple modulators of MAO in the cytosol fractions of I-thyroxine treated rats.
