Thyroxine antagonism

Particular attention is given to the development of new mechanistic biomarker assays and bioassays that can be used as indices of the toxicity of mixtures. These biomarker assays are typically based on toxic mechanisms such as brain acetylcholinesterase inhibition, vitamin K antagonism, thyroxin antagonism, Ah-receptor-mediated toxicity, and interaction with the estrogenic receptor. They can give integrative measures of the toxicity of mixtures of compounds where the components of the mixture share the same mode of action. They can also give evidence of potentiation as well as additive toxicity. 

Cocaine produces hyperpyrexia in mammals, due to increased heat production, by the motor excitement and rise of basal metabolic rate, reinforced by the convulsions. It probably acts directly on the midbrain temperature centers. Cocaine lowers the temperature of birds. Procaine lowers the temperature of mammals by increasing heat loss. It is antagonized by thyroxin and by dinitrophenol. 

Larval growth antagonizes effects of thyroxine on metamorphosis. 

In the plasma, increased levels of /3-endorphin, epinephrine, norepinephrine, corticosterone, ACTH, renin, and angiotensin I and decreased levels of growth hormone, thyroxine, triiodothyronine, and thyrotropin were reported with high caffeine doses. The mechanisms responsible for these various effects are largely unknown, and the mediation of adenosine receptors is suggested. The antagonism of benzodiazepine at the receptor level is observed at lower caffeine concentrations (0.5-0.7mM) than those required for phosphodiesterase inhibition. 

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