Iodothyronamines are Oxidatively Deaminated to Iodothyroacetic Acids in vivo

Authors

  • Warren J. L. Wood Dr.,

    1. Department of Physiology and Pharmacology, Oregon Health and Science University, 3181 SW Sam Jackson Park Road, Mail Code L334, Portland, OR 97239 (USA), Fax: (+1) 503-494-4352
    2. Department of Chemistry, University of Portland, 5000 N. Willamette Blvd, Portland, OR 97203 (USA)
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  • Travis Geraci,

    1. Department of Physiology and Pharmacology, Oregon Health and Science University, 3181 SW Sam Jackson Park Road, Mail Code L334, Portland, OR 97239 (USA), Fax: (+1) 503-494-4352
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  • Aaron Nilsen Dr.,

    1. Department of Physiology and Pharmacology, Oregon Health and Science University, 3181 SW Sam Jackson Park Road, Mail Code L334, Portland, OR 97239 (USA), Fax: (+1) 503-494-4352
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  • Andrea E. DeBarber Dr.,

    1. Department of Physiology and Pharmacology, Oregon Health and Science University, 3181 SW Sam Jackson Park Road, Mail Code L334, Portland, OR 97239 (USA), Fax: (+1) 503-494-4352
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  • Thomas S. Scanlan Prof.

    1. Department of Physiology and Pharmacology, Oregon Health and Science University, 3181 SW Sam Jackson Park Road, Mail Code L334, Portland, OR 97239 (USA), Fax: (+1) 503-494-4352
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Abstract

3-Iodothyronamine (T1AM) and 3,3′,5-triiodothyroacetic acid (Triac) are bioactive metabolites of the hormone thyroxine (T4). In the present study, the ability of T1AM and 3,3′,5-triiodothyronamine (T3AM) to be metabolized to 3-iodothyroacetic acid (TA1) and Triac, respectively, was investigated. Both T1AM and T3AM were converted to their respective iodinated thyroacetic acid analogues in both cell and tissue extracts. This conversion could be significantly inhibited with the monamine oxidase (MAO) and semicarbazide-sensitive amine oxidase (SSAO) inhibitor iproniazid. TA1 was found to be present in trace quantities in human serum and in substantial levels in serum from T1AM-treated rats. These results demonstrate that iodothyronamines are substrates for amine oxidases and that this metabolism may be the source of the corresponding endogenous arylacetic acid products Triac and TA1.

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