Identification of a Toxic Mechanism of the Plasticizers, Phtahlic Acid Esters, which are Putative Endocrine Disrupters: Time-dependent Increase in Quinolinic Acid and Its Metabolites in…

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  • FUKUWATARI Tsutomu
    <i>Laboratory of Food Science and Nutrition, Department of Life Style Studies, School of Human Cultures, The University of Shiga Prefecture</i>
  • SUZUKI Yuko
    <i>Laboratory of Food Science and Nutrition, Department of Life Style Studies, School of Human Cultures, The University of Shiga Prefecture</i>
  • SUGIMOTO Etsuro
    <i>Laboratory of Food Science and Nutrition, Department of Life Style Studies, School of Human Cultures, The University of Shiga Prefecture</i>
  • SHIBATA Katsumi
    <i>Laboratory of Food Science and Nutrition, Department of Life Style Studies, School of Human Cultures, The University of Shiga Prefecture</i>

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  • Identification of a Toxic Mechanism of the Plasticizers, Phtahlic Acid Esters, which are Putative Endocrine Disrupters: Time-dependent Increase in Quinolinic Acid and Its Metabolites in Rats Fed di(2-ethylhexyl)phthalate.

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  We have reported that the administration of di(2-ethylhexyl)phthalate (DEHP) increased the formations of quinolinic acid (QA) and its lower metabolites on the tryptophan-niacin pathway. To discover the mechanism involved in disruption of the tryptophan-niacin pathway by DEHP, we assessed the daily urinary excretion of QA and its lower metabolites, and enzyme activities on the tryptophan-niacin pathway. Rats were fed with a niacin-free, 20% casein diet or the same diet supplemented with 0.1% DEHP or 0.043% phthalic acid and 0.067% 2-ethylhexanol added for 21 days. Feeding of DEHP increased the urinary excretions of QA and its lower metabolites in a time-dependent manner, and the increase of these excretions reached a peak at 11 days, but feeding of phthalic acid and 2-ethylhexanol had no effect. Feeding of DEHP, however, did not affect any enzyme activity including α-amino-β-carboxymuconate-ε-semialdehyde decarboxylase (ACMSD), affecting the formation of QA, on the tryptophan-niacin pathway.<br>

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