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Peroxisome induction studies on di(2-ethylhexyl)terephthalate.

D C Topping, G P Ford, J G Evans

    Toxicology and Industrial Health
    |June 1, 1987
    PubMed
    Summary

    Di(2-ethylhexyl)terephthalate (DEHT) showed minimal effects on rat liver and metabolism at high doses, unlike di(2-ethylhexyl)phthalate (DEHP). DEHT

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    Area of Science:

    • Toxicology
    • Metabolism
    • Hepatology

    Background:

    • Di(2-ethylhexyl)phthalate (DEHP) is known to induce peroxisome proliferation.
    • Understanding the toxicological profile of alternative plasticizers like di(2-ethylhexyl)terephthalate (DEHT) is crucial.

    Purpose of the Study:

    • To compare the effects of DEHT and DEHP on rat liver and lipid metabolism.
    • To investigate the dose-dependent toxicity and metabolic fate of DEHT.

    Main Methods:

    • Rats were fed diets containing 0% to 2.5% DEHT or 1.2% DEHP for 21 days.
    • Evaluated feed consumption, body weight gain, serum lipids, enzyme activities, and hepatic peroxisome proliferation.
    • Analyzed DEHT metabolism in rats.

    Main Results:

    • DEHT caused decreased feed consumption and weight gain only at 2.5%, with minimal impact on liver weight and peroxisomes.
    • DEHP at 1.2% significantly increased liver weight, lipid metabolism enzymes, and peroxisome content.
    • DEHT metabolism yields 2-ethylhexanol and terephthalic acid, with 2-ethylhexanol being less potent in peroxisome induction than DEHP metabolites.

    Conclusions:

    • DEHT exhibits a lower potential for peroxisome proliferation and liver effects compared to DEHP.
    • Metabolic differences, particularly the lower production of active metabolites from DEHT, explain the observed toxicological disparities.

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