Absorption and metabolism of three phthalate diesters by the rat small intestine

White, Russell D.; Carter, D.E.; Earnest, David L.; Mueller, John F.

doi:10.1016/0015-6264(80)90194-7

Cited by 73 publications

(31 citation statements)

References 13 publications

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“…The reproducible increase in T max and corresponding decrease in C max /D seen at the higher doses, suggests that uptake of the monoester is dose limited. This is likely due to saturation of the intestinal lipases, which convert the poorly absorbed diester to the rapidly absorbed monoester phthalate (White et al, 1980). Despite this reduced uptake, AUC/D and MRT are increased at higher doses, suggesting that metabolite clearance is also saturated.…”

Section: Discussionmentioning

confidence: 85%

Kinetics of selected di-n-butyl phthalate metabolites and fetal testosterone following repeated and single administration in pregnant rats

et al. 2009

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Section: Discussionmentioning

confidence: 85%

Kinetics of selected di-n-butyl phthalate metabolites and fetal testosterone following repeated and single administration in pregnant rats

et al. 2009

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“…Intestinal preparations from three animal species (baboon, rat, and ferret) and from humans also catalyzed the monohydrolysis of phthalate diesters, including that of DEHP to MEHP (Lake et al, 1977). It has been suggested that esterases within the mucosal epithelium actively hydrolyze DEHP (and other diesters) during absorption (White et al, 1980). In addition, cholinesterase inhibitors can significantly reduce the hydrolysis of phthalate acid esters and thus interfere with their metabolism (Heck et al, 1980).…”

Section: Metabolismmentioning

confidence: 97%

Toxicity and metabolism of monoethylhexyl phthalate and diethylhexyl phthalate: A survey of recent literature

Thomas

Northup²

1982

Journal of Toxicology and Environmental Health

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The literature dealing with monoethylhexyl phthalate (MEHP), the principal metabolite of di (2-ethylhexyl) phthalate (DEHP), a widely used plasticizer, is discussed. MEHP has been shown to be moderately toxic and, following oral administration, undergoes omega- and omega- 1 oxidation to yield the same metabolites as does DEHP. In plasma there is an equilibrium between MEHP absorbed to albumin and in free solution, whereas DEHP is bound to lipoproteins. Studies involving orally administered MEHP revealed the mild hepatic changes occurred but there was no bioaccumulation of the monoester. Studies of the rat and rabbit indicated that MEHP has no teratogenic effects.

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“…However, the concentrations of MEHP we found in human urine were lower than those of other phthalate monoesters, particularly the phthalates with fewer carbons in the alkyl side chains, despite the likely higher availability of DEHP. This could result from several factors, including differences in exposure, systemic absorption from the gastrointestinal tract (White et al 1980), metabolism (Albro and Moore 1974;Williams andBlanchfield 1974, 1975), and excretion. Phthalates with short alkyl side chains undergo oxidative metabolism to a lesser extent (Albro and Moore 1974;Williams andBlanchfield 1974, 1975), compared with phthalates with long alkyl side chains.…”

mentioning

confidence: 99%

Mono(2-ethyl-5-hydroxyhexyl) phthalate and mono-(2-ethyl-5-oxohexyl) phthalate as biomarkers for human exposure assessment to di-(2-ethylhexyl) phthalate.

Kato

Silva

Reidy

et al. 2004

Environ Health Perspect

234

134

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Exposure to di-(2-ethylhexyl) phthalate (DEHP) is prevalent based on the measurement of its hydrolytic metabolite mono-(2-ethylhexyl) phthalate (MEHP) in the urine of 78% of the general U.S. population studied in the 1999-2000 National Health and Nutrition Examination Survey (NHANES). However, despite the high level of production and use of DEHP, the urinary MEHP levels in the NHANES samples were lower than the monoester metabolites of phthalates less commonly used than DEHP, suggesting metabolic differences between phthalates. We measured MEHP and two oxidative DEHP metabolites, mono-(2-ethyl-5-oxohexyl) phthalate (MEOHP) and mono (2-ethyl-5-hydroxyhexyl) phthalate (MEHHP) to verify whether these other metabolites account for a greater proportion of DEHP metabolic products in 127 paired human urine and serum samples. We found that the urinary levels of MEHHP and MEOHP were 10-fold higher than levels of MEHP; concentrations of urinary MEOHP and MEHHP were strongly correlated (r = 0.928). We also found that the serum levels of MEOHP and MEHHP were comparatively lower than those in urine. Furthermore, the glucuronide-bound conjugates of the oxidative metabolites were the predominant form in both urine and serum. MEOHP and MEHHP cannot be formed by serum enzymes from the hydrolysis of any contamination from DEHP potentially introduced during blood collection and storage. Therefore, concentrations of MEHHP and MEOHP in serum may be a more selective measure of DEHP exposure than is MEHP. However, additional data on the absorption, distribution, metabolism, and elimination of these oxidative metabolites are needed to completely understand the extent of DEHP exposure from the serum concentrations of oxidative DEHP metabolites.

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Absorption and metabolism of three phthalate diesters by the rat small intestine

Cited by 73 publications

References 13 publications

Kinetics of selected di-n-butyl phthalate metabolites and fetal testosterone following repeated and single administration in pregnant rats

Kinetics of selected di-n-butyl phthalate metabolites and fetal testosterone following repeated and single administration in pregnant rats

Toxicity and metabolism of monoethylhexyl phthalate and diethylhexyl phthalate: A survey of recent literature

Mono(2-ethyl-5-hydroxyhexyl) phthalate and mono-(2-ethyl-5-oxohexyl) phthalate as biomarkers for human exposure assessment to di-(2-ethylhexyl) phthalate.

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