Mono- phthalate MEHP

Di-2-ethylhexyl phthalate DEHP Mono-(2-ethylhexyl) phthalate MEHP... 

Eor example, in the intestinal tract and liver of both humans and animals DEHP is rapidly hydrolyzed by esterases to yield mono-(2-ethylhexyl) phthalate (MEHP) and 2-ethylhexanol [25]. The latter metabolite is subsequently oxidized enzymatically to 2-ethyl hexanoic acid (2-EHXA) [26]. MEHP, 2-hethylhexanol, and/or their metabolites are the immediate inducers of the majority of enzymes known to be affected by exposure of DEHP [27]. Due to the high importance of the primary and secondary PAE metabolites in the human exposure smdies, during the last years a big number of smdies have been conducted to prove that some of them are appropriate biomarkers to calculate human PAE intake [28-30] and that their determination is easier than calculate it through food intake, which are more time consuming and subjects to several error sources. 

Boruchoff SA. Hypotension and cardiac arrest in rats after infusion of mono(2-ethylhexyl)phthalate (MEHP), a contaminant of stored blood. N Engl J Med 1987 316 1218-19. 

Peck, C.C., Odom, D.G, Friedman, H I., Albro, P.W., Hass, J.R., Brady, J.T. Jess, D A. (1979) Di-2-ethylhexyl phalate (DEHP) and mono-2-ethylhexyl phthalate (MEHP) accnmnlation in whole blood and red cell concentrates. Transfusion, 19, 137-146 Persson, P.E., Penttinen, H. Nnorteva, P. (1978) DEHP in the vicinity of an industrial area in Finland. Environ. Pollut., 16, 163-166... 

DEHP can break down in the presence of other chemicals to produce mono(2-ethylhexyl)-phthalate (MEHP) and 2-ethylhexanol. Many of the properties of MEHP are like those of DEHP, and therefore its fate in the environment is similar. In the presence of oxygen, DEHP in water and soil can be broken down by microorganisms to carbon dioxide and other simple... 

Responsible Metabolite. Since DEHP is metabolized to a variety of compounds following oral exposure, the question has been raised as to which of DEHP metabolites is responsible for the testicular effects of DEHP. Evidence suggests that mono(2-ethylhexyl) phthalate (MEHP) might be the toxic metabolite in the testes. In one study, 1,055 mg/kg/day of DEHP administered for 5 days to rats did not affect testicular weight or structure, but an equimolar dose of MEHP had a significant effect (Sjoberg et al. 1986a). 

Lhuguenot JC, Mitchell AM, Milner G, et al. 1985. The metabolism of di(2-ethylhexyl)phthalate (DEHP) and mono(2-ethylhexyl)phthalate (MEHP) in rats in vivo and in vitro dose and time dependency of metabolism Toxicol Appl Pharmacol 80 11-22. 

Rock G, Secours NE, Franklin CA, et al. 1978. The accumulation of mono-2-ethylhexyl phthalate (MEHP) during storage of whole blood andplasma. Transfusion 18 553-558. 

DEHP is absorbed by the oral and parenteral routes. It is not absorbed in any significant amount through intact skin. Intravenously or orally administered DEHP is rapidly metabolized to derivatives of mono-(2-ethylhexyl) phthalate (MEHP). The MEHP metabolites are mainly excreted in the urine and the bile. The estimated half-life of DEHP in humans following intravenous administration is 28 min. 

In vitro and in vivo data on Cynomolgus monkeys (Table 17.3) and other species of monkeys (i.e., marmoset and Rhesus) indicate that the key events in the PPARa activator MOA are relatively nonresponsive in monkeys. Palmitoyl-CoA oxidase activity was evaluated in monkeys after in vivo exposure to a variety of PPARa activators [e.g., bezafibrate, clofibrate, DEHP, mono-2-ethylhexyl phthalate (MEHP), fenofibrate, nafenopin, and LY171883], and changes were minimal or nonexistent relative to controls (Klaunig et al. 2003). Moreover, Cynomolgus monkeys exposed to DEHP, DINP, or clofibrate failed to exhibit an increase in cell proliferation (Doull et al. 1999 Pugh et al. 2000). Cynomolgus monkeys treated for two weeks with clinically relevant doses of the PPARa activators fenofibrate or ciproflbrate exhibited increases in the number of hepatic peroxisomes (Hoivik et al. 

D BP Di-n-butyl phthalate, MnBP Mono-n-hutyl phthalate, BBP Benzyl butyl phthalate, MBnP Monobenzyl phthalate, DEHP Di-(2-ethylhexyl) phthalate, MEHP Mono-2-ethylhexyl phthalate, DnOP Di-n-octyl phthalate, MnOP Mono-n-octyl phthalate, DiNP Di-iso-nonyl phthalate, MiNP Mono-iso-nonyl phthalate, DiDP Di-iso-deeyl phthalate, MiDP Mono-iso-decyl phthalate expressed as the number of carbon atoms in the alkyl side ehain... 

As PEs are rapidly metabolized, measurement of the metabolites is generally accepted when the amount of exposure to humans is evaluated. PEs are mainly metabolized into phthalate monoesters and excreted into the urine (Fig. 1). Albro and Lavenhar reported 30 or more metabolites of DEHP metabolism. The exposure amount of mono(2-ethylhydroxyhexyl) phthalate (MEHHP) in which mono(2-ethylhexyl) phthalate (MEHP) is subjected to oxidation by co-1 and mono(2-ethyl-5-oxohexyl) phthalate (MEOHP) that is an oxide of MEHHP, etc. has been reported. MEHP oxides such as MEHHP and MEOHP were excreted into the urine at a high ratio compared to MEHP, when they were measured after DEHP exposure.It is known that PEs other than DEHP are metabolized into the mono form. The rate of metabolism is 69% when dibutyl phthalate is metabolized into monobutyl phthalate and 73% when dibutyl benzyl phthalate is metabolized into monobutyl benzyl phthalate. Because it is considered... 

MEHP Mono(2-ethylhexyl)phthalate (2) Proton affinity... 

Studies on health effects of PAEs in humans have remained controversial due to limitations of the study design. Some findings in human populations are consistent with animal data, suggesting that PAEs and their metabolites produce toxic effects in the reproductive system. Some studies associate monoesters PAEs with semen parameters, sperm DNA damage, and hormones in human population, but none of them are statistically significant. Urinary monomethyl phthalate (MMP), monobenzyl phthalate (MBzP), mono- -butyl phthalate (MBP), MEHP, and monoethyl phthalate (MEP) were associated with poor sperm morphology and vigor, and with low sperm concentration, motility, and linearity [31-35]. However, it is not yet possible to conclude whether phthalate exposure is harmful for human reproduction. 

Induction of peroxisome proliferation following treatment with DEHP is not due to the parent compound, but to DEHP metabolites. Studies with MEHP in vitro have demonstrated that the proximate peroxisome proliferators are mono(2-ethyl-5-oxohexyl) phthalate (metabolite VI) and mono(2-ethyl-5-hydroxyhexyl) phthalate, (metabolite IX) and that for 2-ethylhexanol, the proximate proliferator is 2-ethylhexanoic acid (Elcombe and Mitchell 1986 Mitchell et al. 1985a). Similar findings were observed by Maloney and Waxman (1999), who showed that MEHP (but not DEHP) activated mouse and human PPARa and PPARy, while 2-ethylhexanoic acid activated mouse and human PPARa only, and at much higher concentrations. Based on its potency to induce enzyme activities, such as the peroxisomal fatty acid (3-oxidation cycle and carnitine acetyltransferase, DEHP might be considered a relatively weak proliferator. 

Synonyms 1,2-Benzenedicarboxylic acid, mono-(2-ethylhexyl) ester MEHP Monoethylhexyl phthalate Phthalic acid, mono-(2-ethylhexyl) ester... 

Moyer B, Hbcon ML (2012) Rejuoductive effects in FI adult females exposed in utero to moderate to high doses of mono-2-ethylhexylphthalate (MEHP). Reprod Toxicol 34(l) 43-50 National Research Council (2008) Phthalates and cumulative risk assessment the task ahead. National Academy of Sciences, http //clpub.epa.gov/ncea/cfm/recordisplay.cfm deid=202508 Download. Accessed 15 Nov 2013... 

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