Journal of applied toxicology : JAT, 5(6), 368-371 (1985-12-01)
Di(2-ethylhexyl)phthalate (DEHP) inhibited UDP-glucuronyltransferase activity of rat liver in vitro and in vivo. Diethyl phthalate and dimethoxyethyl phthalate also inhibited this enzyme in vitro. On the other hand, DEHP did not inhibit the activity of the cytosolic enzyme N-acetyltransferase; it
Environmental monitoring and assessment, 115(1-3), 451-471 (2006-05-02)
Screening-level ecological risk assessments of di(2-ethylhexyl)phthalate (DEHP) for aquatic organisms in Japan were conducted using estimated statistical values based on surface water and sediment monitoring data and effect threshold values based on a large aquatic toxicity database. An alternative method
Journal of applied toxicology : JAT, 4(1), 35-41 (1984-02-01)
The rat foetus, in contrast with the maternal liver and placenta, has little or no ability to hydrolyse di-(2-methoxyethyl)-phthalate (DMEP) to mono-2-methoxyethyl)-phthalate (MMEP). At short times after the administration of DMEP to the dam on the 14th day of gestation
Journal of occupational health, 49(3), 172-182 (2007-06-19)
Di(2-ethylhexyl)phthalate (DEHP), a commonly used industrial plasticizer, causes liver tumorigenesis presumably via activation of peroxisome proliferator-activated receptor alpha (PPARalpha). The mechanism of DEHP tumorigenesis has not been fully elucidated, and to clarify whether DEHP tumorigenesis is induced via PPARalpha, we
The secondary metabolite of dimethoxyethyl phthalate (DMEP), methoxyacetic acid (MAA), but neither the diester nor either of its primary metabolites, monomethoxyethyl phthalate (MMEP) and 2-methoxyethanol (ME), interferes with normal growth and development of organogenesis phase rat embryos in culture. These
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