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di 2 ethylhexyl phthalate/zea mays
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Pagina 1 a partire dal 72 risultati
Di-2-ethylhexyl phthalate in thermally oxidized corn oil.
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Relative sensitivity of developmental and immune parameters in juvenile versus adult male rats after exposure to di(2-ethylhexyl) phthalate.
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The developing immune system displays a relatively high sensitivity as compared to both general toxicity parameters and to the adult immune system. In this study we have performed such comparisons using di(2-ethylhexyl) phthalate (DEHP) as a model compound. DEHP is the most abundant phthalate in the
Exposure to di-(2-ethylhexyl) phthalate transgenerationally alters anxiety-like behavior and amygdala gene expression in adult male and female mice.
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Phthalates are industrial plasticizers and stabilizers commonly found in polyvinyl chloride plastic and consumer products, including food packaging, cosmetics, medical devices, and children's toys. Di-(2-ethylhexyl) phthalate (DEHP), one of the most commonly used phthalates, exhibits
Effects of Di(2-ethylhexyl)phthalate on Bone Metabolism in Ovariectomized Mice.
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[Effects of in utero exposure to di(2-ethylhexyl) phthalate on sexual development in female offspring].
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OBJECTIVE
To evaluate the ability of di(2-ethylhexyl) phthalate (DEHP) with inducing damage in sexual development of female offspring rats after maternal exposure.
METHODS
On gestational day (GD) 12, pregnant Wistar rats were weighed, encoded and randomly assigned to 5 groups (10 dams per group).
[Effects of di-(2-ethylhexyl) phthalate exposure on reproductive development and PPARs in prepubertal female rats].
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OBJECTIVE
To investigate the effects of di-(2-ethylhexyl) phthalate (DEHP) exposure on pubertal development and reproductive endocrine function in prepubertal female rats and its possible mechanisms.
METHODS
40 female SD rats at 3-week-old were randomly divided into a control group (corn oil) and
Citrate ester substitutes for di-2-ethylhexyl phthalate: In vivo reproductive and in vitro cytotoxicity assessments
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Di-2-ethylhexyl phthalate (DEHP) is frequently used as a plasticizer for wrapping films, in toys, and in medical devices. Previous studies demonstrated that DEHP in mouse reduced testicular and epididymis weights, suppressed levels of serum testosterone, luteinizing hormone, and follicle-stimulating
Exposure to di(2-ethylhexyl) phthalate and diisononyl phthalate during adulthood disrupts hormones and ovarian folliculogenesis throughout the prime reproductive life of the mouse.
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Di(2-ethylhexyl) phthalate (DEHP) is a phthalate commonly used for its plasticizing capabilities. Because of the wide production and use of DEHP, humans are exposed to DEHP on a daily basis. Diisononyl phthalate (DiNP) is often used as a DEHP replacement chemical, and because of the increased use of
Opposite effects of high- and low-dose di-(2-ethylhexyl) phthalate (DEHP) exposure on puberty onset, oestrous cycle regularity and hypothalamic kisspeptin expression in female rats.
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Di-(2-ethylhexyl) phthalate (DEHP) is ubiquitous in the environment and has been proposed to lead to reproductive disruption. In this study, we systematically investigated the effects of different doses of DEHP exposure on female hypothalamic-pituitary-gonadal axis development. Female Sprague-Dawley
Adverse effects of di-(2-ethylhexyl) phthalate on Leydig cell regeneration in the adult rat testis.
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The objective of the present study is to determine whether di-(2-ethylhexyl) phthalate (DEHP) exposure at adulthood affects regeneration of rat Leydig cells. 90-day-old Long-Evans rats received intraperitoneal injection of 75 mg/kg ethane dimethanesulfonate (EDS) to eliminate mature Leydig cells,
Di(2-ethylhexyl) phthalate induces apoptosis through peroxisome proliferators-activated receptor-gamma and ERK 1/2 activation in testis of Sprague-Dawley rats.
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Di(2-ethylhexyl) phthalate (DEHP) is a well-known hepatic and reproductive toxicant whose toxicity may be mediated by peroxisome proliferators-activated receptor (PPAR). This study examined the effects of DEHP on the expression of PPAR-regulated genes involved in testicular cells apoptosis.
From the Cover: Teratogenic Effects of in Utero Exposure to Di-(2-Ethylhexyl)-Phthalate (DEHP) in B6:129S4 Mice.
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Intrauterine exposure to phthalates is known to cause disorders of male reproductive function including androgen insufficiency, decreased fertility, and germ cell defects in rodents. In this study, we set out to investigate the effects of intrauterine exposure to di-(2-ethylhexyl)-phthalate (DEHP)
Placental P-glycoprotein inhibition enhances susceptibility to Di-(2-ethylhexyl)-phthalate induced cardiac malformations in mice: A possibly promising target for congenital heart defects prevention.
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Nonadditive developmental toxicity in mixtures of trichloroethylene, Di(2-ethylhexyl) phthalate, and heptachlor in a 5 x 5 x 5 design.
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In order to identify nonadditive effects on development, three compounds were combined using five dosages of each agent (a 5 x 5 x 5 full-bacterial design). Trichloroethylene (TCE), di(2-ethylhexyl) phthalate (DEHP), and heptachlor (HEPT), in corn oil, were administered by gavage to Fischer-344 rats
Gene expression in rat placenta after exposure to di(2-ethylhexyl) phthalate
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The organic compound di(2-ethylhexyl) phthalate (DEHP) is widely used as a plasticizer in many products. Exposure to DEHP has been reported to lead to adverse pregnancy outcomes by suppressing placenta growth and development. The aim of this study was to determine the gene expression profiles of rat
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