Antiandrogenic effects in male rats perinatally exposed to a mixture of di(2-ethylhexyl) phthalate and di(2-ethylhexyl) adipate

Jarfelt, Kirsten; Dalgaard, Majken; Hass, Ulla; Borch, Julie; Jacobsen, Helene; Ladefoged, Ole

doi:10.1016/j.reprotox.2004.11.005

Cited by 108 publications

(64 citation statements)

References 23 publications

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“…Perinatal exposure to certain phthalates leads to anti-androgenic effects such as reduced anogenital distance (AGD), retained nipples, hypospadias, undescended testes, epididymal agenesis and low sperm counts in male rats [2][3][4]. These four phthalates have been classified for reproductive toxicity in the European Union, and are therefore prohibited for use in cosmetics, some food contact materials, toys and childcare articles.…”

Section: Introductionmentioning

confidence: 99%

Reproductive and behavioral effects of diisononyl phthalate (DINP) in perinatally exposed rats

Boberg¹,

Christiansen²,

Axelstad³

et al. 2011

Reproductive Toxicology

144

121

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Section: Introductionmentioning

confidence: 99%

Reproductive and behavioral effects of diisononyl phthalate (DINP) in perinatally exposed rats

Boberg¹,

Christiansen²,

Axelstad³

et al. 2011

Reproductive Toxicology

144

121

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“…The cauda epididymis was thawed, weighed, and prepared as described by Jarfelt et al (2005), and samples were analyzed using a 10! u.v.…”

Section: Sperm Count Analysismentioning

confidence: 99%

“…The presence of dysgenetic tubules in testis in exposed groups is a finding that is commonly seen with exposure to certain phthalates including DEHP and DBP (Jarfelt et al 2005, Mahood et al 2007, and these effects are assumed to be related to the phthalate content of the mixture, but are not directly related to the sperm count reduction.…”

Section: Reproductive Aging In Malesmentioning

confidence: 99%

Late-life effects on rat reproductive system after developmental exposure to mixtures of endocrine disrupters

et al. 2014

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This study examined late-life effects of perinatal exposure of rats to a mixture of endocrine-disrupting contaminants. Four groups of 14 time-mated Wistar rats were exposed by gavage from gestation day 7 to pup day 22 to a mixture of 13 anti-androgenic and estrogenic chemicals including phthalates, pesticides, u.v.-filters, bisphenol A, parabens, and the drug paracetamol. The groups received vehicle (control), a mixture of all 13 chemicals at 150-times (TotalMix150) or 450-times (TotalMix450) high-end human exposure, or 450-times a mixture of nine predominantly anti-androgenic chemicals (AAMix450). Onset of puberty and estrous cyclicity at 9 and 12 months of age were assessed. Few female offspring showed significantly regular estrus cyclicity at 12 months of age in the TotalMix450 and AAMix450 groups compared with controls. In 19-month-old male offspring, epididymal sperm counts were lower than controls, and in ventral prostate an overrepresentation of findings related to hyperplasia was observed in exposed groups compared with controls, particularly in the group dosed with anti-androgens. A higher incidence of pituitary adenoma at 19 months of age was found in males and females in the AAMix450 group. Developmental exposure of rats to the highest dose of a human-relevant mixture of endocrine disrupters induced adverse effects late in life, manifested as earlier female reproductive senescence, reduced sperm counts, higher score for prostate atypical hyperplasia, and higher incidence of pituitary tumors. These delayed effects highlight the need for further studies on the role of endocrine disrupters in hormone-related disorders in aging humans.

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“…DEHP is rapidly metabolized to its major metabolite mono(2-ethylhexyl)phthalate (MEHP) in liver, and MEHP is even more toxic than the parent compound. DEHP disturbs the quality and/or quantity of sperms, induces testicular atrophy in rodents (Parks et al, 2000;Jarfelt et al, 2005;Borch et al, 2006;Erkekoglu et al, 2011), and was shown to increase p21 expression in rat testis (Ryu et al, 2007). MEHP was reported to selectively induce oxidative stress and release cytochrome c from mitochondria in germ cells, thereby inducing apoptosis of spermatocytes and causing testicular atrophy (Kasahara et al, 2002).…”

Section: Introductionmentioning

confidence: 99%

Induction of ROS, p53, p21 in DEHP- and MEHP-exposed LNCaP cells-protection by selenium compounds

Erkekoğlu

Rachidi

Yuzugullu

et al. 2011

Food and Chemical Toxicology

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Keywords: DEHP MEHP p53 p21 ROS Selenium a b s t r a c t This study was designed to investigate the hypothesis that the toxic effects of di(2-ethylhexyl)phthalate (DEHP), the most abundantly used plasticizer and ubiquitous environmental contaminant that cause alterations in endocrine and spermatogenic functions in animals is mediated through the induction of reactive oxygen species (ROS) and activation of nuclear p53 and p21 proteins in LNCaP human prostate adenocarcinoma cell line. Protective effects of two selenocompounds, sodium selenite (SS) and selenomethionine (SM) were also examined. It was demonstrated that 24 h exposure of the cells to 3 mM DEHP or its main metabolite, mono(2-ethylhexyl)phthalate (MEHP, 3 lM) caused strongly amplified production of ROS. Both SS (30 nM) and SM (10 lM) supplementations reduced ROS production, and p53 and p21 activation that induced significantly only by MEHP-exposure. The overall results of this study indicated that the induction of oxidative stress is one of the important mechanisms underlying the toxicity of DEHP and this is mainly through the effects of the metabolite, MEHP. Generated data also emphasized the critical role of Se in modulation of intracellular redox status, implicating the importance of the appropriate Se status in cellular response against testicular toxicity of phthalates.

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Antiandrogenic effects in male rats perinatally exposed to a mixture of di(2-ethylhexyl) phthalate and di(2-ethylhexyl) adipate

Cited by 108 publications

References 23 publications

Reproductive and behavioral effects of diisononyl phthalate (DINP) in perinatally exposed rats

Reproductive and behavioral effects of diisononyl phthalate (DINP) in perinatally exposed rats

Late-life effects on rat reproductive system after developmental exposure to mixtures of endocrine disrupters

Induction of ROS, p53, p21 in DEHP- and MEHP-exposed LNCaP cells-protection by selenium compounds

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