Short-term effects of di-(2-ethylhexyl) phthalate on testes, liver, kidneys and pancreas in mice

Miura, Yumi; Naito, Makoto; Ablake, Maira; Terayama, Hayato; Yi, Shuang-Qin; Qu, Ning; Cheng, Lin-xian; Suna, Shigeru; Jitsunari, Fumihiko; Itoh, Masahiro

doi:10.1111/j.1745-7262.2007.00220.x

Cited by 38 publications

(16 citation statements)

References 18 publications

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“…This increase could be attributed to impairment of the kidney functioning [20] . The significant difference in the group treated with Dehp also similar to previous work done by Raymond et al and Miura et al [21][22][23] . This is to show that combining effect of Bpaand Dehp can impede the functioning of the liver and kidney.…”

Section: Discussionsupporting

confidence: 89%

Pathophysiological Assessment of Bisephenol A and Di (2-ethylhexyl)Phthalate on Hepatic and Renal Function Parameters of Albino Wistar Rats

Omorodion¹,

Achukwu²,

Ogbuabor³

2019

Am. J. Biomed. Sci.

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The ubiquitous nature of plastics has raised concerns pertaining to continuous exposure to plastic polymers and human health risks of particular concern are the use of endocrine-disrupting chemicals (EDCs) in plastic production, including Di(2-ethylhexyl) phthalate (DEHP) and Bisphenol A (BPA). The aim of this work is to evaluate the pathological effect of bisephenol a and di(2-etylhexyl)phthalate on weight, liver and liver function parameters of albino wistar rats. An experimental study involving 60 Wistar rats was carried out. The rats were divided into four groups of 15 Wistar rat each in a group. The group I received normal rats pellet and water and served as control group, group II received 5mg/kg/day of BPA mixed with rat pellet orally, group III received 0.5mg/kg daily of DEHP mixed with rat pellet while group IV received orally mixture of 0.5mg/kg BPA and 0.5mg/kg DEHP + rat pellet. The rats were fed for 30 consecutive days after which they were sacrificed and an analysis was carried out on them. The laboratory analysis revealed significant variations in the concentration of liver function test, kidney function test and weight size in group II, III, and IV comparison with group I (control). In conclusion, the present work reveals that Bpa and Dehp alters the proper functioning of the hepatic and renal functioning and can also lead to severe weight loss.

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Section: Discussionsupporting

confidence: 89%

Pathophysiological Assessment of Bisephenol A and Di (2-ethylhexyl)Phthalate on Hepatic and Renal Function Parameters of Albino Wistar Rats

Omorodion¹,

Achukwu²,

Ogbuabor³

2019

Am. J. Biomed. Sci.

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“…It has been established that DEHP disrupts oxidative balance associated with production of a strongly oxidative damaging milieu [41], [42], increased the production of reactive oxygen species (ROS) and decreased production of protective antioxidants, as evidenced by significant decreases in glutathione peroxidase 1 (GPx1) (∼20%) and superoxide dismutase (SOD) (∼30%) activities and glutathione (GSH) levels (∼20%) in DEHP treatment (1000 mg/kg) rats [43], and might ultimately leading to carcinogenesis [44], [45]. There are several other lines of evidence relating DEHP to reproduction, such as altering the expression of several key genes in embryonic zinc homeostasis [46], inhibited equine oocyte maturation [47] and blocked mouse follicle growth through an oxidative stress pathway [48].…”

Section: Discussionmentioning

confidence: 99%

The Effects of Di-(2-ethylhexyl)-phthalate Exposure on Fertilization and Embryonic Development In Vitro and Testicular Genomic Mutation In Vivo

Huang

et al. 2012

PLoS ONE

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The present study was undertaken to determine the reproductive hazards of Di-(2-ethylhexyl)-phthalate (DEHP) on mouse spermatozoa and embryos in vitro and genomic changes in vivo. Direct low-level DEHP exposure (1 μg/ml) on spermatozoa and embryos was investigated by in vitro fertilization (IVF) process, culture of preimplanted embryos in DEHP-supplemented medium and embryo transfer to achieve full term development. Big Blue® transgenic mouse model was employed to evaluate the mutagenesis of testicular genome with in vivo exposure concentration of DEHP (500 mg/kg/day). Generally, DEHP-treated spermatozoa (1 μg/ml, 30 min) presented reduced fertilization ability (P<0.05) and the resultant embryos had decreased developmental potential compared to DMSO controls (P<0.05). Meanwhile, the transferred 2-cell stage embryos derived from treated spermatozoa also exhibited decreased birth rate than that of control (P<0.05). When fertilized oocytes or 2-cell stage embryos were recovered by in vivo fertilization (without treatment) and then exposed to DEHP, the subsequent development proceed to blastocysts was different, fertilized oocytes were significantly affected (P<0.05) whereas developmental progression of 2-cell stage embryos was similar to controls (P>0.05). Testes of the Big Blue® transgenic mice treated with DEHP for 4 weeks indicated an approximately 3-fold increase in genomic DNA mutation frequency compared with controls (P<0.05). These findings unveiled the hazardous effects of direct low-level exposure of DEHP on spermatozoa's fertilization ability as well as embryonic development, and proved that in vivo DEHP exposure posed mutagenic risks in the reproductive organ – at least in testes, are of great concern to human male reproductive health.

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“…For example, adult male C57BL/6 mice exposed to perfluorooctanoic acid (PFOA), a POP used industrially as a surfactant, exhibited reduced adipose mass [51], while the fungicide triphenyltin (fentin, TPT) attenuated weight gain in golden hamsters [52]. Likewise, other models examining the metabolic effects of DEHP have shown protection from diet-induced obesity in C57BL/6J mice [53], weight loss in male Crlj:CD1 mice [54], and reduced weight gain and adipose mass in male Wistar rats [55,56]. Collectively, these studies suggest that a structurally and functionally diverse array of environmental contaminants have the capacity to modulate body weight and fat mass; however, much less is known about the mechanisms by which these compounds act to promote alterations in adipose mass or function.…”

Section: Edcs Promote Adiposity and Weight Gain In Animal Modelsmentioning

confidence: 99%

Adipocytes under assault: Environmental disruption of adipose physiology

Regnier

Sargis

2014

Biochimica et Biophysica Acta (BBA) - Molecular Basis of Diseas

106

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The burgeoning obesity epidemic has placed enormous strains on individual and societal health mandating a careful search for pathogenic factors, including the contributions made by endocrine disrupting chemicals (EDCs). In addition to evidence that some exogenous chemicals have the capacity to modulate classical hormonal signaling axes, there is mounting evidence that several EDCs can also disrupt metabolic pathways and alter energy homeostasis. Adipose tissue appears to be a particularly important target of these metabolic disruptions. A diverse array of compounds has been shown to alter adipocyte differentiation, and several EDCs have been shown to modulate adipocyte physiology, including adipocytic insulin action and adipokine secretion. This rapidly emerging evidence demonstrating that environmental contaminants alter adipocyte function emphasizes the potential role that disruption of adipose physiology by EDCs may play in the global epidemic of metabolic disease. Further work is required to better characterize the molecular targets responsible for mediating the effects of EDCs on adipose tissue. Improved understanding of the precise signaling pathways altered by exposure to environmental contaminants will enhance our understanding of which chemicals pose a threat to metabolic health and how those compounds synergize with lifestyle factors to promote obesity and its associated complications. This knowledge may also improve our capacity to predict which synthetic compounds may alter energy homeostasis before they are released into the environment while also providing critical evidentiary support for efforts to restrict the production and use of chemicals that pose the greatest threat to human metabolic health.

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Short-term effects of di-(2-ethylhexyl) phthalate on testes, liver, kidneys and pancreas in mice

Abstract: The results indicate that DEHP-induced aspermatogenesis is caused by the high sensitivity of the testicular tissues to MEHP rather than the specific accumulation or uptake of circulating MEHP into the testes.

Cited by 38 publications

References 18 publications

Pathophysiological Assessment of Bisephenol A and Di (2-ethylhexyl)Phthalate on Hepatic and Renal Function Parameters of Albino Wistar Rats

Pathophysiological Assessment of Bisephenol A and Di (2-ethylhexyl)Phthalate on Hepatic and Renal Function Parameters of Albino Wistar Rats

The Effects of Di-(2-ethylhexyl)-phthalate Exposure on Fertilization and Embryonic Development In Vitro and Testicular Genomic Mutation In Vivo

Adipocytes under assault: Environmental disruption of adipose physiology

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