Decrease in the Concentration of Vitamin E in Blood and Tissues Caused by Di(2‐Ethylhexyl) Phthalate, a Commonly Used Plasticizer in Blood Storage Bags and Medical Tubing

Manojkumar, V; Nair, K.G. Padmakumaran; Santhosh, Anitha; Deepadevi, K.V.; Arun, P.; Lakshmi, L. R.; Kurup, Parameswara Achutha

doi:10.1046/j.1423-0410.1998.7520139.x

Cited by 25 publications

(14 citation statements)

References 22 publications

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“…In Experiment 1, the addition of DEHP at any used concentration did not affect mt distribution pattern, intracellular ROS localization, apparent energy status and mt/ROS colocalization whereas it increased ROS levels. This observation prompted us to hypothesize that the DEHP-induced ooplasmic ROS levels increase could be responsible for altered oocyte maturation, also in agreement with previous studies reporting that oxidative stress may be an important mechanism underlying the toxic effects of DEHP [18]-[20]. However, 0.12 µM was the only dose that inhibited oocyte maturation while all tested doses increased ooplasmic ROS levels.…”

Section: Discussionsupporting

confidence: 88%

“…It has been reported that oxidative stress (OS) may be an important mechanism underlying the toxic effects of DEHP [16]-[18]. Oxidative stress occurs if disequilibrium between reactive oxygen species (ROS) production and antioxidative capacity of the cell takes place [19] and it has also been implicated in the etiology of some forms of female infertility [20].…”

Section: Introductionmentioning

confidence: 99%

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In Vitro Acute Exposure to DEHP Affects Oocyte Meiotic Maturation, Energy and Oxidative Stress Parameters in a Large Animal Model

et al. 2011

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Phthalates are ubiquitous environmental contaminants because of their use in plastics and other common consumer products. Di-(2-ethylhexyl) phthalate (DEHP) is the most abundant phthalate and it impairs fertility by acting as an endocrine disruptor. The aim of the present study was to analyze the effects of in vitro acute exposure to DEHP on oocyte maturation, energy and oxidative status in the horse, a large animal model. Cumulus cell (CC) apoptosis and oxidative status were also investigated. Cumulus-oocyte complexes from the ovaries of slaughtered mares were cultured in vitro in presence of 0.12, 12 and 1200 µM DEHP. After in vitro maturation (IVM), CCs were removed and evaluated for apoptosis (cytological assessment and TUNEL) and intracellular reactive oxygen species (ROS) levels. Oocytes were evaluated for nuclear chromatin configuration. Matured (Metaphase II stage; MII) oocytes were further evaluated for cytoplasmic energy and oxidative parameters. DEHP significantly inhibited oocyte maturation when added at low doses (0.12 µM; P<0.05). This effect was related to increased CC apoptosis (P<0.001) and reduced ROS levels (P<0.0001). At higher doses (12 and 1200 µM), DEHP induced apoptosis (P<0.0001) and ROS increase (P<0.0001) in CCs without affecting oocyte maturation. In DEHP-exposed MII oocytes, mitochondrial distribution patterns, apparent energy status (MitoTracker fluorescence intensity), intracellular ROS localization and levels, mt/ROS colocalization and total SOD activity did not vary, whereas increased ATP content (P<0.05), possibly of glycolytic origin, was found. Co-treatment with N-Acetyl-Cysteine reversed apoptosis and efficiently scavenged excessive ROS in DEHP-treated CCs without enhancing oocyte maturation. In conclusion, acute in vitro exposure to DEHP inhibits equine oocyte maturation without altering ooplasmic energy and oxidative stress parameters in matured oocytes which retain the potential to be fertilized and develop into embryos even though further studies are necessary to confirm this possibility.

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Section: Discussionsupporting

confidence: 88%

Section: Introductionmentioning

confidence: 99%

In Vitro Acute Exposure to DEHP Affects Oocyte Meiotic Maturation, Energy and Oxidative Stress Parameters in a Large Animal Model

et al. 2011

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“…Because some studies have suggested that DEHP-induced elevation of oxidative stress contributes to hepatotoxicity and testicular toxicity (23)(24)(25), the influence of oxidative stress in DEHP-induced glomerulonephritis was examined. Immunoblot analysis showed that total amounts of 4-HNE-modified proteins, a lipid peroxidation marker, were increased markedly and dosage dependently in glomeruli of DEHP-exposed PPAR␣-null mice at 22 mo but increased only mildly in exposed wild-type mice ( Figure 5A).…”

Section: Dehp Elevates Oxidative Stress In Glomerulimentioning

confidence: 99%

Peroxisome Proliferator–Activated Receptor α Protects against Glomerulonephritis Induced by Long-Term Exposure to the Plasticizer Di-(2-Ethylhexyl)Phthalate

Kamijo¹,

Hora²,

Nakajima³

et al. 2007

Journal of the American Society of Nephrology

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Safety concerns about di-(2-ethylhexyl)phthalate (DEHP), a plasticizer and a probable endocrine disruptor, have attracted considerable public attention, but there are few studies about long-term exposure to DEHP. DEHP toxicity is thought to involve peroxisome proliferator-activated receptor ␣ (PPAR␣), but this contention remains controversial. For investigation of the long-term toxicity of DEHP and determination of whether PPAR␣ mediates toxicity, wild-type and PPAR␣-null mice were fed a diet that contained 0.05 or 0.01% DEHP for 22 mo. PPAR␣-null mice that were exposed to DEHP exhibited prominent immune complex glomerulonephritis, most likely related to elevated glomerular oxidative stress. Elevated NADPH oxidase, low antioxidant enzymes, and absence of the PPAR␣-dependent anti-inflammatory effects that normally antagonize the NFB signaling pathway accompanied the glomerulonephritis in PPAR␣-null mice. The results reported here indicate that PPAR␣ protects against the nephrotoxic effects of long-term exposure to DEHP. , a probable endocrine disruptor, is used widely as a plasticizer for production of many types of polyvinyl chloride (PVC) consumer products. DEHP provides PVC items with the desired mechanical properties, including flexibility and strength. The presence of DEHP in the environment has been confirmed, as has product-related human exposure to DEHP; recent safety assessments of DEHP thereby have attracted much public interest (1). DEHP continually enters the human body via food, water, and the atmosphere. Moreover, substantial human exposure to DEHP occurs via PVC-containing medical devices that are used in intravenous therapy, enteral and parenteral nutrition support, blood transfusion, hemodialysis, cardiopulmonary bypass, and extracorporeal membrane oxygenation (2). Maximal medical exposure has been estimated to be near the US no-observed-adverse-effect level (3.7 to 14 mg/kg body wt per d). Many previous experimental animal studies yielded no obvious evidence of DEHP toxicities at these low exposure levels, but periods of exposure in the studies generally were brief. Long-term exposure to DEHP is important for safety assessment of real-world toxicity.Past experimental animal studies using short-term exposure to high-dosage DEHP have demonstrated hepatotoxicity, testicular toxicity, renal toxicity, developmental disturbance, reproductive toxicity, and teratogenicity (3-5). The peroxisome proliferator-activated receptor ␣ (PPAR␣), a member of the steroid/nuclear receptor superfamily of ligand-dependent transcription factors, has been implicated as a causative factor in these toxicities (6). PPAR␣ is expressed abundantly in the rodent liver, testis, kidney, heart, digestive tract, and retina (7) and participates in diverse physiologic functions, including maintenance of lipid and glucose homeostasis (8 -11), regulation of cell proliferation (12), and modulation of inflammatory responses (13). In humans, some ligands for this receptor, termed peroxisome proliferators, are used clinically as hypolipid...

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“…In addition, histological damage in testis, kidney and liver during pregnancy and suckling [63], cryptorchidism after prenatal exposition [64] and persistent thyroid hyperactivity [65] were observed. Then, polycystic kidney disease and a decrease in kidney function [66,67] as well as a dose-dependent decrease of cell viability in kidney epithelial cells [68], hypotension and cardiac arrest [69], decrease in the concentration of vitamin E in liver and testis [70] and finally peroxisome proliferation in liver, kidney and brain [71][72][73][74] were also reported. …”

Section: Evidence Of Toxicity In Experimental Animalsmentioning

confidence: 99%

“…In 1995 Smith et al [47] observed acute toxicity in cultured human lung fibroblasts, probably subsequent to the synergistic action of plasticizer and stabilizer, while in 1998 Fischer et al [79] showed a dose-dependent impairment in leukocyte oxidative metabolism in vitro. More recently, an increase in lipid peroxidation of erythrocytes and consequent hemolysis, presumably due to oxidative damage to the cell membrane, as well as a decrease in the concentration of vitamin E in blood stored in DEHP-plasticized bags have been reported [70,80,81].…”

Section: Evidence Of Toxicity In Human Tissues and Biological Fluidsmentioning

confidence: 99%

Potential Hazards of Exposure to Di-(2-Ethylhexyl)-Phthalate in Babies

Latini

2000

Neonatology

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Many plastic items are made of polyvinylchloride (PVC) blended with plasticizers. The most frequently used plasticizer is di-(2-ethylhexyl)-phthalate (DEHP). DEHP migrates at a constant rate from plastics to the environment: it has been detected in water, soil and food and is therefore considered as a widespread environmental contaminant. Over the past several years, a number of publications concerning toxic effects of DEHP on animals and humans have been reported. Although DEHP is suggested to be of low acute toxicity, long-term exposure, especially in human beings at risk such as pregnant women and children, requires more in-depth studies. If DEHP toxicity in humans were to be confirmed, it would be advisable in the future to replace current PVC plasticizers, especially if they come into contact with babies, with better-quality materials.

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Decrease in the Concentration of Vitamin E in Blood and Tissues Caused by Di(2‐Ethylhexyl) Phthalate, a Commonly Used Plasticizer in Blood Storage Bags and Medical Tubing

Abstract: DEHP even at very low doses caused a decrease in the concentration of vitamin E in liver and tests of rats given this substance. Blood stored in DEHP-plasticized bags also showed a decrease in the concentration of vitamin E.

Cited by 25 publications

References 22 publications

In Vitro Acute Exposure to DEHP Affects Oocyte Meiotic Maturation, Energy and Oxidative Stress Parameters in a Large Animal Model

In Vitro Acute Exposure to DEHP Affects Oocyte Meiotic Maturation, Energy and Oxidative Stress Parameters in a Large Animal Model

Peroxisome Proliferator–Activated Receptor α Protects against Glomerulonephritis Induced by Long-Term Exposure to the Plasticizer Di-(2-Ethylhexyl)Phthalate

Potential Hazards of Exposure to Di-(2-Ethylhexyl)-Phthalate in Babies

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