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di 2 ethylhexyl phthalate/edema
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p53-dependent apoptosis contributes to di-(2-ethylhexyl) phthalate-induced hepatotoxicity.
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Di-(2-ethylhexyl) phthalate (DEHP) is used extensively in many personal care and consumer products, resulting in widespread non-occupational human exposure through multiple routes and media. DEHP has various deleterious effects including hepatotoxicity. p53 protein is a central sensor in cell
Effects of phthalate acid esters on zebrafish larvae: Development and skeletal morphogenesis.
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This study evaluated the acute developmental toxicity of six priority phthalic acid esters (PAEs) including dimethyl phthalate (DMP), diethyl phthalate (DEP), dibutyl phthalate (DBP), di-2-ethylhexyl phthalate (DEHP), di-n-octyl phthalate (DNOP), and benzyl butyl phthalate (BBP) in zebrafish
A multi-omics approach reveals molecular mechanisms by which phthalates induce cardiac defects in zebrafish (Danio rerio)
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The potential risks of phthalates affecting human and animal health as well as the environment are emerging as serious concerns worldwide. However, the mechanism by which phthalates induce developmental effects is under debate. Herein, we found that embryonic exposure of zebrafish to
Plasticisers, another burden for asthmatics?
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The widely used plasticiser di(2-ethylhexyl)phthalate (DEHP) has been reported to have some toxicological effects on pulmonary tissue. Inhalation of DEHP may cause pulmonary edema and bronchial asthma. Moreover intravenous injection of DEHP induces pulmonary inflammation and hemorrhage of the lungs.
The effect of mono(2-ethylhexyl)phthalate on an isolated perfused rat heart-lung preparation.
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Di(2-ethylhexyl)phthalate (DEHP), the plasticizer used in the biomedical production of blood storage bags, hemodialysis systems, cardiopulmonary bypass (CPB) circuitry, and intubation tubes, is extracted from the plastic material when it comes into contact with biological fluids and is converted to
Clofibrate and gemfibrozil induce an embryonic malabsorption syndrome in zebrafish.
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Nutrient availability is one of the major non-genetic factors determining embryonic growth and larval or fetal size. Due to the high human consumption of blood lipid regulators, fibrates have recently been reported as pollutants in rivers. Our study investigated the developmental toxicity of
Di2-ethylhexyl phthalate disrupts thyroid hormone homeostasis through activating the Ras/Akt/TRHr pathway and inducing hepatic enzymes.
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Di(2-ethylhexyl) phthalate (DEHP), as a widespread environmental pollutant and an endocrine disruptor, can disturb the homeostasis of thyroid hormones (THs). In order to elucidate roles of the MAPK and PI3K/Akt pathways and hepatic enzymes in thyroid-disrupting effects of DEHP, Sprague-Dawley rats
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