2019
DOI: 10.1007/s11356-019-04219-w
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Di (2-ethylhexyl) phthalate induces cardiac disorders in BALB/c mice

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Cited by 32 publications
(17 citation statements)
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“…Additionally, the biochemical mechanism through which cardiotoxicity occurs have been reported. DEHP exposure in mice can induce oxidative stress, inhibit acetylcholinesterase activity, and lead to structural alternation of surrounding blood vessels, as reported in previous literature [13]; these disruptions provide evidence that exposure to DEHP may promote the progression of atherosclerosis. Furthermore, Ferguson and associates indicated that mono-n-butyl phthalate (MnBP), the metabolite of di-n-butyl phthalate (DnBP), and the metabolites of DEHP were significantly and positively associated with markers of oxidative stress (bilirubin) and inflammation (fibrinogen, alkaline phosphatase) based on data from participants in the National Health and Nutrition Examination Survey [14].…”
Section: Introductionsupporting
confidence: 81%
“…Additionally, the biochemical mechanism through which cardiotoxicity occurs have been reported. DEHP exposure in mice can induce oxidative stress, inhibit acetylcholinesterase activity, and lead to structural alternation of surrounding blood vessels, as reported in previous literature [13]; these disruptions provide evidence that exposure to DEHP may promote the progression of atherosclerosis. Furthermore, Ferguson and associates indicated that mono-n-butyl phthalate (MnBP), the metabolite of di-n-butyl phthalate (DnBP), and the metabolites of DEHP were significantly and positively associated with markers of oxidative stress (bilirubin) and inflammation (fibrinogen, alkaline phosphatase) based on data from participants in the National Health and Nutrition Examination Survey [14].…”
Section: Introductionsupporting
confidence: 81%
“…Martinelli suggested that DEHP exposure to animal skeletal muscle could disrupt glucose metabolism [58]. Amara showed that DEHP exposed mice have altered lipid profiles with higher triglycerides, cholesterol and high and low lipoproteins [59]. Human children aged 6-18 exposed to the metabolite MEHP had increased obesity, triglycerides, and increased blood pressure [60].…”
Section: Metabolic and Genetic Toxicitymentioning
confidence: 99%
“…Given its interaction with PPAR nuclear receptors, this is one potential mechanism by which DEHP exposure can disrupt energy metabolism and contribute to metabolic disorders. Indeed, Amara et al reported that DEHP exposure (5–200 mg/kg) altered the serum lipid profile of mice by increasing total cholesterol, triglycerides, low and high density lipoproteins (Amara et al, 2019). The authors also reported an increase in inflammatory and oxidative stress markers, which coincided with increased myocardial injury in DEHP‐treated animals.…”
Section: Di‐2‐ethylhexyl Phthalatementioning
confidence: 99%