ArticleBioscience reports2020
MEHP interferes with mitochondrial functions and homeostasis in skeletal muscle cells.
Article in Bioscience reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 26 citations in OpenAlex.
- High-concentration MEHP triggers mtDNA depletion in undifferentiated HepaRG and C2C12 cultures and disrupts mitochondrial homeostasis in both HepaRG culture states.Toxicological sciences : an official journal of the Society of Toxicology · 2026Article
- Hepatic lipid accumulation induced by mono-(2-ethylhexyl) phthalate and potential ERBB2-associated inflammatory signaling in NAFLD.Frontiers in pharmacology · 2026Article
- Underexplored terrain: effects of high priority environmental toxicants on skeletal muscle.Journal of toxicology and environmental health. Part B, Critical reviews · 2026Review
- Epigenetic signatures of phthalate exposure and potential risks: a DNA methylation analysis using Infinium MethylationEPIC BeadChip.Environmental epigenetics · 2025Article
- DEHP exposure impairs human skeletal muscle cell proliferation in primary culture conditions: preliminary study.Cytotechnology · 2023Article
- Maternal rodent exposure to di-(2-ethylhexyl) phthalate decreases muscle mass in the offspring by increasing myostatin.Journal of cachexia, sarcopenia and muscle · 2022Article
- Alteration of the NEpigenomics · 2022Article
- Article
- Association of urinary phthalate metabolites with sarcopenia in US adults: NHANES 1999-2006.Environmental science and pollution research international · 2022Article
- MEHP induces alteration of mitochondrial function and inhibition of steroid biosynthesis in MA-10 mouse tumor Leydig cells.Toxicology · 2021Article
- Article
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Di (2-ethylhexyl) phthalate (DEHP) is a plasticizer frequently leached out from polyvinyl chloride (PVC) products and is quickly metabolized to its monoester equivalent mono(2-ethylhexyl) phthalate (MEHP) once enters organisms. Exposure to DEHP/MEHP through food chain intake has been shown to modified metabolism but its effect on the development of metabolic myopathy of skeletal muscle (SKM) has not been revealed so far. Here, we found that MEHP repressed myogenic terminal differentiation of proliferating myoblasts (PMB) and confluent myoblasts (CMB) but had weak effect on this process once it had been initiated. The transition of mitochondria (MITO) morphology from high efficient filamentary network to low efficient vesicles was triggered by MEHP, implying its negative effects on MITO functions. The impaired MITO functions was further demonstrated by reduced MITO DNA (mtDNA) level and SDH enzyme activity as well as highly increased reactive oxygen species (ROS) in cells after MEHP treatment. The expression of metabolic genes, including PDK4, CPT1b, UCP2, and HO1, was highly increased by MEHP and the promoters of PDK4 and CPT1b were also activated by MEHP. Additionally, the stability of some subunits in the oxidative phosphorylation system (OXPHOS) complexes was found to be reduced by MEHP, implying defective oxidative metabolism in MITO and which was confirmed by repressed palmitic acid oxidation in MEHP-treated cells. Besides, MEHP also blocked insulin-induced glucose uptake. Taken together, our results suggest that MEHP is inhibitory to myogenesis and is harmful to MITO functions in SKM, so its exposure should be avoided or limited.
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Registered trials
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