Oral Intake of Plasticizer Di-(2-ethylhexyl) Phthalate Disrupts Cerebellar Myelination via Thyroid Signaling in Aging Mice.
Abstract
Aging is a significant global health challenge, with neurodegenerative diseases severely affecting the quality of life in the elderly. Di-(2-ethylhexyl) phthalate (DEHP), a commonly used plasticizer in food packaging, has been identified as an environmental contaminant with thyroid hormone (TH) disruption and neurotoxic effects. Myelination in the central nervous system is crucial for neurological function, and oligodendrocytes play a central role in this process by forming myelin around axons. THs regulate oligodendrocyte differentiation and the expression of myelin-related genes. This study investigates whether environmental exposure to DEHP in aging mice disrupts thyroid hormone signaling and contributes to myelin damage. 22-month-old male C57BL/6J mice were orally administered DEHP at doses of 0, 0.2, 20, and 200 mg/kg·bw/day (mg/kg·bw/d) for 30 days (d). Nissl staining revealed significant neuronal loss in the cerebellum at higher DEHP doses. Luxol Fast Blue staining showed notable hypomyelination in DEHP-treated mice. Immunofluorescence results demonstrated an increase in oligodendrocyte progenitor cells (NG2
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Research summary
The paper claims that oral intake of DEHP disrupts thyroid hormone signaling, leading to myelination damage in aging mice. This research is relevant as it explores the impact of environmental toxins on neurodegeneration and myelination, which are critical factors in the aging process and age-related diseases.
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