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La contaminación por microplásticos PET transmitida por los alimentos compromete la barrera intestinal a través de
Chuxin Zhang1, Yitao Yan2, Xu Li1
1School of Forensic Medicine, Shanxi Medical University, Shanxi Key Laboratory of Forensic Medicine, and Key Laboratory of Forensic Toxicology, Ministry of Public Security, Jinzhong 030600, China.
Journal of agricultural and food chemistry
|February 9, 2026
Resumen
Los microplásticos de poli (tereftalato de etileno) (PET-MPs) causan lesiones intestinales al dañar las mitocondrias, activando la AMPK e induciendo rupturas del ADN. La inhibición de la AMPK puede mitigar estos efectos nocivos, revelando una vía clave en la toxicidad microplástica.
Área de la Ciencia:
- Salud Ambiental Salud del medio ambiente.
- Toxicología Toxicología.
- Biología celular Biología celular.
Sus antecedentes:
- Los microplásticos de poli (tereftalato de etileno) (PET-MP) son contaminantes comunes en la dieta.
- Los mecanismos subyacentes a la toxicidad del PET-MP en el intestino humano no se comprenden bien.
Objetivo del estudio:
- Para investigar la toxicidad de los PET-MPs digeridos por el aparato digestivo en las células epiteliales intestinales humanas.
- Para dilucidar los mecanismos moleculares de la lesión intestinal inducida por PET-MP.
Principales métodos:
- Utilizó un modelo de cocultivo de epitelio intestinal humano expuesto a PET-MPs digeridos durante 24 horas.
- Realizó metabolomías no dirigidas para identificar vías celulares perturbadas.
- Se realizan ensayos de validación funcional, incluidas pruebas de función mitocondrial y evaluaciones de daños en el ADN.
- Investigó el papel de la vía de señalización de AMPK y su inhibición.
Principales resultados:
- Los PET-MPs digeridos indujeron citotoxicidad, estrés oxidativo, alteración de la barrera y desregulación de las citoquinas.
- Metabolomics identificó la vía de señalización de AMPK como un nodo clave afectado.
- Los PET-MPs causaron daño mitocondrial, lo que condujo al agotamiento de ATP y la posterior activación de AMPK.
- La detención de la proliferación celular mediada por AMPK activado y las rupturas de doble cadena de ADN.
- La inhibición farmacológica de AMPK redujo los defectos de la barrera y el daño del ADN.
Conclusiones:
- Se identifica un nuevo eje de disfunción mitocondrial-activación de AMPK-daño al ADN como un mecanismo central en la lesión intestinal inducida por PET-MP.
- Estos hallazgos proporcionan información mecanicista crucial sobre los riesgos para la salud asociados con la exposición a microplásticos.
- Dirigirse a la vía AMPK puede ofrecer una estrategia terapéutica para mitigar el daño intestinal inducido por microplásticos.
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