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Updated: Feb 13, 2026

Sampling, Sorting, and Characterizing Microplastics in Aquatic Environments with High Suspended Sediment Loads and Large Floating Debris
Published on: July 28, 2018
Microplastic-induced alterations in the intestinal environment: Aging as a modulating factor
Alicia Sánchez1, Diego Ríos1, Mireia Mártinez1
1Instituto de Agroquímica y Tecnología de Alimentos (IATA-CSIC), Calle Agustín Escardino 7, Paterna (Valencia) 46980, Spain.
None:
Microplastics (MPs) present in the diet can affect the intestinal environment. Alterations in gut microbiota, as well as oxidative stress and inflammation in intestinal tissue, have been reported. However, most studies rely on commercial microspheres and non-aged particles, which do not reflect realistic environmental exposure. Environmental aging can modify MP properties and potentially their toxicity. The aim of this study was to evaluate the in vivo intestinal toxicity of a subchronic oral exposure to MPs derived from PVC packaging samples that have undergone an aging process. Female BALB/c mice were exposed by oral gavage to aged or non-aged PVC MPs (0.02 mg/day) for 70 days. Intestinal toxicity was assessed by measuring oxidative stress markers (ROS/RNS, lipid peroxidation, reduced glutathione), inflammatory cytokines (IL-1β, TNF-α), histological alterations, gut microbiota composition and metabolism (short-chain fatty acids, SCFAs), and fecal albumin. Microplastic accumulation in intestinal tissue was determined using microwave-assisted digestion and µRaman spectroscopy. Exposure to both aged and non-aged PVC MPs increased oxidative stress, with higher ROS/RNS (20-43 %) and lipid peroxides (27-34 %), and promoted inflammation, with elevated IL-1β (229 %) and TNF-α (68-163 %). Histological analysis showed reduced crypt depth and increased mucus-secreting cells. MPs also altered gut microbiota composition and reduced SCFA levels (32-82 %). Notably, intestinal toxicity differed between aged and non-aged MPs. Overall, subchronic exposure to PVC MPs disrupts intestinal homeostasis through oxidative and inflammatory mechanisms and microbiota dysbiosis, with toxicity influenced by particle aging.
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