Microplastics (MPs) appear to promote the development of endometrial cancer (EC) by activating specific molecular pathways, according to a study recently published in Environmental Pollution.
There is growing research on the effect of microplastics on women’s reproductive health. Studies show that microplastics can accumulate in various organs, generating oxidative stress that leads to cell death and scarring.
The study authors hypothesize that the endometrium may be particularly vulnerable to microplastic-mediated damage. They aimed to further characterise its effects by analysing 32 endometrial samples: normal tissue, endometrial hyperplasia, and EC.
The results showed that microplastics were common across all samples, with 13 polymers identified. The most frequent were polyethylene, polypropylene, ethylene–acrylic acid and polystyrene.
“Research has shown that many seafood products—fish and shellfish—contain MP particles in their bodies and can enter the human body through the food chain. MPs are also frequently found in everyday foods, including table salt, bottled water, honey, and beer,” the authors wrote.
The researchers observed that EC tissues harboured significantly higher microplastic levels than normal endometrium. More precisely, the detection rates were 66.7% in normal tissue, 83.3% in endometrial hyperplasia and 80.0% in EC samples.
Further investigations revealed distinct biochemical profiles between EC tissues with high and low microplastic levels; tissues with higher microplastic loads showed markedly different protein-expression profiles.
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Differentially affected pathways included glycine, serine and threonine metabolism; aminoacyl-tRNA biosynthesis; and pantothenate and CoA biosynthesis.
The authors propose that MP accumulation may contribute to EC development by perturbing amino-acid and coenzyme pathways, thereby shaping a pro-tumour metabolic environment. However, they note that the study cannot prove causality.
“Although causality cannot be established, these findings suggest a potential link between MP accumulation and EC-related metabolic dysregulation,” the authors wrote. “This work advances current understanding of the environmental factors potentially involved in gynecological cancer pathogenesis and underscores the emerging threat of MP pollution to women’s reproductive health.”
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