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Combined exposure to lead and microplastics increased risk of glucose metabolism in mice via the Nrf2 / NF‐κB pathway

Environmental Toxicology 2024 13 citations

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A mouse study found that combined exposure to lead and microplastics (PVC and polyethylene) disrupted glucose metabolism more severely than either pollutant alone, causing insulin resistance and damaging the pancreas. The combined exposure triggered inflammation and oxidative stress through a specific signaling pathway. This research suggests that microplastics and heavy metals, which often occur together in the environment, may work together to increase the risk of metabolic diseases like diabetes in people.

Polymers
Models
Study Type Environmental

The purpose of this study was to explore the effects of combined lead (Pb) and two types of microplastic (MP) (polyvinyl chloride [PVC] and polyethylene [PE]) exposure on glucose metabolism and investigate the role of the nuclear factor erythroid 2-related factor 2 (Nrf2)/nuclear factor-kappa B (NF-κB) signaling pathway in mediating these effects in mice. Adult C57BL/6J mice were randomly divided into four groups: control, Pb (100 mg/L), MPs (containing 10 mg/L PE and PVC), and Pb + MPs, each of which was treated with drinking water. Treatments were conducted for 6 weeks. Co-exposure to Pb + MPs exhibited increase glycosylated serum protein levels, insulin resistance, and damaged glucose tolerance compared with the control mice. Additionally, treatment with Pb + MPs caused more severe damage to hepatocytes than when exposed to them alone concomitantly, exposed to Pb + MPs exhibited improved the levels of interleukin-6, tumor necrosis factor-alpha, and malondialdehyde, but reduced superoxide dismutase, glutathione peroxidase, and catalase assay in livers. Furthermore, they increase the Kelch-like ECH-associated protein 1 (Keap1) and phosphorylated p-NF-κB protein levels but reduced the protein levels of heme oxygenase-1 and Nrf2, as well as increased Keap1 mRNA and Nrf2 mRNA. Co-exposure to Pb + MP impacts glucose metabolism via the Nrf2 /NF-κB pathway.

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