0
Article ? AI-assigned paper type based on the abstract. Classification may not be perfect — flag errors using the feedback button. Tier 2 ? Original research — experimental, observational, or case-control study. Direct primary evidence. Human Health Effects Sign in to save

Polystyrene microplastics modulation of hexavalent chromium toxicity in quails: transcriptomic and toxicological insights

Environmental Chemistry and Ecotoxicology 2025 2 citations ? Citation count from OpenAlex, updated daily. May differ slightly from the publisher's own count. Score: 58 ? 0–100 AI score estimating relevance to the microplastics field. Papers below 30 are filtered from public browse.
Dongfang Liu, Kaiwei Song, Miaomiao Li, Biqi Han, Zhanjun Lv, Jiayi Li, Jiayi Li, SiYu Li, Jingjing Lu, Shuke Ji, Jiatong Ma, Zhigang Zhang

Summary

Researchers exposed quails to both polystyrene microplastics and hexavalent chromium — a cancer-causing heavy metal — for 12 weeks, finding that microplastics worsened the kidney damage caused by chromium by disrupting fat metabolism and energy production. The combination triggered severe kidney scarring (fibrosis) that neither pollutant caused as strongly on its own, illustrating how microplastics can amplify the toxicity of other environmental contaminants.

Hexavalent chromium (Cr(VI)) is a globally recognized carcinogen that can lead to kidney toxicity. Microplastics (MPs) pollution is a serious environmental problem. The presence of Cr(VI) and MPs in the environment not only affects the ecological environment, but also impacts the health of humans and animals. Renal fibrosis represents a frequent final manifestation across a spectrum of chronic kidney conditions. This study aims to investigate whether chronic exposure to Cr(VI) and/or polystyrene (PS) promotes renal injury by altering fatty acid metabolism and energy metabolism, and inducing fibrotic responses. This study established a chronic co-exposure model in quails by simultaneously exposing them to Cr(VI) via drinking water and PS via oral gavage for 12 consecutive weeks. Experiments in vivo and transcriptome sequencing were performed to screen genes for analysis. The research results show that quails exposed to Cr(VI) and PS exhibited abnormal renal lipid and energy metabolism, leading to severe renal fibrosis. Overall, chronic exposure to PS exacerbates renal fibrosis process via promoting lipid dysregulation induced by Cr(VI) in quails. This study enriches the mechanism of nephrotoxicity induced by environmental PS-MPs and Cr(VI) contamination and contributes to the exploration of new preventive and therapeutic strategies. • Hexavalent chromium (Cr(VI)) and polystyrene (PS) have synergistic toxicity. • PS exacerbate Cr(VI)-induced nephrotoxicity in quails. • Cr(VI) induces renal lipid metabolism disorder by inhibiting fatty acid degradation. • PS aggravate Cr(VI)-induced renal energy metabolism disorders in quails. • PS enhance Cr(VI)-induced renal fibrosis in quails.

Sign in to start a discussion.

More Papers Like This

Article Tier 2

Exposure to Environmentally Relevant Concentrations of Polystyrene Microplastics Increases Hexavalent Chromium Toxicity in Aquatic Animals

Researchers found that environmentally relevant concentrations of polystyrene microplastics significantly increased the toxicity of hexavalent chromium across multiple aquatic species, acting as vectors that amplify heavy metal harm.

Article Tier 2

Microplastics and nanoplastics co-exposure modulates chromium bioaccumulation and physiological responses in rats

Rats exposed to a mix of microplastics and nanoplastics along with hexavalent chromium, a toxic heavy metal, accumulated significantly more chromium in their liver, heart, brain, and skin than rats exposed to chromium alone. This shows that plastic particles can act as carriers that increase the amount of toxic metals absorbed by the body, potentially amplifying the health risks of metal pollution.

Article Tier 2

Microplastics Exacerbate Cadmium-Induced Kidney Injury by Enhancing Oxidative Stress, Autophagy, Apoptosis, and Fibrosis

Researchers exposed mice to microplastics and cadmium for three months and found that microplastics significantly worsened cadmium-induced kidney injury. The combined exposure enhanced oxidative stress, autophagy, cell death, and tissue scarring in the kidneys beyond what cadmium alone caused. The study suggests that microplastics may act as amplifiers of heavy metal toxicity in organ systems.

Article Tier 2

Synergistic kidney toxicity of polylactic acid nanoplastics and Cr(VI): Ferroptosis aggravated by mitophagy

Researchers investigated the combined kidney toxicity of polylactic acid nanoplastics and hexavalent chromium in mice. The study found that co-exposure produced synergistic kidney damage through ferroptosis aggravated by mitophagy, suggesting that even bioplastic-derived nanoplastics can enhance heavy metal toxicity when both contaminants are present together.

Article Tier 2

Synergistic toxicity of PFAS and microplastic mixtures across five human cell lines

Researchers tested the combined toxicity of PFAS chemicals and microplastics on five types of human cells representing the kidney, liver, prostate, skin, and lung. They found that mixtures of these common environmental contaminants produced synergistic harmful effects, particularly in kidney and liver cells, including increased oxidative stress and DNA damage. The study suggests that the combined exposure to PFAS and microplastics, which frequently co-occur in the environment, may pose greater health risks than either pollutant alone.

Share this paper