We can't find the internet
Attempting to reconnect
Something went wrong!
Hang in there while we get back on track
Synergistic kidney toxicity of polylactic acid nanoplastics and Cr(VI): Ferroptosis aggravated by mitophagy
Summary
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.
Nanoplastics (NPs) and chromium (Cr) are ubiquitous in the environment, causing severe pollution and posing significant potential threats to human health. Polylactic acid (PLA) and Cr are among widely used bioplastic and heavy metal, respectively, both capable of contaminating water sources through corresponding pathways and posing substantial risks to human health. Nanoplastics can act as carriers for heavy metals, thereby enhancing their bioaccumulation and toxicity. Therefore, this study investigated the effects of combined exposure to Cr(VI) and PLA NPs on mice kidneys and its potential mechanisms. Results indicated that exposure to PLA NPs alone did not exhibit significant toxic effects on the kidneys. However, combined exposure to Cr(VI) and PLA NPs caused severe kidney damage in mice. This indirectly suggests that Cr(VI) and PLA NPs exhibit synergistic toxicity rather than simple additive effects. Furthermore, combined exposure exacerbated the toxic mechanism by inducing mitochondrial damage and excessive reactive oxygen species (ROS) production, thereby triggering mitophagy. Overactivated mitophagy exacerbated lipid peroxidation by releasing free iron, thereby amplifying ROS-mediated ferroptosis. This study investigates the synergistic renal toxicity of Cr(VI) and PLA NPs, providing scientific evidence for the combined toxicity mechanism of exposure to MNPs and heavy metals.
Sign in to start a discussion.
More Papers Like This
Co-exposure to environmentally relevant concentrations of cadmium and polystyrene nanoplastics induced oxidative stress, ferroptosis and excessive mitophagy in mice kidney
A mouse study found that combined exposure to cadmium (a toxic metal) and polystyrene nanoplastics caused more kidney damage than either pollutant alone. The combination triggered a harmful chain reaction involving oxidative stress, iron buildup, and excessive breakdown of cellular energy factories called mitochondria. This is significant because people are often exposed to both nanoplastics and heavy metals simultaneously, and their combined effects may be worse than expected.
Iron's silent betrayal: Ferritinophagy-driven mitochondrial damage mediates polylactic acid nanoplastics and Cr(VI)-induced cardiac injury
Researchers found that co-exposure of mice to biodegradable polylactic acid nanoplastics and hexavalent chromium causes synergistic cardiac injury by inducing ferritinophagy — a process where cells break down iron-storage proteins — triggering iron overload and excess mitochondrial reactive oxygen species that damage heart tissue.
Combined exposure to polystyrene nanoplastics and bisphenol A results in mitochondrial damage and ferroptosis via the PI3K-AKT signaling pathway in mice kidneys
Researchers exposed mice to polystyrene nanoplastics combined with bisphenol A for six weeks and found that co-exposure caused significant kidney damage through mitochondrial dysfunction and a form of cell death called ferroptosis. The combined exposure was more harmful than either contaminant alone, operating through the PI3K-AKT signaling pathway. The findings suggest that nanoplastics acting as carriers for co-pollutants like BPA may amplify toxic effects on kidney tissue.
Ferroptosis and hepatic fibrosis induced by cooperative exposure to polylactic acid nanoplastics and copper: Emphasis on gut microbiota dysbiosis
Researchers investigated the combined hepatotoxicity of polylactic acid nanoplastics and copper in mice, focusing on the gut-liver axis. The study found that co-exposure caused synergistic liver damage through ferroptosis, characterized by disrupted glutathione and iron homeostasis, along with gut microbiota dysbiosis and hepatic fibrosis more severe than either pollutant alone.
Polystyrene microplastics modulation of hexavalent chromium toxicity in quails: transcriptomic and toxicological insights
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.