We can't find the internet
Attempting to reconnect
Something went wrong!
Hang in there while we get back on track
Combined effects of nanoplastics and 3-BHA at environmentally relevant concentrations significantly aggravated kidney injury via TGF-β/SMAD signaling pathway in mice
Summary
Researchers investigated combined exposure to nanoplastics and the synthetic antioxidant 3-BHA at environmentally relevant concentrations, finding that the combination caused greater disruption to renal function than either contaminant alone, suggesting synergistic kidney toxicity.
The increasing presence of nanoplastics (NPs) and synthetic antioxidants like 3-tert -Butyl-4-hydroxyanisole (3-BHA) in the environment has attracted widespread attention about their combined toxicological effects on human health, particularly on renal function. This study explored to the combined impacts of NPs and 3-BHA at environmentally relevant concentrations on sub-chronic kidney injury in mice. Firstly, our results confirmed that the accumulation of 80 nm NPs in renal tissues, leading to structural abnormalities such as reduced mitochondrial cristae and increased empty bubbles in mice by transmission electron microscope (TEM) analysis. Secondly, NPs and 3-BHA co-treatment resulted in significant renal developmental abnormalities including decreased kidney weight, as well as reduced organ index of kidney/body weight in mice. Besides, the histopathological staining revealed that severe renal damage characterized by thickened tubular epithelium, glomerular atrophy, and inflammatory cell infiltration were observed in kidney tissues after co-exposure. Additionally, co-exposure increased collagen fiber deposition and enhanced renal fibrosis, which showing elevated expression levels of renal function markers such as BUN, CRE, Cys-C and β2-MG. Oxidative stress and renal apoptosis were significantly aggravated, as evidenced by increased CAT, GSH-Px, and SOD levels together with TUNEL staining and expressions of apoptosis-related genes. Furthermore, co-exposure of NPs and 3-BHA caused the activation of TGF-β/Smad signaling pathway, promoting epithelial-to-mesenchymal transition (EMT) and extracellular matrix deposition, which are key processes in renal fibrosis. Thirdly, RNA-Seq analysis identified disruptions in energy metabolism and redox balance, with terms associated with oxidative phosphorylation and mitochondrial ATP synthesis were significantly enriched after NPs and 3-BHA co-exposure. Finally, pharmacological inhibition of TGF-β/Smad signaling using hydrochlorothiazide (HCTZ) could partially rescue the renal damage, cell apoptosis, inflammation and fibrosis after co-treatment. In summary, these results demonstrated the synergistic nephrotoxic effects of nanoplastics and 3-BHA in mice, which mainly mediated through oxidative stress, inflammation/apoptosis and TGF-β/SMAD signaling pathway. These information point to the critical need for further exploration of the combined effects of environmental pollutants on human kidney function.
Sign in to start a discussion.
More Papers Like This
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.
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.
Polystyrene nanoplastics exacerbate gentamicin-induced nephrotoxicity in adult rat by activating oxidative stress, inflammation and apoptosis pathways
Researchers co-exposed rats to polystyrene nanoplastics and the antibiotic gentamicin and found that the combination caused significantly greater kidney damage than either substance alone, amplifying oxidative stress, inflammation, and mitochondrial apoptosis in a synergistic manner.
Coexposure to microplastic and Bisphenol A exhacerbates damage to human kidney proximal tubular cells
This study exposed human kidney cells to polyethylene microplastics and bisphenol A (BPA, a common plastic chemical) together and found the combination was significantly more damaging than either substance alone. The co-exposure reduced cell survival and increased both oxidative stress and inflammation in the kidney cells. Since both microplastics and BPA are commonly found in the human body, their combined effect on kidney health is a real concern.
Single and joint exposure to nanoplastics and bisphenols: a comparative assessment of in vitro hazards
This study compared the individual and combined toxicity of nanoplastics and bisphenol compounds in biological test systems, finding synergistic effects at certain exposure combinations. The results indicate that co-exposure to these two common plastic-associated contaminants may be more harmful than either alone.