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Pharmacological inhibition of endoplasmic reticulum stress ameliorates polystyrene nanoplastic-induced renal injury in female Wistar rats
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Tiny plastic particles called nanoplastics, found in everyday items and increasingly in our environment, caused kidney damage in rats by triggering a harmful cell stress response that leads to tissue injury. Researchers found that a drug called 4-PBA (already studied for other health conditions) reversed much of this damage, hinting at a possible way to protect kidneys from plastic pollution exposure. While this study was done in rats, not humans, it adds to growing concerns about how the microplastics and nanoplastics we're exposed to daily might affect our organs over time.
Nanoplastics are a relatively new pollutant that has raised growing concern about their deleterious effects on humans. Endoplasmic reticulum (ER) stress is a cellular stress response that helps maintain protein balance in response to internal or external stimuli. The aim of this research was to modulate ER stress in renal tissues by administering 4-PBA to mitigate the nephrotoxicity induced by polystyrene nanoplastics (PSNPs). For this purpose, 24 healthy female Wistar rats were randomly divided into four groups: vehicle control group, PSNPs group, PSNPs + 4-PBA 500 mg/kg group, and PSNPs + 4-PBA 1000 mg/kg group (n = 6). During the experiment, PSNPs (10 mg/kg) were given for 5 weeks, whereas 4-PBA was given for the last two weeks. At the end of the experiment, animals were sacrificed, and tissue samples from the kidney and blood were collected and stored immediately. PSNPs exposure resulted in severe renal dysfunction, including increased serum creatinine, MDA, and nitrite, whereas body weight, kidney weight, and GSH were decreased. Markers related to ER stress, including GRP78, CHOP, and caspase-12, were found to be upregulated, along with distorted renal histopathology in the PSNPs-exposed group. The administration of 4-PBA leads to improvement in histological alterations and biochemical parameters, as well as attenuation of GRP78, CHOP, and caspase-12 expression levels. The results of this study indicate that 4-PBA may serve as a potent intervention to treat PSNP-induced nephrotoxicity. Also, apoptosis through GRP78/CHOP-dependent ER stress signalling plays a significant role in the development of PSNPs-induced nephrotoxicity.
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4-Phenylbutyric acid attenuates endoplasmic reticulum stress-mediated polystyrene microplastic-induced nephrotoxicity in Wistar rats
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Scientists found that microplastic particles caused kidney damage in rats by triggering stress inside cells, leading to worse kidney function and tissue damage. A compound called 4-PBA, already studied for other health conditions, helped protect the kidneys and reverse much of this damage when given to the rats. While this is early animal research, it suggests microplastics may pose real risks to kidney health and hints at a possible way to protect against that damage in the future.
Polystyrene microplastics induced nephrotoxicity associated with oxidative stress, inflammation, and endoplasmic reticulum stress in juvenile rats
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This study found that polystyrene microplastics caused kidney damage in young rats through a combination of oxidative stress, inflammation, and a cellular stress response called endoplasmic reticulum stress. The microplastics also reduced body weight growth and affected multiple organs including the heart and ovaries. These findings suggest that microplastic exposure during development could be particularly harmful to kidney health in young, growing organisms.
Nephroprotective role of edaravone against polystyrene nanoplastic-induced endoplasmic reticulum stress in Wistar rats
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Researchers exposed Wistar rats to polystyrene nanoplastics and found significant kidney damage mediated through endoplasmic reticulum stress, marked by elevated oxidative stress markers, histopathological abnormalities, and upregulation of ER stress proteins GRP78, CHOP, and caspase-12 — damage that was substantially reduced by co-administration of the antioxidant edaravone.
Evaluation of the hepatorenal subacute toxicity of polystyrene nanoplastics on immunohistochemical, histopathological, endoplasmic reticulum stress, and biochemical changes: The protective role of ellagic acid
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Researchers demonstrated that 28-day oral exposure to polystyrene nanoplastics in rats caused liver and kidney toxicity—marked by elevated oxidative stress, inflammation, endoplasmic reticulum stress, and histopathological damage—and that co-administration of the antioxidant ellagic acid significantly attenuated these harmful effects.
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Researchers investigated how microplastic exposure affects animal cells through a stress response in a cellular structure called the endoplasmic reticulum. They found that microplastics triggered this stress pathway, which amplified toxic effects including inflammation and cell death. The study suggests that endoplasmic reticulum stress may be an important and previously underappreciated mechanism through which microplastics cause damage to tissues.
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