Tissue & cell · 2026
Polystyrene microplastics induce nephrotoxicity through impaired mitochondrial homeostasis: An integrated experimental study.
СтатьяНазвание и аннотация: Перевод пока не подготовлен
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Abdel Ghany Fatma, Yousef Mokhtar I, El-Tabakh Mohamed A M, Kamel Maher A, El Wakil Abeer
Аннотация
OBJECTIVE: The present study aimed to investigate the nephrotoxic effects of polystyrene microplastics (PS-MPs) and to elucidate the underlying mechanisms associated with oxidative stress, transcriptional dysregulation of mitochondrial homeostasis, inflammation, apoptosis, and renal bioaccumulation.
METHODS: Experimental animals were exposed to increasing concentrations of PS-MPs. Renal accumulation of PS-MPs was confirmed by pyrolysis-gas chromatography/mass spectrometry (Py-GC/MS). Renal function biomarkers, oxidative stress parameters, antioxidant enzyme activities, inflammatory and apoptotic markers, mitochondrial biogenesis, dynamics, and mitophagy regulators were assessed using biochemical and molecular analyses. Histopathological examination of renal tissue was performed using hematoxylin and eosin staining. Principal Component Analysis (PCA) was conducted to evaluate relationships among all measured parameters.
RESULTS: Py-GC/MS detected characteristic PS-derived pyrolysis products only in the 10, 20, and 40 µg/kg groups, with estimated signals increasing in a dose-dependent manner, suggesting dose-dependent renal accumulation of PS-derived material. PS-MP exposure induced significant renal dysfunction, evidenced by elevated creatinine, urea, uric acid, and urea/creatinine ratio. Oxidative stress was markedly increased, as demonstrated by elevated TBARS levels and depletion of GSH and antioxidant enzymes (GPx, GR, GST, SOD, and CAT). Histopathological examination revealed progressive glomerular congestion, tubular degeneration, epithelial desquamation, fibrosis, and inflammatory infiltration. In parallel, NF-κB and caspase-3 levels were significantly elevated, indicating enhanced inflammatory and apoptotic responses. Moreover, PS-MPs were associated with coordinated transcriptional dysregulation of mitochondrial homeostasis-related genes, characterized by suppression of PGC-1α, TFAM, MFN2, OPA1, and PINK1 expression, accompanied by increased DRP1 levels. PCA further demonstrated distinct separation between control and exposed groups, strongly associating PS-MP exposure with oxidative stress, transcriptional dysregulation of mitochondrial homeostasis-related genes, inflammation, apoptosis, and renal injury.
CONCLUSION: PS-MPs induce marked nephrotoxicity, accompanied by oxidative stress, coordinated transcriptional dysregulation of mitochondrial homeostasis-related genes, inflammatory activation, and apoptosis. These findings identify the kidney as a major target organ for microplastic accumulation and toxicity and provide valuable mechanistic insights into PS-MP-induced renal injury.
METHODS: Experimental animals were exposed to increasing concentrations of PS-MPs. Renal accumulation of PS-MPs was confirmed by pyrolysis-gas chromatography/mass spectrometry (Py-GC/MS). Renal function biomarkers, oxidative stress parameters, antioxidant enzyme activities, inflammatory and apoptotic markers, mitochondrial biogenesis, dynamics, and mitophagy regulators were assessed using biochemical and molecular analyses. Histopathological examination of renal tissue was performed using hematoxylin and eosin staining. Principal Component Analysis (PCA) was conducted to evaluate relationships among all measured parameters.
RESULTS: Py-GC/MS detected characteristic PS-derived pyrolysis products only in the 10, 20, and 40 µg/kg groups, with estimated signals increasing in a dose-dependent manner, suggesting dose-dependent renal accumulation of PS-derived material. PS-MP exposure induced significant renal dysfunction, evidenced by elevated creatinine, urea, uric acid, and urea/creatinine ratio. Oxidative stress was markedly increased, as demonstrated by elevated TBARS levels and depletion of GSH and antioxidant enzymes (GPx, GR, GST, SOD, and CAT). Histopathological examination revealed progressive glomerular congestion, tubular degeneration, epithelial desquamation, fibrosis, and inflammatory infiltration. In parallel, NF-κB and caspase-3 levels were significantly elevated, indicating enhanced inflammatory and apoptotic responses. Moreover, PS-MPs were associated with coordinated transcriptional dysregulation of mitochondrial homeostasis-related genes, characterized by suppression of PGC-1α, TFAM, MFN2, OPA1, and PINK1 expression, accompanied by increased DRP1 levels. PCA further demonstrated distinct separation between control and exposed groups, strongly associating PS-MP exposure with oxidative stress, transcriptional dysregulation of mitochondrial homeostasis-related genes, inflammation, apoptosis, and renal injury.
CONCLUSION: PS-MPs induce marked nephrotoxicity, accompanied by oxidative stress, coordinated transcriptional dysregulation of mitochondrial homeostasis-related genes, inflammatory activation, and apoptosis. These findings identify the kidney as a major target organ for microplastic accumulation and toxicity and provide valuable mechanistic insights into PS-MP-induced renal injury.