We can't find the internet
Attempting to reconnect
Something went wrong!
Hang in there while we get back on track
Polystyrene microplastics (PS-MPs) disturb skeleto-muscular energy metabolism and tissue architecture following sub-acute exposure: A dose-responsive study
AI summary Read the abstract
Wistar rats given polystyrene microplastics in drinking water (0.5–50 mg/L) for 28 days showed dose-dependent disruption of skeletal muscle energy metabolism — including reduced ATP production and altered mitochondrial activity — along with histological changes in muscle tissue architecture.
Polystyrene microplastic (PS-MP), known as a white pollutant, exhibited adverse effects on aquatic and terrestrial animals. The present study aims to evaluate the dose-dependent effect of polystyrene microplastics on skeletal muscle energy metabolism in Wistar rats. PS-MP was administered orally in Wistar rats at doses of 0.5 mg/L, 5 mg/L, and 50 mg/L in drinking water for 28 days daily. After the treatment, metabolic profile and tissue histological analyses were performed. Average food consumption by the treated rats was decreased by PS-MPs. Glycogen and pyruvate contents were depleted in a dose-responsive fashion. Lactate dehydrogenase and transaminase activities were decreased by PS-MP exposure. Free amino nitrogen was mobilized from blood to skeletal muscle in response to stress. Protein content depleted in the muscular tissue whereas enhanced carbonylated protein formation. Pronase and cathepsin activities were increased by PS-MP. Inhibited TCA cycle enzyme activities were observed in the target tissue. Moreover, muscle hypertrophy, nuclear migration, and fibrillation were seen in histological sections. Decreased food consumption by PS-MP exposure could promote glucose scarcity in blood. Depletion of muscular glycogen may result from increased glycogenolysis to replenish loss of blood glucose. Reduction in pyruvate content may result from decreased glycolysis which could perturb the lactate dehydrogenase function. Lack of transaminase in the target tissue was indicative of tissue damage. Muscular protein breakdown might be due to oxidative denaturation of native proteins as well as increased proteolysis. Due to less pyruvate production, the TCA cycle enzyme functions were suppressed. Histopathological studies established significant degenerative changes in muscular morphology following PS-MP exposure. The present study suggests that PS-MP perturbed skeleto-muscular energy metabolism and promoted muscle fiber degeneration following sub-acute exposure.
More Papers Like This
Influence of Polystyrene Microplastics on Mitochondrial Oxidative Damage in Renal and Muscular Tissues of the Freshwater Fish
AI summary Read the abstract
Researchers exposed freshwater fish to environmentally relevant concentrations of polystyrene microplastics for up to 15 days and examined mitochondrial damage in kidney and muscle tissues. The exposure disrupted antioxidant defenses, increased oxidative stress, and altered metabolic enzyme activities in both tissue types. Histological examination revealed significant tissue damage including necrosis and degeneration, suggesting that microplastics can cause organ-level toxicity in fish through mitochondrial oxidative stress.
Polystyrene microplastics induce skeletal muscle atrophy through disruption of anabolic signaling and mitochondrial function
AI summary
Researchers exposed muscle cells to polystyrene microplastics and found dose-dependent muscle atrophy driven by suppressed IGF-1/PI3K/Akt/mTOR anabolic signaling, elevated oxidative stress, and mitochondrial dysfunction—effects comparable to the steroid dexamethasone—suggesting microplastics may be an unrecognized environmental contributor to muscle wasting.
Polystyrene microplastics induce nephrotoxicity through impaired mitochondrial homeostasis: An integrated experimental study
AI summary Read the abstract
In an animal study, exposure to polystyrene microplastics built up in the kidneys and caused kidney damage, including harmful oxidative stress, inflammation, and disrupted function of mitochondria, the energy-producing parts of cells. Higher doses caused more buildup and more tissue damage, pointing to the kidney as a key target for microplastic harm.
Dissection of the potential mechanism of polystyrene microplastic exposure on cardiomyocytes
AI summary Read the abstract
Researchers investigated how polystyrene microplastics affect human heart muscle cells at concentrations reflecting estimated daily human intake levels. They found that the microplastics caused oxidative stress, mitochondrial dysfunction, and disrupted calcium signaling in the cells. The study suggests that microplastic exposure may contribute to cardiovascular risks by directly damaging heart cell function at the cellular level.
Probing Long-Term Impacts: Low-Dose Polystyrene Nanoplastics Exacerbate Mitochondrial Health and Evoke Secondary Glycolysis via Repeated and Single Dosing
AI summary Read the abstract
This study exposed human intestinal cells to low doses of polystyrene nanoplastics over 12 days and found that repeated exposure caused cumulative damage to mitochondria, the energy-producing structures inside cells. Even concentrations considered environmentally realistic impaired cellular energy production and forced cells to switch to a less efficient backup energy system. This suggests that long-term, everyday nanoplastic exposure through food could gradually harm gut health in ways that might not be immediately noticeable.
Research digests by email
When a large batch of papers lands in the Atlas, we read through it and send a short write-up of what stood out.