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Cellular, Subcellular, and Bioenergetic Effects of Functionalized Nanoplastics and Emerging Plasticizers on Rainbow Trout Gill Epithelial Cells
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Scientists tested tiny plastic particles (nanoplastics) and plastic softening chemicals on fish gill cells to understand how these pollutants might harm living tissue at the cellular level. They found that positively charged plastic particles were the most damaging, disrupting the cell's "power plants" (mitochondria) and reducing their ability to produce energy—even at doses too low to kill the cells outright. This matters because it shows plastic pollution can cause hidden cellular damage before any visible harm appears, and since fish are a common entry point for microplastics into the food chain, understanding these effects helps scientists predict risks that could
Nanoplastics are emerging contaminants of concern in freshwater ecosystems and have been shown to be ingested and assimilated tissues of fish and other organisms. Understanding the nano-bio interactions and potential impacts of these pollutants is essential. While previous work has focused on traditional whole organism endpoints of toxicity (i.e., reproduction, survival and growth) at lethal concentrations, there remains a critical gap in understanding the sublethal effects and mechanisms of action in environmentally relevant models. For many pollutants we are just beginning to understand how pollutants act through impacts on cellular metabolism and morphology. Additionally, plasticizers within plastics are an additional understudied aspect in plastic pollution. Plasticizers represent a major class of additives that are not covalently bonded to the polymer matrix and are prone to leaching into aquatic environments. While legacy plasticizers have been extensively researched, emerging alternative replacements remain poorly characterized and the cellular effects of combined nanoplastic-plasticizer exposure remain unclear. In this dissertation, we utilized pristine polystyrene spheres using three model particles of differing functional groups representing positive, negative and neutral surfaces charges since surface charge is well-established as an important factor in determining biological impacts. RTgill-W1 (Oncorhynchus mykiss, Rainbow trout gill epithelia), were used as a model to investigate sensitive cellular impacts. By employing high-content imaging, phenotypic profiling, and mitochondrial bioenergetic analyses we found that surface chemistry played a major role in cellular and subcellular responses. With a traditional cytotoxicity assay, we determined that PS-NH2 NPs (amine-functionalized polystyrene nanoplastics) significantly decreased cell viability compared to its neutral and negatively charged counterparts. Additionally, distinct phenotypic responses at sublethal concentrations suggested early nano-bio interactions in subcellular compartments where no cytotoxicity was observed due to impacts to cellular actin and the mitochondria. The results suggested that the mitochondria may be a primary target of NP-induced stress and provided the rationale for further investigation even though multiple organelles were affected. Subsequent analyses demonstrated that PS-NH2 NPs disrupted mitochondrial bioenergetics. By conducting the Seahorse XF Mito Stress Test, a high-throughput respirometer, we found that PS-NH2 NPs decreased basal and maximal respiration, altered ATP-linked respiration (Adenosine Triphosphate) and induced changes to mitochondrial morphology indicating disruption of mitochondrial function. These findings expand mechanistic knowledge of PS NP toxicity and suggest that the mitochondria may play a key role in governing nanoplastic-induced cellular responses in particles of cationic surface chemistry. These results present opportunities for further study of identifying which specific complex of the electron transport chain is impaired and if increase in proton leakage is associated with a reduction in the cardiolipin content of the inner mitochondrial membrane allowing the exploration of novel mechanisms enhancing our understanding in nano-mito interactions. The second knowledge gap is the need to better characterize the cellular and subcellular effects of emerging alternative plasticizers, and of that combined nano-plasticizer exposure. The current work investigated how RTgill-W1 are perturbed by replacement compounds and will be paired with polyethylene terephthalate nanoplastics (nanoPET) to compare effects between nanoPET with and without the selected additive of bis(2-ethylhexyl) adipate (DOA) by applying phenotypic profiling. The results demonstrated that replacement plasticizers and NPs with additive are not biologically inert, generating distinct phenotypic fingerprints and shared subcellular targets. Combined nanoPET-DOA treatments revealed both additive-driven and particle specific effects, with mitochondrial responses dominated by the plasticizers and other features reflecting particle-specific effects.
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Unveiling the underlying mechanism: Metabolic reprogramming and oxidative stress mediate nanoplastic-induced hepatotoxicity in a freshwater fish (Pseudorasbora parva)
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Scientists studied how tiny plastic particles (nanoplastics) affect fish livers and found that the smallest particles (80 nanometers) caused the most damage by disrupting the body's ability to fight harmful chemicals and process energy. The smallest plastic particles were especially harmful because they damaged the fish's natural defense systems and changed how their cells make energy. While this study was done in fish, it raises concerns about how these tiny plastic particles in our environment might also harm human health.
The Effect of Nano Plastic Toxicity on the Gill Tissue of Goldfish )Carassius auratus(
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Scientists exposed goldfish to tiny plastic particles (nanoplastics, smaller than microplastics) in water at levels similar to polluted environments, and found the particles damaged the fish's gill tissue, harming their ability to breathe and regulate salt balance. This matters because these same tiny plastics are increasingly found in our water, food, and even human blood and organs—if they can damage delicate tissue in fish, researchers are concerned they may pose similar risks to human health, though more research is needed to confirm this in people.
Functionalized Polystyrene Nanoplastics Drive Distinct Mitochondrial Bioenergetic and Phenotypic Responses in Rainbow Trout Gill Epithelia
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Researchers exposed rainbow trout gill epithelial cells to differently functionalized polystyrene nanoplastics and measured mitochondrial bioenergetics alongside phenotypic profiling, finding that surface chemistry drives distinct cellular stress signatures and that morphological data captured toxic responses that bioenergetics measurements alone missed.
Evaluation of Microplastics and Oxidative Stress Biomarkers in Marine Fish
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Scientists found tiny plastic bits (from things like packaging and synthetic fabrics) inside the gills, guts, and muscle of three popular seafood fish, and these plastics were linked to cell damage from oxidative stress—basically, wear and tear at the cellular level that varied depending on the fish species. This matters because it suggests the fish we eat may be absorbing plastic pollution in ways that affect their health, and since we eat the muscle tissue too, it raises questions about what we might be consuming along with our seafood—though more research is needed to know exactly how this impacts human health.
Mitochondrial dysfunction and DNA damage reveal nanoplastic-induced cytotoxicity in the sea cucumber Apostichopus japonicus
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Scientists exposed sea cucumber cells to tiny plastic particles (nanoplastics) and found they damaged cell "power plants" (mitochondria), triggered stress that harms DNA, and caused cell death—even at low doses. While this study was done in sea creatures, not humans, it adds to growing evidence that the ever-smaller plastic particles now found throughout our oceans and food chain can cause real cellular damage, raising concern about what similar exposure might mean for human health down the line.
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When a large batch of papers lands in the Atlas, we read through it and send a short write-up of what stood out.