Molecular effects of polystyrene nanoplastics toxicity in zebrafish embryos (Danio rerio)

Martín-Folgar, Raquel; Torres-Ruiz, Mónica; Alba, Mercedes de; Cañas-Portilla, Ana I.; González, Margarita; Morales, Mónica

doi:10.1016/j.chemosphere.2022.137077

Cited by 18 publications

(13 citation statements)

References 60 publications

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“…This result agrees with those obtained in Zfe, Crassostrea virginica, and Sterechinus neumayeri exposed to NPs [94][95][96]. In contrast, our previous results showed down-regulation of Bcl2 activity after NPs exposure in Zfe [21]. This discrepancy in results may be due to the difference in response to PS NPs from a whole organism or from a specific cell culture of hNSC, as in the Zfe model observe the response of all cell types within the individual, and not only neural cells.…”

Section: Plos Onesupporting

confidence: 92%

“…Previous studies have described that NPs can stimulate reactive oxygen species (ROS) production and cause oxidative stress in human cells [64], Zfe [17,21,[63][64][65], and in Daphnia pulex and Karenia mikimotoi [66]. Increased ROS can generate oxidative stress, mitochondrial damage, amplified inflammatory cytokines and proapoptotic factors that could induce apoptosis in cells and in animals [56,[67][68][69][70].…”

Section: Oxidative Stress Response: Cu/zn Sod1 Mnsod2 and Catmentioning

confidence: 99%

“…To address this work, gene expression of different metabolic pathways, such as stress response (hsp27/hspB1, hsp60, hsp70/hspA5, and hsp90α), DNA repair (xrcc1, gad45a, rad51), oxidative damage response (Cu/ZnSOD 1, MnSOD 2), apoptotic response (Cas3a, Cas7, p53, Bcl2), and mitochondrial response (Cox5A), were analyzed after PS NP exposure, as biomarkers of NPs damage. Cells were exposed to concentrations similar to those present in the environment and/or used in previous studies (0.5, 2.5, and 10 μg/mL) for 4 days [11,21,[31][32][33][34]. Currently, there is limited information on the neurotoxicity of NPs in mammals [22] and there are no data on the concentration and bioaccumulation of these nanomaterials in humans.…”

Section: Introductionmentioning

confidence: 99%

“…It has been suggested that oxidative stress can cause cellular damage that can lead to neuronal disorders, as they produce inhibition of acetylcholinesterase (AChE) activity and alter neurotransmitter levels [ 19 , 20 ]. In addition, studies from our group, demonstrate that PS NPs cause increased gene expression of oxidative stress markers, apoptosis, inflammation, and inhibition of neurotransmitter ( AChE ) gene expression in zebrafish embryos (Zfe) [ 21 ]. Furthermore, these particles are able to enter the Zfe central nervous system (CNS), and cause deleterious effects, as well as endocrine system effects and behavioral alterations [ 11 ].…”

Section: Introductionmentioning

confidence: 99%

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Molecular effects of polystyrene nanoplastics on human neural stem cells

Martin-Folgar,

González-Caballero,

Torres-Ruiz

et al. 2024

PLoS ONE

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Nanoplastics (NPs) have been found in many ecological environments (aquatic, terrestrial, air). Currently, there is great concern about the exposition and impact on animal health, including humans, because of the effects of ingestion and accumulation of these nanomaterials (NMs) in aquatic organisms and their incorporation into the food chain. NPs´ mechanisms of action on humans are currently unknown. In this study, we evaluated the altered molecular mechanisms on human neural stem cell line (hNS1) after 4 days of exposure to 30 nm polystyrene (PS) NPs (0.5, 2.5 and 10 μg/mL). Our results showed that NPs can induce oxidative stress, cellular stress, DNA damage, alterations in inflammatory response, and apoptosis, which could lead to tissue damage and neurodevelopmental diseases.

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Section: Plos Onesupporting

confidence: 92%

Section: Oxidative Stress Response: Cu/zn Sod1 Mnsod2 and Catmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Molecular effects of polystyrene nanoplastics on human neural stem cells

Martin-Folgar,

González-Caballero,

Torres-Ruiz

et al. 2024

PLoS ONE

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“…In particular, the 70 kDa-HSP (Hsp70) family promotes the proteolytic removal of oxidatively damaged proteins by the proteasome ( 18 ) and closely interact with the nitric oxide generation systems ( 19 ). Hsp70 is represents a marker of oxidative response in different experimental models, including Danio rerio (commonly called zebrafish) ( 20 – 22 ).…”

Section: Introductionmentioning

confidence: 99%

Effects of carnosine on the embryonic development and TiO2 nanoparticles-induced oxidative stress on Zebrafish

Caruso

Scalisi²,

Pecoraro³

et al. 2023

Front. Vet. Sci.

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Oxidative stress is due to an unbalance between pro-oxidants, such as reactive oxygen (ROS) and nitrogen (RNS) species, and antioxidants/antioxidant system. Under physiological conditions these species are involved in different cellular processes such as cellular homeostasis and immune response, while an excessive production of ROS/RNS has been linked to the development of various diseases such as cancer, diabetes, and Alzheimer's disease. In this context, the naturally occurring dipeptide carnosine has shown the ability to scavenge ROS, counteract lipid peroxidation, and inhibit proteins oxidation. Titanium dioxide nanoparticles (TiO2-NPs) have been widely used to produce cosmetics, in wastewater treatment, in food industry, and in healthcare product. As consequence, these NPs are often released into aquatic environments. The Danio rerio (commonly called zebrafish) embryos exposure to TiO2-NPs did not affect the hatching rate, but induced oxidative stress. According to this scenario, in the present study, we first investigated the effects of carnosine exposure and of a sub-toxic administration of TiO2-NPs on the development and survival of zebrafish embryos/larvae measured through the acute embryo toxicity test (FET-Test). Zebrafish larvae represent a useful model to study oxidative stress-linked disorders and to test antioxidant molecules, while carnosine was selected based on its well-known multimodal mechanism of action that includes a strong antioxidant activity. Once the basal effects of carnosine were assessed, we then evaluated its effects on TiO2-NPs-induced oxidative stress in zebrafish larvae, measured in terms of total ROS production (measured with 2,7-dichlorodihydrofluorescein diacetate probe) and protein expression by immunohistochemistry of two cellular stress markers, 70 kDa-heat shock protein (Hsp70) and metallothioneins (MTs). We demonstrated that carnosine did not alter the phenotypes of both embryos and larvae of zebrafish at different hours post fertilization. Carnosine was instead able to significantly decrease the enhancement of ROS levels in zebrafish larvae exposed to TiO2-NPs and its antioxidant effect was paralleled by the rescue of the protein expression levels of Hsp70 and MTs. Our results suggest a therapeutic potential of carnosine as a new pharmacological tool in the context of pathologies characterized by oxidative stress such as neurodegenerative disorders.

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