Carboxyl graphene oxide nanoparticles induce neurodevelopmental defects and locomotor disorders in zebrafish larvae

Cao, Zigang; Su, Meile; Wang, Honglei; Zhou, Liqun; Meng, Zhen; Xiong, Gaofeng; Liao, Xinjun; Lu, Huiqiang

doi:10.1016/j.chemosphere.2020.128611

Cited by 41 publications

(21 citation statements)

References 34 publications

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“…Astaxanthin can rescue cardiac toxicity of zebrafish embryos caused by benoxacor exposure 53 . Carboxyl graphene oxide nanoparticles induced neurodevelopmental defects by increasing ROS level, and astaxanthin inhibits ROS accumulation 54 . In our study, Astaxanthin treatment relieves neurotoxicity induced by chlorphoxim through decreasing ROS level.…”

Section: Discussionsupporting

confidence: 53%

Chlorphoxim induces neurotoxicity in zebrafish embryo through activation of oxidative stress

Xiong

Wang

Dong

et al. 2022

Environmental Toxicology

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It is known that chlorphoxim is a broad-spectrum and high-effective pesticide. With the wide use in agricultural practice, chlorphoxim residue is also frequently detected in water, but its potential toxicity to aquatic life is still unclear. In this study, zebrafish is used as a model to detect the toxicity of chlorphoxim. Our results showed that exposure of high concentration of chlorphoxim at 96 h post-fertilization (hpf) resulted in a high mortality and pericardium edema rate, a low hatchability rate and heart rate. The nervous system damage, swimming behavior alteration and acetylcholinesterase (AChE) inhibition were measured in zebrafish embryos after a 6 days post-fertilization (dpf) of chlorphoxim exposure. The expression of neural-related genes is abnormal in zebrafish embryos. Chlorphoxim exposure significantly increases oxidative stress in zebrafish embryos by inhibiting antioxidant enzyme (SOD and CAT) and activating reactive oxygen species (ROS). As expected, chlorphoxim exposure induces apoptosis by enhancing the expression of apoptotic genes (Bax, Bcl2, and p53). Astaxanthin (ATX), an effective antioxidant, was found to be able to rescue the neurotoxicity of chlorphoxim through relieving oxidative stress and apoptosis.Altogether, the results showed that chlorphoxim exposure led to severe neurotoxicity to zebrafish embryos, which was contributed to a more comprehensive understanding of the safety use of the organophosphorus pesticide.

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Section: Discussionsupporting

confidence: 53%

Chlorphoxim induces neurotoxicity in zebrafish embryo through activation of oxidative stress

Xiong

Wang

Dong

et al. 2022

Environmental Toxicology

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“…5-HT is the principal neurotransmitter for modulating various brain functions and psychiatric conditions such as depression and antisocial behavior [ 22 , 23 ]. The alteration of genes that are involved in GABA and 5-HT synthesis, metabolism and receptor trafficking may result in dysfunction of the corresponding neurotransmitter systems [ 22 , 24 , 25 ]. It was reported that two typical neonicotinoids, imidacloprid and thiamethoxam, could induce abnormality in locomotor activity, alter the expression of genes that are involved in GABA and 5-HT transmission, and cause neurotoxicity in zebrafish [ 26 ].…”

Section: Introductionmentioning

confidence: 99%

Early-Stage High-Concentration Thiacloprid Exposure Induced Persistent Behavioral Alterations in Zebrafish

Xie

2022

IJERPH

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As a major neonicotinoid insecticide, thiacloprid (THCP) is frequently detected in aquatic environments worldwide due to its heavy use, posing potential threats to aquatic organisms. In this study, zebrafish (Danio rerio) embryos were exposed to THCP (1, 10, 100, 1000 and 10,000 μg/L) for 5 days and then recovered in THCP-free water for 20 days to investigate the effects of early-stage THCP exposure on the development, antioxidant defense, and neurotransmitter systems of zebrafish, and explore their recovery mechanism. The results show that THCP exposure induced developmental toxicity and oxidative stress in zebrafish. The hypoactivity, behavioral alterations (decreased avoidance and edge preference behaviors) and neurotoxicity were found throughout the exposure-recovery experiments. THCP exposure altered the expression of γ-aminobutyric acid (GABA)- and serotonin (5-HT)-related genes accompanied by the decrease in GABA and 5-HT contents. However, after recovery, GABA content returned to the control level, but 5-HT did not, indicating that only the serotonergic system was persistently disrupted. Overall, our results suggest that the disruption of the serotonergic system and oxidative stress may aggravate neurotoxicity and that the former was the main reason for the depressive-like behavior. This study could help to unravel the mechanisms of the behavioral alterations induced by early-stage THCP exposure in zebrafish.

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“…Surprisingly, they found an elevated level of oxidative stress and disrupted development of the nervous system of zebrafish larvae, manifested as abnormalities in locomotor activity. Furthermore, acetylcholine esterase and ATPase activity and expression of genes related to Parkinson’s disease were up-regulated [ 70 ].…”

Section: Developmental Carbon Nanotoxicitymentioning

confidence: 99%

Reproductive and Developmental Nanotoxicity of Carbon Nanoparticles

et al. 2022

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The presented review aims to summarize the knowledge regarding the reproductive and developmental toxicity of different types of carbon nanoparticles, such as graphene, graphene oxide, multi- and single-walled nanotubes, fullerenes, and nanodiamonds. Carbon nanoparticles have unique chemical and physical properties that make them an excellent material that can be applied in many fields of human activity, including industry, food processing, the pharmaceutical industry, or medicine. Although it has a high degree of biocompatibility, possible toxic effects on different tissue types must also be taken into account. Carbon nanoparticles are known to be toxic to the respiratory, cardiovascular, nervous, digestive system, etc., and, according to current studies, they also have a negative effect on reproduction and offspring development.

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Carboxyl graphene oxide nanoparticles induce neurodevelopmental defects and locomotor disorders in zebrafish larvae

Cited by 41 publications

References 34 publications

Chlorphoxim induces neurotoxicity in zebrafish embryo through activation of oxidative stress

Chlorphoxim induces neurotoxicity in zebrafish embryo through activation of oxidative stress

Early-Stage High-Concentration Thiacloprid Exposure Induced Persistent Behavioral Alterations in Zebrafish

Reproductive and Developmental Nanotoxicity of Carbon Nanoparticles

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