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Carbon Quantum Dots Protect Against Neuronal Cell Death

In an article recently published in the journal ACS Chemical Neuroscience, researchers discussed the attenuation of paraquat (PQ)-induced neuronal compromise in vitro and in vivo by carbon quantum dots derived from citric acid (Cit).

Study: Citric Acid-Derived Carbon Quantum Dots Attenuate Paraquat-Induced Neuronal Compromise In Vitro and In Vivo. Image Credit: MattLphotography/Shutterstock.com

Protein aggregation and the concurrent pathophysiology of their respective illnesses are linked to the soluble-to-toxic change of amyloid proteins. The main etiological culprits for the onset and development of neurodegenerative diseases continue to be environmental variables.

Applications of PQ in the Treatment of Neurodegenerative Diseases

The agricultural and xenobiotic agent PQ, which is used as a herbicide in the cultivation of crucial crops, including soy, corn, and cotton, is of particular relevance. A rising range of neurodegenerative disorders, including Parkinson's disease (PD), has been related to research on PQ. Here, PQ targeted to reactive oxygen species (ROS) production causes oxidative stress, mitochondrial failure, dopaminergic neuron degeneration, and protein aggregation. Therefore, it is essential to create novel strategies with strong antioxidant activity and favorable biocompatibility to treat neurodegenerative illnesses given the rapid growth of nanotechnology.

Carbon Quantum Dots

The usage of carbon nanomaterials (CNMs) in biomedicine is very common. Carbon quantum dots (CQDs) have been successfully used in environmental applications (as sensors) and as prognosticators. Recent research has shown that graphene quantum dots (GQDs) can interfere with IAPP aggregation and decrease the fibrillization of PD-associated amyloid -synuclein.

In other research, it was discovered that biocompatible carbon quantum dots produced from naphthalene interfered with the transition of HEWL from soluble to poisonous. According to reports, carbon quantum dots have significant antioxidant activity due to their capacity to scavenge free radicals. Citric acid has low toxicity and great biocompatibility and is one of the most widely used precursors for creating carbon quantum dots. However, more research is required to confirm that the formation of carbon quantum dots enhances citric acid's antioxidant action.

Utility of Citric Acid-Sourced Carbon Quantum Dots

In this study, the authors assessed the neuroprotective effects of citric acid-sourced carbon quantum dots (Cit-CQDs) on PQ-insulted human neuroblastoma-derived SHSY5Y cell lines and on a nematode that had been exposed to paraquat (Caenorhabditis elegans).

The findings showed that Cit-carbon quantum dots could lower the levels of paraquat-induced ROS in SH-SY5Y cells and scavenge free radicals in test tube experiments. Additionally, Cit-carbon quantum dots guarded the cell line against paraquat, which would otherwise cause cell death. Nematodes that were exposed to Cit-carbon quantum dots improved survival rates as compared to controls 72 hours after paraquat exposure.

Dopamine (DA) neurons were destroyed by paraquat, which impaired worm locomotion. However, when the nematodes were incubated with Cit-carbon quantum dots before being exposed to a neurotoxicant, the neurons were unharmed. The accumulated evidence pointed to Cit-carbon quantum dots as a neuroprotective agent for cell lines and organisms against neuronal injury and death brought on by xenotoxicants.

According to the study, Cit-carbon quantum dots were a potentially useful bio-based nanomaterial that can be produced using green chemistry to treat neurodegenerative diseases.

The team looked at whether Cit-carbon quantum dots could act in a xenotoxicant model of neuronal damage both in vitro and in vivo. The findings demonstrated that carbon quantum dots made from citric acid precursors were effectively protecting against PQ-induced neurotoxicity and neuronal death using undifferentiated SH-SY5Y cell lines and C. elegans. Importantly, Cit-carbon quantum dots helped reduce organismal mortality caused by PQ compromise.

The researchers conducted this investigation to show the prophylactic effect of Cit-carbon quantum dots and their capacity to prevent neuronal cell death by blocking and scavenging the PD cascade, which caused dopaminergic neuron loss and cell dysfunction. The vitality of C. elegans and neuroblastoma cells (SH-SY5Y) both with and without Cit-carbon quantum dots was used to assess the toxicity of PQ. The neuroblastoma cells were used to investigate the toxicity of Cit-carbon quantum dots and PQ (SH-SY5Y). The percentage of cell death as a function of Cit-carbon quantum dots and PQ was measured to determine the cytotoxicity profile of Cit-carbon quantum dots in the cell line.

Neuroprotective Effects of Cit-Sourced Carbon Quantum Dots

The size of the Cit-CQDs ranged from 10 to 60 nanometers. A wide peak in the ultraviolet (UV)–visible (vis) spectrum at 330 nanometers indicated the presence of conjugated moieties capable of photoluminescence. The presence of oxidized groups (CO; COH) and conjugated centers (CC), which validated the solubility and photoluminescence capabilities of Cit-CQDs, was demonstrated by the infrared (IR) spectrum. The reduction in UV-vis intensity with increasing Cit-CQD concentration demonstrated the dose-dependent free radical scavenging capacity of the aforementioned CQDs.

The antioxidant capacity and effectiveness of Cit-CQDs were shown by the microgram range of Cit-CQDs that exhibited ROS scavenging capabilities. After 24 hours of exposure, the number of dead cells increased along with the concentration of Cit-CQDs. At concentrations below 500 grams/milliliter, Cit-CQDs were more cytotoxic than the untreated and vehicle controls. Unlike the vehicle group, Cit-CQDs exhibited no toxicity at lower doses.

Compared to the vehicle control group, PQ showed exceptional toxicity to the cell at values above 250 Molar. The cytoprotective effect of Cit-CQDs was statistically significant in reducing cell death from 500 Molar PQ insult from 60% to 30%. In SH-SY5Y cells, exposure to PQ caused increased ROS levels. From 24 to 72 hours after the PQ insult, survival for a 1 milliMolar dosage decreased from 90% to 65%. Compared to the untreated control, PQ treatment caused about 75% of the nematodes to show a drop in GFP fluorescence. Furthermore, treatment with Cit-CQDs led to the specific neuroprotection of DA neurons.

Conclusions and Future Perspectives

In conclusion, this study demonstrated that a particular type of carbon nanomaterial, CQDs made of citric acid protects against oxidative stress, neuronal loss, and increased organismal mortality brought on by environmental toxins. The authors mentioned that Cit-CQDs and possibly other CQDs could be a useful tool in the fight against sporadic neurodegenerative diseases.

Reference

Henriquez, G., Ahlawat, J., Fairman, R., et al. (2022). Citric Acid-Derived Carbon Quantum Dots Attenuate Paraquat-Induced Neuronal Compromise In Vitro and In Vivo. ACS Chemical Neuroscience https://pubs.acs.org/doi/10.1021/acschemneuro.2c00099​​​​​​​​​​​​​​

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Surbhi Jain

Written by

Surbhi Jain

Surbhi Jain is a freelance Technical writer based in Delhi, India. She holds a Ph.D. in Physics from the University of Delhi and has participated in several scientific, cultural, and sports events. Her academic background is in Material Science research with a specialization in the development of optical devices and sensors. She has extensive experience in content writing, editing, experimental data analysis, and project management and has published 7 research papers in Scopus-indexed journals and filed 2 Indian patents based on her research work. She is passionate about reading, writing, research, and technology, and enjoys cooking, acting, gardening, and sports.

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