Citric Acid-Derived Carbon Quantum Dots Attenuate Paraquat-Induced Neuronal Compromise In Vitro and In Vivo .
Gabriela HenriquezJyoti AhlawatRobert FairmanMahesh NarayanPublished in: ACS chemical neuroscience (2022)
The potent environmental herbicide and weedicide paraquat is linked to neuromotor defects and Parkinson's disease (PD). We have evaluated the neuroprotective role of citric acid-sourced carbon quantum dots (Cit-CQDs) on paraquat-insulted human neuroblastoma-derived SH-SY5Y cell lines and on a paraquat-exposed nematode ( Caenorhabditis elegans ). Our data reveal that Cit-CQDs are able to scavenge free radicals in test tube assays and mitigate paraquat-elevated reactive oxygen species (ROS) levels in SH-SY5Y cells. Furthermore, Cit-CQDs protect the cell line from paraquat, which otherwise elicits cell death. Cit-CQDs-challenged nematodes demonstrate enhanced survival rates 72 h post-paraquat exposure compared to controls. Paraquat ablates dopamine (DA) neurons, which results in compromised locomotor function in nematodes. However, the neurons remained intact when the nematodes were incubated with Cit-CQDs prior to neurotoxicant exposure. The collective data suggest Cit-CQDs offer neuroprotection for cell lines and organisms from xenotoxicant-associated neuronal injury and death. The study suggests Cit-CQDs as a potentially viable green chemistry-synthesized, biobased nanomaterial for intervention in neurodegenerative disorders.
Keyphrases
- pulmonary fibrosis
- cell death
- quantum dots
- reactive oxygen species
- cerebral ischemia
- randomized controlled trial
- endothelial cells
- spinal cord
- induced apoptosis
- cell cycle arrest
- spinal cord injury
- machine learning
- sensitive detection
- signaling pathway
- big data
- dna damage
- uric acid
- metabolic syndrome
- subarachnoid hemorrhage
- blood brain barrier
- gram negative
- endoplasmic reticulum stress
- brain injury
- multidrug resistant
- energy transfer
- risk assessment
- oxide nanoparticles