# Development and testing of Carbon Quantum Dot architectures to arrest neurotoxicant-insult- related outcomes

> **NIH NIH R16** · UNIVERSITY OF TEXAS EL PASO · 2022 · $153,375

## Abstract

Exposure to pesticides, fungicides and herbicides is linked to neuronal injury, neuronal loss and the onset and progress of
neurodegeneration. Environmental and household use of pesticides such as rotenone, Maneb, paraquat, Cyprodinil, etc
initiates mitochondrial dysfunction. The resulting elevation in levels of reactive oxygen species (ROS) and reactive nitrogen
species (RNS) triggers ubiquitin-proteasome (UPS) dysregulation, alters cellular-proteomics’ status and the provokes the
aggregation of amyloid proteins in neurons. Aggregation-prone amyloids such as alpha-synuclein, amyloid β, and mutant
Huntingtin protein (mHTT) form toxic oligomers and protofibrils that create pores in cell membranes, disrupt Ca2+
homeostasis, facilitate neurotransmitter leakage and provoke neuronal death, on-setting neurodegenerative disorders such
as Parkinson’s (PD), Alzheimer’s (AD) and Huntington’s (HD) diseases. Efforts at limiting environmental toxicant-driven
neurodegenerative onset with small molecules have enjoyed limited success. Here, we explore whether a novel class of
carbon nano materials, viz. carbon quantum dots (CQDs), can restore cellular homeostasis and prevent behavioral deficits
in organisms under pesticide exposure. CQDs are easily synthesized from biowaste-containing carbon precursors such as
fruit peel, waste paper and organic acids via green-chemical techniques. They possess low cytotoxicity and are inherently
antioxidant. Importantly, they can be chemically functionalized and doped. When chemically tuned, they find applications
in biosensing, tissue imaging, drug-delivery and can cross the blood-brain barrier. Preliminary data from our lab has revealed
that organo-acid-derived CQDs can interfere in amyloid aggregation and mitigate ROS-stress in cells. They were uptaken
by nematodes and protected them from paraquat toxicity. We hypothesize that CQDs ameliorate environmental toxicant-
associated neuronal corruption. We test this hypothesis in Aim 1, by determining whether CQDs can intervene in amyloid
fibril-forming trajectories. We also attempt to extend our understanding of how functionalized CQDs interact with toxic
intermediates such as oligomers and protofibrils to passivate them. In Aim 2, using a number of proteomic and
neurometabolomic readouts, we establish whether functionalized CQDs can reset pesticide-driven cellular dyshomeostasis
in model neuroblastoma-derived cells. In Aim 3, we will test their ability to restore neuronal loss and behavioral deficits in
C. elegans using strains prone to amyloidogenesis and/or via pesticide-exposure. In the former scenario, worms strains
expressing mHTT, amyloid β or alpha-synuclein will be exposed to CQDs while the latter objective is completed by introducing
CQDs into pesticide-challenged worms. By quantitatively co-relating amyloid aggregation and locomotor compromise with
CQD-type and dose, we will test our hypothesis at the organismal level. Findings from the completion of the proposed work
...

## Key facts

- **NIH application ID:** 10412365
- **Project number:** 1R16GM145575-01
- **Recipient organization:** UNIVERSITY OF TEXAS EL PASO
- **Principal Investigator:** Mahesh Narayan
- **Activity code:** R16 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2022
- **Award amount:** $153,375
- **Award type:** 1
- **Project period:** 2022-08-01 → 2026-06-30

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10412365

## Citation

> US National Institutes of Health, RePORTER application 10412365, Development and testing of Carbon Quantum Dot architectures to arrest neurotoxicant-insult- related outcomes (1R16GM145575-01). Retrieved via AI Analytics 2026-05-24 from https://api.ai-analytics.org/grant/nih/10412365. Licensed CC0.

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