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Updated: May 3, 2026
Novel Whole-tissue Quantitative Assay of Nitric Oxide Levels in Drosophila Neuroinflammatory Response
Published on: December 4, 2013
A common fungal volatile organic compound induces a nitric oxide mediated inflammatory response in Drosophila
Arati A Inamdar1, Joan W Bennett1
1Department of Plant Biology and Pathology, Rutgers, The State University of New Jersey, New Brunswick, New Jersey, 08901.
Abstract:
Using a Drosophila model, we previously demonstrated truncated life span and neurotoxicity with exposure to 1-octen-3-ol, the volatile organic compound (VOC) responsible for much of the musty odor found in mold-contaminated indoor spaces. In this report, using biochemical and immunological assays, we show that exposure to 0.5 ppm 1-octen-3-ol induces a nitric oxide (NO) mediated inflammatory response in hemocytes, Drosophila innate immune cells. Moreover, exposed Drosophila brains show increased peroxynitrite expression. An increase in nitrite levels is observed with toluene and 1-octen-3-ol but not with 1-butanol. Pharmacological inhibitors of nitric oxide synthase (NOS) namely, L-NAME, D-NAME and minocycline, and NOS mutants show improvements of life span among 1-octen-3-ol exposed flies. Exposure to 1-octen-3-ol also induces NOS expression in larval tracheal tissues and remodels tracheal epithelial lining. These findings suggest a possible mechanistic basis for some of the reported adverse health effects attributed to mold exposure and demonstrates the utility of this in vivo Drosophila model to complement existing model systems for understanding the role of inflammation in VOC-mediated toxicity.
Insights
Mold-related volatile organic compound (VOC) 1-octen-3-ol causes inflammation and shortens lifespan in Drosophila by increasing nitric oxide (NO). Inhibiting nitric oxide synthase (NOS) improves fly survival, suggesting a mechanism for mold-related health issues.
Area of Science:
- Environmental Health
- Toxicology
- Immunology
Background:
- 1-octen-3-ol, a volatile organic compound (VOC) from mold, causes neurotoxicity and shortens lifespan.
- The specific mechanisms underlying VOC-induced toxicity, particularly inflammation, remain incompletely understood.
Purpose of the Study:
- To investigate the role of nitric oxide (NO) in the toxicity of 1-octen-3-ol using a Drosophila model.
- To explore the impact of 1-octen-3-ol exposure on innate immune cells and neuronal tissues.
Main Methods:
- Biochemical and immunological assays were performed on Drosophila exposed to 1-octen-3-ol.
- Nitrite levels, peroxynitrite expression, and nitric oxide synthase (NOS) expression were measured.
- Pharmacological inhibitors of NOS and NOS mutants were used to assess lifespan.
Main Results:
- Exposure to 1-octen-3-ol induced a NO-mediated inflammatory response in Drosophila hemocytes.
- Increased peroxynitrite and nitrite levels were observed in exposed Drosophila brains and tissues.
- Inhibiting NOS or using NOS mutants significantly improved lifespan in 1-octen-3-ol exposed flies.
- 1-octen-3-ol exposure induced NOS expression and tracheal remodeling.
Conclusions:
- Nitric oxide plays a critical role in the toxicity of 1-octen-3-ol, contributing to inflammation and reduced lifespan.
- The Drosophila model effectively demonstrates the link between VOC exposure, NO-mediated inflammation, and adverse health effects.
- These findings provide mechanistic insights into the health impacts of mold-contaminated indoor environments.
