FB2026_01 , released March 12, 2026
FB2026_01 , released March 12, 2026
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Citation
Pappus, S.A., Mishra, M. (2018). A Drosophila Model to Decipher the Toxicity of Nanoparticles Taken Through Oral Routes.  Adv. Exp. Med. Biol. 1048(): 311--322.
FlyBase ID
FBrf0238072
Publication Type
Review
Abstract
In recent era, nanoparticles (NPs) are widely used in food, medicine and body implants. Besides it's wide use being a foreign particle it may have some noxious effect on the body. To understand the mechanistic role of NPs toxicity, Drosophila appeared to be a superior model organism. Toxicity of several nanoparticles were accessed using Drosophila. The NPs, after oral route of exposure enter into the gut, crosses the barrier of peritrophic membrane and induces apoptosis. The toxicity of NPs within gut resulted in developmental delay, with decrease in pupa count, fly hatching along with weight loss. The adult fly hatched after nanoparticle treatment shows increasing phenotypic defect in various sensory organs as well as in different body parts. Besides phenotypic defect some of the nanoparticle results altered behavioural phenotypes like larva crawling or adult climbing. Alteration of both phenotypic as well as behavioural assay clearly hints that signalling pathway like Notch, Wnt, EGFR etc. get affected due to exposure of nanoparticle. Results from various labs prove that nanoparticle can mediate developmental defect by altering signalling pathways. Since many of the signalling pathways are conserved the effect seen in model organisms cannot be overlooked. All the nanoparticles used in food and medicine should be modified to nullify the toxic effect before used in food and medicine.
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Secondary IDs
    Language of Publication
    English
    Additional Languages of Abstract
    Parent Publication
    Publication Type
    Journal
    Abbreviation
    Adv. Exp. Med. Biol.
    Title
    Advances in Experimental Medicine and Biology
    Publication Year
    1976-
    ISBN/ISSN
    0065-2598
    Data From Reference
    Chemicals (6)
    Genes (3)
    Human Disease Models (1)