4.3 Article

Reactive oxygen species: the root cause of nanoparticle-induced toxicity in Drosophila melanogaster

Journal

FREE RADICAL RESEARCH
Volume 55, Issue 6, Pages 671-687

Publisher

TAYLOR & FRANCIS LTD
DOI: 10.1080/10715762.2021.1914335

Keywords

Nanoparticles; reactive oxygen species; antioxidant enzymes; redox mechanism; redox imbalance

Funding

  1. Department of Biotechnology, Ministry of Science and Technology [SERB/EMR/2017/003054, BT/PR21857/NNT/28/1238/2017, Odisha DBT 3325/ST(BIO)-02/2017]

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Nanotechnology is widely used in various industries, but also carries toxicity risks, mainly related to the generation of reactive oxygen species. Insufficient antioxidant enzymes to combat ROS may lead to DNA damage, cell damage, cytotoxicity, apoptosis, and abnormal physiological and genetic conditions.
Nanotechnology is a rapidly developing technology in the twenty-first century. Nanomaterials are extensively used in numerous industries including cosmetics, food, medicines, industries, agriculture, etc. Along with its wide application toxicity is also reported from studies of various model organisms including Drosophila. The toxicity reflects cytotoxicity, genotoxicity, and teratogenicity. The current study correlates the toxicity as a consequence of reactive oxygen species (ROS) generated owing to the presence of nanoparticles with the living cell. ROS mainly includes hydroxyl ions, peroxide ions, superoxide anions, singlet oxygen, and hypochlorous acids. An elevated level of ROS can damage the cells by various means. To protect the body from excess ROS, living cells possess a set of antioxidant enzymes which includes peroxidase, glutathione peroxidase, and catalase. If the antioxidant enzymes cannot nullify the elevated ROS level than DNA damage, cell damage, cytotoxicity, apoptosis, and uncontrolled cell regulations occur resulting in abnormal physiological and genotoxic conditions. Herewith, we are reporting various morphological and physiological defects caused after nanoparticle treatment as a function of redox imbalance.

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