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SODIUM NITROPRUSSIDE TOXICITY IN D rosophila melanogaster : DELAYED PUPATION, REDUCED ADULT EMERGENCE, AND INDUCED OXIDATIVE/NITROSATIVE STRESS IN ECLOSED FLIES
Author(s) -
Lozinsky Oleksandr V.,
Lushchak Oleh V.,
Storey Janet M.,
Storey Kenneth B.,
Lushchak Volodymyr I.
Publication year - 2012
Publication title -
archives of insect biochemistry and physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.576
H-Index - 66
eISSN - 1520-6327
pISSN - 0739-4462
DOI - 10.1002/arch.21033
Subject(s) - biology , sodium nitroprusside , aconitase , oxidative stress , catalase , superoxide dismutase , toxicity , glutathione reductase , antioxidant , drosophila melanogaster , biochemistry , nitric oxide , enzyme , endocrinology , medicine , glutathione peroxidase , gene
The toxicity of sodium nitroprusside ( SNP ) was tested on the D rosophila melanogaster model system. Fly larvae were raised on food supplemented with SNP at concentrations of 0.01–1.5 mM. Food supplementation with SNP caused a developmental delay in flies and reduced adult eclosion. Biochemical analyses such as levels of oxidative stress markers and activities of antioxidant and associated enzymes were carried out on 2‐day‐old flies emerged from control and SNP ‐fed larvae. Larval exposure to SNP resulted in lower activities of aconitase and catalase in adult flies relative to the control cohort. However, larval treatment with SNP led to higher carbonyl protein content and higher activities of superoxide dismutase, glucose‐6‐phosphate dehydrogenase, thioredoxin reductase, and glutathione‐ S ‐transferase in flies. Among the parameters tested, aconitase activity and developmental end points may be useful early indicators of toxicity caused by SNP . The study also suggests that the toxicity of SNP may arise not just from its direct effects, but also from its decomposition products such as nitric oxide and iron ions.