Abstract
Genomic instability, one of cancer’s hallmarks, is induced by genotoxins from endogenous and exogenous sources, including reactive oxygen species (ROS), diet, and environmental pollutants. A sensitive in vivo genotoxicity test is required for the identification of human hazards to reduce the potential health risk. The somatic mutation and recombination test (SMART) or wing spot test is a genotoxicity assay involving Drosophila melanogaster (fruit fly) as a classical, alternative human model. This review describes the principle of the SMART assay in conjunction with its advantages and disadvantages and discusses applications of the assay covering all segments of health-related industries, including food, dietary supplements, drug industries, pesticides, and herbicides, as well as nanoparticles. Chemopreventive strategies are outlined as a global health trend for the anti-genotoxicity of interesting herbal extract compounds determined by SMART assay. The successful application of Drosophila for high-throughput screening of mutagens is also discussed as a future perspective.
Highlights
Maintaining a stable genome is of the greatest importance for the proper functioning of life
This review summarizes the basic principle of the somatic mutation and recombination test (SMART) assay and its application, from past to present, in human hazard assessment covering food and drug safety, nanoparticles, pesticide and herbicide assessment, and environmental safety
The somatic mutation and recombination test (SMART) or wing spot test relies on the genetic damage induction of dividing wing disc cells, resulting in loss of heterozygosity (LOH) during larval development, which can be obviously seen on the adult wings as mutant wing spots [10]
Summary
Maintaining a stable genome is of the greatest importance for the proper functioning of life. Mutagen/genotoxic agents can be divided into two groups as (i) endogenous genotoxins such as reactive oxygen species (ROS) that oxidize guanine, leading to the formation of the most common DNA adducts, 8-oxoguanine (8-oxoG) [7]. These highly mutagenic lesions can pair to either cytosine (C) or adenine (A) in the DNA leading to T-to-G mutations [8]. Another source is (ii) exogenous genotoxins, including those present in food, medicine, cosmetics, air pollution, radiation, and sunlight.
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