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Updated: Aug 25, 2025
Assessment of Chemical Toxicity in Adult Drosophila Melanogaster
Published on: March 24, 2023
Canavalia ensiformis lectin induced oxidative stress mediate both toxicity and genotoxicity in Drosophila
Antônio Marcos de Oliveira Dos Santos1, Antônia Eliene Duarte2, Adrielle Rodrigues Costa3
1Department of Genetics, Federal University of Rio Grande do Sul, Porto Alegre, RS, Brazil.
Abstract:
Mannose/glucose-binding lectin from Canavalia ensiformis seeds (Concanavalin A - ConA) has several biological applications, such as mitogenic and antitumor activity. However, most of the mechanisms involved in the in vivo toxicity of ConA are not well known. In this study, the Drosophila melanogaster model was used to assess the toxicity and genotoxicity of different concentrations of native ConA (4.4, 17.5 and 70 μg/mL) in inhibited and denatured forms of ConA. The data show that native ConA affected: the survival, in the order of 30.6 %, and the locomotor performance of the flies; reduced cell viability to levels below 50 % (4.4 and 17.5 μg/mL); reduced nitric oxide levels; caused lipid peroxidation and increased protein and non-protein thiol content. In the Comet assay, native ConA (17.5 e 70 μg/mL) caused DNA damage higher than 50 %. In contrast, treatments with inhibited and denatured ConA did not affect oxidative stress markers and did not cause DNA damage. We believe that protein-carbohydrate interactions between ConA and carbohydrates of the plasma membrane are probably the major events involved in these activities, suggesting that native ConA activates mechanisms that induce oxidative stress and consequently DNA damage.
Insights
Native Concanavalin A (ConA) induces toxicity and DNA damage in Drosophila melanogaster by increasing oxidative stress. Inhibited or denatured ConA did not show these toxic effects, highlighting the importance of protein-carbohydrate interactions.
Area of Science:
- Toxicology
- Genetics
- Biochemistry
Background:
- Mannose/glucose-binding lectin from Canavalia ensiformis seeds (Concanavalin A - ConA) exhibits biological applications like mitogenic and antitumor activity.
- The in vivo toxicity mechanisms of ConA remain largely uncharacterized.
Purpose of the Study:
- To investigate the toxicity and genotoxicity of native, inhibited, and denatured ConA using the Drosophila melanogaster model.
- To elucidate the mechanisms underlying ConA-induced toxicity, focusing on oxidative stress and DNA damage.
Main Methods:
- Drosophila melanogaster were exposed to varying concentrations of native, inhibited, and denatured ConA.
- Assessed survival rates, locomotor performance, cell viability, nitric oxide levels, lipid peroxidation, and thiol content.
- Evaluated DNA damage using the Comet assay.
Main Results:
- Native ConA significantly reduced fly survival and locomotor performance, decreased cell viability, and altered oxidative stress markers (nitric oxide, lipid peroxidation, thiols).
- Native ConA (17.5 and 70 μg/mL) induced significant DNA damage (>50%) as evidenced by the Comet assay.
- Inhibited and denatured ConA treatments did not induce oxidative stress or DNA damage.
Conclusions:
- Native ConA triggers oxidative stress and subsequent DNA damage in vivo, likely through protein-carbohydrate interactions with cell membranes.
- The observed toxicity and genotoxicity are dependent on the native conformation of ConA, suggesting specific molecular interactions are involved.
