Glyphosate-based herbicide exposure causes antioxidant defence responses in the fruit fly Drosophila melanogaster.

Comp Biochem Physiol C Toxicol Pharmacol

Programa de Pós-Graduação em Ciências Fisiológicas - Fisiologia Animal Comparada, Instituto de Ciências Biológicas, Universidade Federal do Rio Grande - FURG. Av. Itália km 8, Campus Carreiros, 96203-900 Rio Grande, RS, Brazil. Electronic address:

Published: February 2017

Glyphosate is a non-selective and post-emergent herbicide that affects plant growth. Animal exposure to this herbicide can lead to adverse effects, such as endocrine disruption, oxidative stress and behavioural disorders. Drosophilids have been utilized previously as an effective tool in toxicological tests. In the present study, the effects of a glyphosate-based herbicide (Roundup [Original]) were investigated regarding oxidative stress, the antioxidant defence system and acetylcholinesterase (AChE) activity in Drosophila melanogaster. Flies (of both genders) that were 1 to 3days old were exposed to different glyphosate concentrations (0.0g/L=control, 1.0g/L, 2.0g/L, 5.0g/L and 10.0g/L) [corrected] in the diet for 24h and 96h. After the exposure periods, reactive oxygen species (ROS) levels, antioxidant capacity against peroxyl radicals (ACAP) and lipid peroxidation (LPO) levels were quantified. In addition, the mRNA expression of antioxidant genes (i.e., keap1, sod, sod2, cat, irc, gclc, gclm, gss, trxt, trxr-1 and trxr-2) was evaluated via RT-PCR. Additionally, AChE activity was evaluated only after the 96h exposure period. The results indicated that Roundup exposure leads to a reduction in ROS levels in flies exposed for 96h. ACAP levels and gene expression of the antioxidant defence system exhibited an increase from 24h, while LPO did not show any significant alterations in both exposure periods. AChE activity was not affected following Roundup exposure. Our data suggest that Roundup exposure causes an early activation of the antioxidant defence system in D. melanogaster, and this can prevent subsequent damage caused by ROS.

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http://dx.doi.org/10.1016/j.cbpc.2016.03.006DOI Listing

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