Abstract

Imidacloprid (Imid), a systemic neonicotinoid insecticide, is broadly used worldwide. It is reported to contaminate aquatic systems. This study was proposed to evaluate oxidative stress and genotoxicity of Imid on Nile tilapia (Oreochromis niloticus) and the protective effect of ascorbic acid (Asc). O. niloticus juveniles (30.4 ± 9.3 g, 11.9 ± 1.3 cm) were divided into six groups (n = 10/replicate). For 21 days, two groups were exposed to sub-lethal concentrations of Imid (8.75 ppm, 1/20 of 72 h-LC50 and 17.5 ppm, 1/10 of 72 h-LC50); other two groups were exposed to Asc (50 ppm) in combination with Imid (8.75 and 17.5 ppm); one group was exposed to Asc (50 ppm) in addition to a group of unexposed fish which served as controls. Oxidative stress was assessed in the liver where the level of enzymatic activities including superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPX) in addition to mRNA transcripts and, Lipid peroxidation (LPO) were evaluated. Moreover, mitotic index (MI) and comet assay were performed, in addition, the erythrocytic micronucleus (MN), and nuclear abnormalities (NA) were observed to assess genotoxicity in fish. Imid exposure induced significant (p ˂ 0.05) changes in the antioxidant profile of the juveniles' liver by increasing the activities and gene expression of SOD, CAT and GPX as well as elevating the levels of LPO. DNA strand breaks in gill cells, erythrocytes and hepatocytes along with erythrocytic MN and NA were also significantly elevated in Imid-exposed groups. MI showed a significant (p ˂ 0.05) decrease associated with Imid exposure. Asc administration induced a significant amelioration towards the Imid toxicity (8.75 and 17.5 ppm). A significant protective potency against the genotoxic effects of Imid was evidenced in Asc co-treated groups. Collectively, results highlight the importance of Asc as a protective agent against Imid-induced oxidative stress and genotoxicity in O. niloticus juveniles.

Highlights

  • Imidacloprid (Imid), a systemic neonicotinoid insecticide, is broadly used worldwide

  • The antioxidative system plays a crucial role in repelling exogenous pollution, and other stimuli that induce the production of the superoxide anion, the intracellular parental form of reactive oxygen species (ROS), which is a highly active molecule and thereby causing various damages to cells and ­organisms[36]

  • Superoxide anion radicals can be catalyzed by superoxide dismutase (SOD) to form oxygen and hydrogen peroxide (­ H2O2)

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Summary

Introduction

Imidacloprid (Imid), a systemic neonicotinoid insecticide, is broadly used worldwide. This study was proposed to evaluate oxidative stress and genotoxicity of Imid on Nile tilapia (Oreochromis niloticus) and the protective effect of ascorbic acid (Asc). A significant protective potency against the genotoxic effects of Imid was evidenced in Asc co-treated groups. Results highlight the importance of Asc as a protective agent against Imid-induced oxidative stress and genotoxicity in O. niloticus juveniles. Xenobiotics or toxic chemicals including Imid may affect the endogenous and exogenous reactive oxygen species (ROS) balance and can subsequently suppress the antioxidant defenses or induce macromolecules oxidative damage in many ­organisms[12,13,14]. Its toxicity in Oncorhynchus mykiss and Danio rerio[15], Cyprinus carpio[2] and O. niloticus[4] was reported In carp fish, it induced severe inflammation, oxidative stress and histopathological lesions in the gills, liver, and b­ rain[16]. Beneficial effects of Asc on adult Oncorhynchus mykiss were ­proven[35]

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