Imidacloprid exposure cause the histopathological changes, activation of TNF-α, iNOS, 8-OHdG biomarkers, and alteration of caspase 3, iNOS, CYP1A, MT1 gene expression levels in common carp (Cyprinus carpio L.).

Selçuk Özdemir,Serdar Altun,Harun Arslan

doi:10.1016/j.toxrep.2017.12.019

Abstract

Imidacloprid (IMI) is a neonicotinoid that is widely used for the protection of crops and carnivores from insects and parasites, respectively. It is well known that imidacloprid exposure has a harmful effect on several organisms. However, there is little information about imidacloprid toxicity in aquatic animals, particularly fish. Thus, in the current study, we assessed the histopathological changes; activation of iNOS, 8-OHdG and TNF-α; and expression levels of caspase 3, iNOS, CYP1A and MT1 genes in the common carp exposed to imidacloprid. For this purpose, fish were exposed to either a low dose (140 mg/L) or a high dose (280 mg/L) of imidacloprid for 24 h, 48 h, 72 h and 96 h. After IMI exposure, we detected hyperplasia of secondary lamellar cells and mucous cell hyperplasia in the gills, as well as hydropic degeneration in hepatocytes and necrosis in the liver. Moreover, 8-OHdG, iNOS and TNF-α activation was found particularly in the gills and liver but also moderately in the brain. Transcriptional analysis showed that caspase 3 expression was altered low dose and high doses of IMI for 72 h and 96 h exposure (p < 0.05), iNOS expression was up-regulated with both low and high doses of IMI and in a time-dependent manner (p < 0.05, p < 0.01, p < 0.001), CYP1A expression was not significantly changed regardless of the dose of IMI and exposure time (p > 0.05) except with low and high doses of IMI for 96 h (p < 0.05), and lastly, MT1 gene expression was up-regulated only in the brain with low doses of IMI for 96 h and high doses of IMI for 48 h, 72 h and 96 h exposure (p < 0.05, p < 0.01). Our results indicated that acute IMI exposure moderately induce apoptosis in the brain but caused severe histopathological lesions, inflammation, and oxidative stress in the gills, liver, and brain of the common carp.

Highlights

Imidacloprid (IMI) is used as an insecticide and was first commercially produced by Bayer in 1991 [1]
Since there are no available studies on IMI. The compound (IMI) toxicity in the common carp, we investigated the potential toxic effects of IMI and assessed inflammation, oxidative stress, DNA damage and apoptosis associated with IMI in this animal model
No apparent lesions were detected in the histopathological examination of brain tissue, apart from some neurodegeneration in samples exposed to the high dose of IMI (280 mg/L) for 96 h

Summary

Introduction

Imidacloprid (IMI) is used as an insecticide and was first commercially produced by Bayer in 1991 [1]. The use of imidacloprid has been a controversial issue since the European Food Safety Authority reported its highly toxic effects on bees and farmers. There are different reports on the environmental toxicity of IMI. The compound (IMI) was selected based on high use, prior linkage with aquatic toxicity in the region, or emerging use with little previous monitoring. The potential adverse effects of IMI exposure in non-target organisms, including humans, animals, and aquatic animals, is of increased interest. It is necessary to assess IMI toxicity in vertebrate fish. This is important for non-target organisms such as humans and animals

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Conclusion