Histopathological and genotoxic effects of chlorpyrifos in rats

Abstract

This study aims to investigate the effects of chlorpyrifos's sub-acute exposure on male rats. Two groups with six animals each were orally treated, respectively, with 3.1 mg/kg b w and 6.2 mg/kg b w of chlorpyrifos during 4 weeks. The genotoxic effect of chlopyrifos was investigated using the comet assay and the micronucleus test. Some hematological and liver's histopathological changes were also evaluated. Results revealed that chlorpyrifos induced histopathological alterations in liver parenchyma. The lymphoid infiltration observed in liver sections and the increase in white blood cells parameter are signs of inflammation. A significant increase in the platelet' count and in polychromatic erythrocytes/normochromatic erythrocytes (PCE/NCE) ratio was observed in chlorpyrifos-treated groups which could be due to the stimulatory effect of chlorpyrifos on cell formation in the bone marrow at lower doses. In addition, the increase of bone marrow micronucleus percentage and the comet tail length revealed a genotoxic potential of chlorpyrifos in vivo.

Chromosome Missegregation and Aneuploidy Induction in Human Peripheral Blood Lymphocytes In vitro by Low Concentrations of Chlorpyrifos, Imidacloprid and α‐Cypermethrin

“…and found dose-dependent comet formation at 24-h and 48-h exposure, which decreased with extended exposure times up to 96 h owing to DNA damage repair. Numerous studies have tested commercial formulations of chlorpyrifos on rats (Ezzi et al, 2016), mice (Chauhan et al, 2016), silkworms (Kalita et al, 2016) and fish (Ismail et al, 2014;Vera-Candioti et al, 2014), reporting the positive genotoxic effects. Even the occupational exposure to mixtures of insecticides including chlorpyrifos formulations has been associated with observed MN induction (Omari, 2011;Singh et al, 2011).…”

Adverse effects of organophosphorus pesticides on the liver: a brief summary of four decades of research

“…Extensive data suggest that free radical formation and oxidative stress can be a major contributor to the toxicity of pesticides (108)(109)(110)(111)(112)(113). OPs are oxidants and impair enzymatic antioxidant defences, including superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), and glutathione S-transferase (GST) (23,34,44,(114)(115)(116)(117)(118)(119)(120)(121)(122)(123)(124)(125)(126)(127)(128)(129). Malathion, methyl parathion, and parathion in HepG2 cell lines, as well as chlorpyrifos, methidathion, chlorfenvinphos, and dimethoate in rat liver and diazinon in fish most probably disrupt membrane lipids through oxidative stress (23,35,61,116,118,(130)(131)(132)(133)(134)(135).…”

“…Goel et al (33) studied liver histoarchitecture in chlorpyrifostreated rats and observed hepatocyte vacuolisation and necrosis, sinusoidal dilatation, and increase in binucleated cells at higher doses and longer exposure to chlorpyrifos. Recent findings by Ezzi et al (34) suggest that chlorpyrifos had a dose-dependent effect on dilated sinusoids, central vein, and portal triad in rats.…”

Comet assay: an essential tool in toxicological research

“…But only a few studies also addressed antigenotoxic effects (~6 %) like, e.g., Sassi et al (2016) who examined genotoxic as Results were drawn from the PubMed (total counts: 9091) and Web of Science™ Core Collection (total counts: 10,037) databases including the years from 1990 to 2016 using the search term "comet assay" well as antigenotoxic effects of Ceratonia siliqua extracts and total oligomer flavonoids in murine leukemia cells. In contrast, most of the publications investigated genotoxic effects of distinct substances like diazinon (Ezzi et al 2016b) or nano particles such as Ni nanoparticles (Magaye et al 2016). A limited number of studies (about 8 %) also analyzed oxidative-induced DNA damage using lesion-specific enzymes like FPG, Endo III or hOGG1 or DNA repair (about 7 %) in combination with the comet assay.…”