Avermectin induced liver injury in pigeon: Mechanisms of apoptosis and oxidative stress

Zhu, Wenjun; Li, Ming; Liu, Ci; Qu, Jianping; Ye, Min; Xu, Shiwen; Li, Shu

doi:10.1016/j.ecoenv.2013.09.021

Cited by 51 publications

(21 citation statements)

References 41 publications

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“…According to the reviews by Yin et al (2008) and Rautou et al (2010), liver cells may be saved from death after stress stimulation by up-regulating autophagy induction of the occurrence of the disease. In view of the above results, we cannot conclusively determine the biological impact of our findings, although our previous studies have found that AVM can induce oxidative stress, apoptosis, and P450 inhibition in pigeon liver tissue (Zhu et al 2013(Zhu et al , 2014; however, the complicated relationship between autophagy, apoptosis and oxidative stress has not been well understood. The significance and mechanism of autophagy induced by AVM in pigeon liver requires further studies in vitro and in vivo.…”

Section: Discussioncontrasting

confidence: 50%

“…According to the Organization for Economic Cooperation and Development (OECD) Guidelines for Testing of Chemicals, the pigeon is a recommended species for toxicology experiments in birds. Previous studies performed by our lab showed that exposure to AVMs resulted in apoptosis, oxidative stress, and inhibition of the P450 enzyme systems in the liver of the king pigeon (Zhu et al 2013(Zhu et al , 2014. Physianthropy studies showed that autophagy is involved in major fields of hepatology (Rautou et al 2010;Yin et al 2008).…”

Section: Abbreviationsmentioning

confidence: 96%

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Autophagy response in the liver of pigeon exposed to avermectin

Wang

Liu

Khoso

et al. 2016

Environ Sci Pollut Res

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Pesticide residues are an important aspect of environmental pollution. Environmental avermectin residues have produced adverse effects in organisms. Many pesticides exert their toxic effects via the mechanism of autophagy. The purpose of this study was to examine the changes in autophagy levels and in autophagy-related genes, including LC3, Beclin 1, Dynein, ATG5, TORC1, and TORC2, resulting from exposure to subchronic levels of AVM in liver tissue in the king pigeon model. We observed abundant autophagic vacuoles with extensively degraded organelles, autophagosomal vacuoles, secondary lysosomes, and double-membrane structures in the liver. The expression levels of the autophagy-related genes LC3-I, LC3-II, Beclin 1, ATG5, and Dynein were up-regulated; however, TORC1 and TORC2 expression levels were down-regulated. These changes occurred in a concentration-dependent manner after AVM exposure for 30, 60, and 90 days in pigeons. Taken together, these results suggested that AVM increased the autophagic flux and that upregulation of autophagy might be closely related to the hepatotoxicity of AVM in birds.

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Section: Discussioncontrasting

confidence: 50%

Section: Abbreviationsmentioning

confidence: 96%

Autophagy response in the liver of pigeon exposed to avermectin

Wang

Liu

Khoso

et al. 2016

Environ Sci Pollut Res

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“…Abamectin is a mixture of B 1a and B 1b avermectins (Meister 1992). MN micronucleus, MMC mitomycin C (4.5 μg/ml, positive control in absence of S9 mix), BP benzo(a)pyrene (2 μg/ml, positive control in presence of S9 mix) * p<0.05, * * p<0.01; significant difference compared with control a Data are presented as mean ± SE of micronuclei/500 binucleated cytokinesis-blocked cells hepatocytes and brain neurons of King pigeon (Chen et al 2013;Zhu et al 2013). Ivermectin, a member of the avermectin family, and its commercial formulation Ivomec® originated cytotoxic effects in CHO K1 cells (Molinari et al 2009).…”

Section: Discussionmentioning

confidence: 99%

Cytotoxic and genotoxic effects of abamectin, chlorfenapyr, and imidacloprid on CHOK1 cells

Al‐Sarar

Abobakr

Bayoumi

et al. 2015

Environ Sci Pollut Res

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The cytotoxicity and genotoxicity of abamectin, chlorfenapyr, and imidacloprid have been evaluated on the Chinese hamster ovary (CHOK1) cells. Neutral red incorporation (NRI), total cellular protein content (TCP), and methyl tetrazolium (MTT) assays were followed to estimate the mid-point cytotoxicity values, NRI50, TCP50, and MTT50, respectively. The effects of the sublethal concentration (NRI25) on glutathione S-transferase (GST), glutathione reductase (GRD), glutathione peroxidase (GPX), and total glutathione content have been evaluated in the presence and absence of reduced glutathione (GSH), vitamin C, and vitamin E. The genotoxicity was evaluated using chromosomal aberrations (CA), micronucleus (MN) formation, and DNA fragmentation techniques in the presence and absence of the metabolic activation system, S9 mix. Abamectin was the most cytotoxic pesticide followed by chlorfenapyr, while imidacloprid was the least cytotoxic one. The glutathione redox cycle components were altered by the tested pesticides in the absence and presence of the tested antioxidants. The results of genotoxicity indicate that abamectin, chlorfenapyr, and imidacloprid have potential genotoxic effects on CHOK1 cells under the experimental conditions.

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“…Another antioxidant defense component of GSH-Px could also catalyze H 2 O 2 decomposition to H 2 O [25]; GSH-Px is well known for catalyzing the reduction of hydrogen peroxide and organic hydroperoxides, thus protecting cells from oxidative damage [26]. However, it would work at relatively low H 2 O 2 concentrations as part of a productive enzyme arsenal.…”

Section: Discussionmentioning

confidence: 99%

The Role of Oxidative Stress in Gastrointestinal Tract Tissues Induced by Arsenic Toxicity in Cocks

Guo

Zhao

Guo

et al. 2015

Biol Trace Elem Res

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Arsenic (As) is a widely distributed trace element which is known to be associated with numerous adverse effects on human beings and animals. Arsenic trioxide (As2O3) is an inorganic arsenical-containing toxic compound. The effect of excessive amounts of As2O3 exposure on gastrointestinal tract tissue damage in cocks is still unknown. This study was conducted to investigate the effect of As2O3 exposure on gastrointestinal tract tissue damage in cocks. In total, 72 1-day-old male Hyline cocks were randomly divided into four groups and fed either a commercial diet or an As2O3 supplement diet containing 7.5, 15, and 30 mg/kg As2O3. The experiment lasted for 90 days and gastrointestinal tract tissue samples (gizzard, glandular stomach, duodenum, jejunum, ileum, cecum, and rectum) were collected at 30, 60, and 90 days. Catalase (CAT), glutathione (GSH), and glutathione peroxidase (GSH-Px) activities; malondialdehyde (MDA) contents; and hydroxyl radical (OH·)-mediated inhibition were examined. Furthermore, the results demonstrated that MDA content in the gastrointestinal tract was increased, while the activities of CAT, GSH, and GSH-Px and the ability to resist OH· was decreased in the As2O3 treatment groups. Extensive damage was observed in the gastrointestinal tract. These findings indicated that As2O3 exposure caused oxidative damage in the gastrointestinal tract of cocks due to alterations in antioxidant enzyme activities and elevation of free radicals.

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Avermectin induced liver injury in pigeon: Mechanisms of apoptosis and oxidative stress

Cited by 51 publications

References 41 publications

Autophagy response in the liver of pigeon exposed to avermectin

Autophagy response in the liver of pigeon exposed to avermectin

Cytotoxic and genotoxic effects of abamectin, chlorfenapyr, and imidacloprid on CHOK1 cells

The Role of Oxidative Stress in Gastrointestinal Tract Tissues Induced by Arsenic Toxicity in Cocks

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