Shi-Wen Xu

Northeast Agricultural University, Charbin, Heilongjiang Sheng, China

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Publications (49)107.58 Total impact

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    ABSTRACT: Nitric oxide (NO) is an essential messenger molecule and is associated with inflammation and oxidative stress. Although NO has important biological functions in mammals, its role in the mechanism that occurs after intestinal injuries in chickens remains unknown. The objective of the present study was to investigate the real role of NO and oxidative stress in the intestinal injuries of chickens induced by selenium (Se) deficiency. A total 150 chickens were randomly divided into the following two groups: a low-Se group (L group, fed a Se-deficient diet containing 0.020 mg/kg Se) and a control group (C group, fed a commercial diet containing 0.2 mg/kg Se). The activities and mRNA levels of glutathione peroxidase (GSH-Px), the production of glutathione (GSH) and NO, and the protein and mRNA levels of inducible nitric oxide synthase (iNOS) were examined in the intestinal tissues (duodenum, jejunum, and rectum) at 15, 25, 35, 45, and 55 days. Methane dicarboxylic aldehyde (MDA) levels were also detected by assay kits. Then, the morphologies of the tissues were observed under the microscope after hematoxylin and eosin staining (H&E staining). The results showed that Se deficiency induced higher inflammatory damage and MDA levels (P < 0.05), which were accompanied by higher levels of iNOS and NO but lower levels of GSH and GSH-Px (P < 0.05). Our results indicated that Se deficiency induced oxidative damage in the intestinal tracts of chickens and that low levels of GSH-Px and high contents of NO may exert a major role in the injury of the intestinal tract induced by Se deficiency.
    Biological Trace Element Research 11/2014; · 1.61 Impact Factor
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    ABSTRACT: Selenoprotein W (SelW) is mainly understood in terms of its antioxidant effects in the cellular defense system. Inflammation is an important indicator of animal tissue injury, and the inflammatory cells may trigger a sophisticated and well-orchestrated inflammatory cascade, resulting in exaggerated oxidative stress. To investigate the role of SelW in inflammatory injury in chicken immune tissues and cultured splenic lymphocyte, in this report, the effects of selenium (Se) on mRNA expressions of SelW and inflammatory factors (iNOS, COX-2, NF-κB, PTGEs, and TNF-α) in the chicken immune organs (spleen, thymus and bursa of Fabricius) and cultured splenic lymphocyte treated with sodium selenite and H2O2, or knocked down SelW with small interfering RNAs (siRNAs) were examined. The results showed that Se-deficient diets effectively decreased the mRNA expression of SelW (P < 0.05), and induced a significantly up-regulation of COX-2, iNOS, NF-κB, PTGEs and TNF-α mRNA levels (P < 0.05). The histopathological analysis showed that immune tissues were obviously injured in the low-Se groups. In vitro, H2O2 induced a significantly up-regulation of the mRNA levels of inflammation-related genes (iNOS, COX-2, NF-κB, PTGEs, and TNF-α) in cultured splenic lymphocyte (P < 0.05). When lymphocytes were pretreated with Se before treated with H2O2, the inflammation-related genes were significantly decreased (P < 0.05). Silencing of SelW significantly up-regulated the inflammation-related genes (iNOS, COX-2, NF-κB, PTGEs, and TNF-α) in cultured splenic lymphocyte (P < 0.05). The results suggested that the expression levels of inflammatory factors (iNOS, COX-2, NF-κB, PTGEs, and TNF-α) and SelW can be influenced by Se in birds. SelW commonly played an important role in the protection of immune organs of birds from inflammatory injury by the regulations of inflammation-related genes.
    BioMetals 10/2014; · 2.69 Impact Factor
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    ABSTRACT: The expression of heat shock proteins (Hsps) commonly increases to provide neuroprotection when brain tissues are under stress conditions. Residues of avermectins (AVMs) have neurotoxic effects on a number of non-target organisms. The aim of this study was to investigate the effects of AVM exposure on the expression levels of Hsp 60, Hsp 70 and Hsp 90 for pigeon (Columba livia) neurons both in vivo and in vitro. The results showed that in general, the mRNA and protein levels of Hsps were increased in treated groups relative to control groups after AVM exposure for 30d, 60d and 90d in the cerebrum, cerebellum and optic lobe in vivo. However, AVM exposure had no significant effects on the transcription expression of Hsps for 90d in the optic lobe and decreased the translation expression of Hsps significantly for 90d in the optic lobe. In vitro, the LC50 of avermectin for King pigeon neurons is between 15μgL(-1) and 20μgL(-1). Following AVM (2.5-20μgL(-1)) exposure, the mRNA expression of the 3 Hsps was up-regulated to different degrees. Compared with the control groups, a significant decrease, a remarkable increase and a non-significant change was found in the protein expression of Hsp 60, Hsp 70 and Hsp 90 separately following AVM (2.5-20μgL(-1)) exposure. Based on these results, we conclude that AVM exposure can induce a protective stress response in pigeons by means of promoting the mRNA and protein expression of Hsps under in vivo and in vitro conditions, thus easing the neurotoxic effects of AVM to some extent.
    Ecotoxicology and Environmental Safety 09/2014; 110C:95-102. · 2.48 Impact Factor
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    ABSTRACT: Animals are exposed to various environmental stresses every day, including the stress associated with living in cold temperatures. The aim of this study was to investigate the possible mechanisms of interaction between lipid metabolism and inflammation induced by cold stress in the livers of chickens. Fifteen-day-old male chicks were randomly allocated into 12 groups (10 chickens per group). After exposure of the chickens to the cold stress, cholesterol fractionation was used to examine high-density lipoprotein (HDL) and low-density lipoprotein (LDL) concentrations. Aminotransferase activities were examined with the use of the aspartate transaminase (AST) and alanine transaminase (ALT) assay. The AMP-activated protein kinase alpha-proliferator-activated receptor alpha (AMPKalpha-PPARalpha) pathway genes (AMPKalpha1, AMPKalpha2, PPARalpha, carnitine palmitoyltransferaseI [CPTI], acetyl-CoA carboxylase [ACC]) and inflammatory cytokines (prostaglandin E synthase [PGEs], inducible nitric oxide synthase [iNOS], heme oxygenase-1 [HO-1], nuclear factor kappa-light-chain-enhancer of activated B cells [NF-kappaB], cyclooxygenase-2 [COX-2], and TNF-alpha-like factor [LITAF]) were also measured. The results showed that during the response to cold stress, serum LDL and HDL cholesterol concentrations increased. Histopathologic analyses provided evidence that liver tissues were seriously injured in the chickens exposed to the cold stress. Serum aminotransferase activities were also increased in the group of animals exposed to the cold stress. Additionally, the expressions of AMPKalpha-PPARalpha pathway genes and inflammatory cytokine genes were significantly increased in the animals exposed to cold temperatures. These results suggested that increased inflammation was a feature associated with a lipid-metabolism disorder in the livers of chickens exposed to cold stress.
    Avian Diseases 09/2014; 58(3):415-26. · 1.11 Impact Factor
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    ABSTRACT: Residues of avermectin (AVM) drugs have toxic effects on non-target organisms. Analyses of cytochrome P450 enzymes are among the most frequently employed indicators in pharmacology and toxicology studies. In this study, the responses of cytochrome P450 enzymes and pathological changes in the liver and kidney tissues of King pigeons (Columba livia) following subchronic exposure to avermectin for 30, 60 and 90d were investigated. Dose- and time-dependent decreases in the activities of P450 enzymes (i.e., aminopyrine-N-demethylase, erythromycin N-demethylase, aniline 4-hydroxylase and NADPH-cytochrome C reductase) and down-regulation of the P450 and b5 contents were observed. The microscopic structures were clearly altered, the severity of these alterations increased with the concentration of AVM and the exposure time. These results imply that AVM can inhibit the P450 enzyme systems in the liver and kidney tissues of pigeons. This research provides insight into the safe use of AVM and a comprehensive evaluation of the toxicological effects of AVM in birds.
    Environmental Toxicology and Pharmacology 08/2014; 38(2):562-569. · 1.86 Impact Factor
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    ABSTRACT: Selenium (Se) influences the metabolism of thyroid hormones in mammals. However, the role of Se deficiency in the regulation of thyroid hormones in chickens is not well known. In the present study, we examined the levels of thyroidal triiodothyronine (T3), thyroidal thyroxine (T4), free triiodothyronine, free thyroxine (FT4), and thyroid-stimulating hormone in the serum and the mRNA expression levels of 25 selenoproteins in chicken thyroids. Then, principal component analysis (PCA) was performed to analyze the relationships between the selenoproteins. The results indicated that Se deficiency influenced the conversion of T4 to T3 and induced the accumulation of T4 and FT4. In addition, the mRNA expression levels of the selenoproteins were generally decreased by Se deficiency. The PCA showed that eight selenoproteins (deiodinase 1 (Dio1), Dio2, Dio3, thioredoxin reductase 2 (Txnrd2), selenoprotein i (Seli), selenoprotein u (Selu), glutathione peroxidase 1 (Gpx1), and Gpx2) have similar trends, which indicated that they may play similar roles in the metabolism of thyroid hormones. The results showed that Se deficiency inhibited the conversion of T4 to T3 and decreased the levels of the crucial metabolic enzymes of the thyroid hormones, Dio1, Dio2, and Dio3, in chickens. In addition, the decreased selenoproteins (Dio1, Dio2, Dio3, Txnrd2, Seli, Selu, Gpx1, and Gpx2) induced by Se deficiency may indirectly limit the conversion of T4 to T3 in chicken thyroids. The information presented in this study is helpful to understand the role of Se in the thyroid function of chickens.
    Biological Trace Element Research 08/2014; · 1.61 Impact Factor
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    ABSTRACT: As an effective insecticidal and nematicidal agent, avermectin (AVM) has been widely used in agricultural production and stock farming areas. Subsequently, the residues of AVM or its active metabolites in animal manure pose a toxic threat to non-target organisms in the environment. As the most characteristic epigenetic phenomena, DNA methylation status is a useful biological signal for the toxicity assessment of environmental chemical toxicants. In this study, analyses of the overall level of genomic DNA methylation were performed, and the expression levels of DNA methyltransferases (DNMTs), as well as demethylase methyl-CpG-binding domain protein 2 (MBD2), in pigeon brain tissues after subchronic exposure (with a AVM concentration of 20 mg/kg, 40 mg/kg and 60 mg/kg, respectively) to AVM for 30, 60 and 90 days were investigated. Global DNA hypomethylation and down-regulation of DNMT mRNA expression occurred in a dose-time-dependent manner in pigeon brains. The expression level of MBD2, which functions as a demethylase, was significantly enhanced in a dose-dependent but not time-dependent manner. In addition, the elevated expression level of MBD2 had a more robust effect on genomic DNA hypomethylation compared to changes in DNMT expression. Taken together, these results suggested that subchronic dose exposures of AVM could affect the global DNA methylation status, and this mechanism is closely related to changes in the expression levels of DNMTs and MBD2.
    Chemico-Biological Interactions 08/2014; · 2.98 Impact Factor
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    ABSTRACT: This study describes the effects of selenium (Se) deficiency on the messenger ribonucleic acid (mRNA) expression of 25 selenoproteins (Sels) (including glutathione peroxidases (GPx1-GPx4), thioredoxin reductases (TrxR1-TrxR3), iodothyronine deiodinases (ID1-ID3), selenophosphate synthetase 2 (SPS2), 15-kDa Sel (Sel15), SelH, SelI, SelK, SelM, Sepn1, SelO, Sepx, Selpb, SelS, SelT, SelW, Sepp1, and SelU in the adipose tissues (subcutaneous adipose, visceral adipose, and articular adipose) of chickens. One hundred and fifty 1-day-old chickens were randomly assigned to two groups of 75 each and were fed a low-Se diet (0.032 mg/kg Se) or a control diet (0.282 mg/kg Se). The expression levels of 25 Sel mRNAs were determined on days 35, 45, and 55 from three parts (subcutaneous adipose, visceral adipose, and articular adipose) of the chicken adipose tissues. The results showed that the expression levels of the 25 Sel mRNAs were significantly lower (P < 0.05) in the low-selenium group than in the control group. In addition, the Sel mRNA expression levels in the three adipose tissues were observed to decrease in a time-dependent manner with increasing feeding time.
    Biological Trace Element Research 06/2014; · 1.61 Impact Factor
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    ABSTRACT: Little is known about the influence of subchronic cadmium exposure on apoptosis in the immune organs of birds and the protective effects on apoptosis by selenium against cadmium. The aim of this study was to investigate the effect of subchronic cadmium exposure on nitric oxide and apoptosis in the immune organs of chicken and the protective roles of selenium against cadmium-induced apoptosis. Two hundred ten 30-day-old chickens were randomly assigned to three groups and were fed a basal diet, cadmium + selenium (as 150 mg of CdCl2 per kg of diet + 10 mg of Na2SeO3 per kg of diet ) or cadmium (as 150 mg of CdCl2 per kg of diet) in basic diets for 15, 30, 45, and 60 days. Then, the production of nitric oxide, messenger RNA (mRNA level), and the activity of inducible nitric oxide synthase, ultrastructural changes, TUNEL assay, and flow cytometric analysis of apoptosis and Bcl-2 and p53 mRNA levels in the immune organs were examined. The results showed that cadmium exposure caused ultrastructural damage and increased production of nitric oxide, mRNA level, and activity of inducible nitric oxide synthase, the degree, and the number of apoptotic cells in a time-dependent manner. Cadmium exposure decreased Bcl-2 mRNA level and increased p53 mRNA level in a time-dependent manner. Selenium supplementation during dietary cadmium reduced the production of nitric oxide, the mRNA level, and activity of inducible nitric oxide synthase, ultrastructural damage, and apoptosis in the immune organs of chicken. It indicated that cadmium induced nitric oxide-mediated apoptosis of immune organs, and selenium played protective effects against cadmium-induced apoptosis in the immune organs of chickens.
    Biological Trace Element Research 05/2014; · 1.61 Impact Factor
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    ABSTRACT: To determine the relationship between dietary selenium (Se) deficiency or excess and liver hydrogen peroxide (H2O2) metabolism in chickens, 1-day-old chickens received insufficient Se (0.028 mg Se per kg of diet) or excess Se (3.0 or 5.0 mg Se per kg of diet) in their diets for 8 weeks. Body and liver weight changes, alanine aminotransferase (ALT) and aspartate aminotransferase (AST) activities, H2O2 content, and activities and mRNA levels of enzymes associated with H2O2 metabolism (catalase (CAT) and superoxide dismutase (SOD) 1-3) were determined in the liver. This study showed that Se deficiency or excess Se intake elicited relative severe changes. Se deficiency decreased growth, while Se excess promoted growth in chickens. Both diets vastly altered the liver function, but no obvious histopathological changes were observed in the liver. Se deficiency significantly lowered SOD and CAT activities, and the H2O2 content in the liver and serum increased. Se excess (3.0 mg/kg) decreased SOD and CAT activities with changes in their mRNA levels, and the H2O2 content increased. The larger Se excess (5.0 mg/kg) showed more serious effects but was not fatal. These results indicated that the H2O2 metabolism played a destructive role in the changes in bird liver function induced by Se deficiency or excess.
    Biological trace element research 05/2014; · 1.92 Impact Factor
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    ABSTRACT: Cadmium (Cd), a potent hepatotoxin, has been reported to induce endoplasmic reticulum (ER) stress in various cell types. However, whether such effect exists in bird is still unclear. To delineate the effects of Cd exposure on ER stress response, we examined the expression of 78-kDa glucose-regulated protein (GRP78) and alteration in calcium homeostasis in primary chicken hepatocytes treated with 2-22µM Cd for 24h. A significant decrease of cell viability was observed in chicken hepatocytes following Cd administration. In cells treated with Cd, GRP78 protein levels increased in a dose-dependent manner. In addition, GRP78 and GRP94mRNA levels were elevated in response to Cd exposure. The increase of the intracellular Ca(2+) concentration in chicken hepatocytes was found during Cd exposure. Cd significantly decreased the CaM mRNA levels in hepatocytes. These results show that Cd regulates the expression of GRP78 and calcium homeostasis in chicken hepatocytes, suggesting that ER stress induced by Cd plays an important role in the mechanisms of Cd cytotoxicity to the bird hepatocytes.
    Ecotoxicology and Environmental Safety 05/2014; 106C:109-114. · 2.48 Impact Factor
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    ABSTRACT: The objective of this study was to examine the effects of avermectin (AVM) on amino acid neurotransmitters and their receptors in the pigeon brain. Four groups two-month-old American king pigeons (n=20/group) were fed either a commercial diet or an AVM-supplemented diet (20mg/kg·diet, 40mg/kg·diet, or 60mg/kg·diet) for 30, 60, or 90days. The contents of aspartic acid (ASP), glutamate (GLU), glycine (GLY), and γ-aminobutyric acid (GABA) in the brain tissues were determined using ultraviolet high-performance liquid chromatography (HPLC). The expression levels of the GLU and GABA receptor genes were analyzed using real-time quantitative polymerase chain reaction (qPCR). The results indicate that AVM exposure significantly enhances the contents of GABA, GLY, GLU, and ASP in the cerebrum, cerebellum, and optic lobe. In addition, AVM exposure increases the mRNA expression levels of γ-aminobutyric acid type A receptor (GABAAR), γ-aminobutyric acid type B receptor (GABABR), N-methyl-d-aspartate 1 receptor (NR1), N-methyl-d-aspartate 2A receptor (NR2A), and N-methyl-d-aspartate 2B receptor (NR2B) in a dose- and time-dependent manner. Moreover, we found that the most damaged organ was the cerebrum, followed by the cerebellum, and then the optic lobe. These results show that the AVM-induced neurotoxicity may be associated with its effects on amino acid neurotransmitters and their receptors. The information presented in this study will help supplement the available data for future AVM toxicity studies.
    Pesticide Biochemistry and Physiology 03/2014; · 2.11 Impact Factor
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    ABSTRACT: Selenium (Se) is an important dietary micronutrient with antioxidative roles. Cadmium (Cd), a ubiquitous environmental pollutant, is known to cause brain lesion in rats and humans. However, little is reported about the deleterious effects of subchronic Cd exposure on the brain of poultry and the protective roles on the brain by Se against Cd. The aim of this study was to investigate the protective effects of Se on Cd-induced brain damage in chickens. One hundred twenty 100-day-old chickens were randomly assigned to four groups and were fed a basal diet, or Se (as 10 mg Na2SeO3/kg dry weight of feed), Cd (as 150 mg CdCl2/kg dry weight of feed), or Cd + Se in their basic diets for 60 days. Then, concentrations of Cd and Se, production of nitric oxide (NO), messenger RNA (mRNA) level and activity of inducible NO synthase (iNOS), level of oxidative stress, and histological and ultrastructural changes of the cerebrum and cerebellum were examined. The results showed that Cd exposure significantly increased Cd accumulation, NO production, iNOS activities, iNOS mRNA level, and MDA content in the cerebrum and cerebellum. Cd treatment obviously decreased Se content and antioxidase activities and caused histopathological changes in the cerebrum and cerebellum. Se supplementation during dietary Cd obviously reduced Cd accumulation, NO production, mRNA level and activity of iNOS, oxidative stress, and histopathological damage in the cerebrum and cerebellum of chickens. It indicated that Se ameliorates Cd-induced brain damage in chickens by regulating iNOS-NO system changes, and oxidative stress induced by Cd and Se can serve as a potential therapeutic for Cd-induced brain lesion of chickens.
    Biological trace element research 02/2014; · 1.92 Impact Factor
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    ABSTRACT: To verify the antioxidative role of SelW in oxidant-induced chicken splenic lymphocyte, in this report, the influence of selenite supplementation and SelW gene silence on H2O2-mediated cell viability and cell apoptosis in cultured splenic lymphocyte derived from spleen of chicken were examined. The cultured cells were treated with sodium selenite and H2O2, or knocked down SelW with small interfering RNAs (siRNAs). The lymphocytes were examined for cell viability, cell apoptosis and mRNA expression levels of SelW and apoptosis-related genes (Bcl-2, Bax, Bak-1, caspase-3 and p53). The results show that the mRNA expression of SelW were effectively increased after treatment with sodium selenite, and H2O2-induced cell apoptosis was significantly decreased and cell viability was significantly increased. 20 μM H2O2 was found to induce cell apoptosis and decrease cell viability, which was alleviated obviously when cells were pretreated with sodium selenite before exposure to 20 μM H2O2. Meanwhile, H2O2 induced a significantly up-regulation of the Bax/Bcl-2 ratio, Bax, Bak-1, caspase-3 and p53 and down-regulation of Bcl-2 (P < 0.05). When lymphocytes were pretreated with Se before treated with H2O2, the Bax/Bcl-2 ratio and mRNA expression of those genes were significantly decreased, and Bcl-2 was increased (P < 0.05). SelW siRNA-transfected cells were more sensitive to the oxidative stress induced by treatment of H2O2 than control cells. Silencing of the lymphocyte SelW gene decreased their cell viability, and increased their apoptosis rate and susceptibility to H2O2. Silencing of SelW significantly up-regulated the Bax/Bcl-2 ratio, Bax, Bak-1, caspase-3 and p53 and down-regulated Bcl-2 (P < 0.05). The present study demonstrates that SelW plays an important role in protection of splenic lymphocyte of birds from oxidative stress.
    Biology of Metals 02/2014; · 2.69 Impact Factor
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    ABSTRACT: Previous studies have determined the effects of dietary selenium (Se) supplementation on selenoprotein N (SelN, SEPN1), selenophosphate synthetase-1 (SPS1), and selenocysteine-synthase (SecS) mRNA abundance in chicken skeletal and cardiac muscles. To investigate collective responses of these genes to dietary Se concentrations ranging from deficiency to moderately high level in muscle tissues of chicken, 1-day-old chickens were exposed to a diet of deficient Se and supplemented with Se (0.15 mg Se/kg and 1.50 mg Se/kg) as sodium selenite in the feed for 35 days. Muscle tissues (flight, breast, leg, and cardiac muscles) were collected and examined for Se content and mRNA levels of SelN on days 1, 15, 25, and 35 days, respectively. Moreover, SPS1 and SecS mRNA levels were analyzed. The results showed that the expression of SelN gene in cardiac muscle responded to dietary Se concentrations. SelN gene was downregulated in the Se deficiency group (L group), and upregulated in the Se excess group (H group) compared with the moderate Se group (M group) (P < 0.05) in cardiac muscle. Se deficiency mainly unregulated SelN mRNA level in skeletal muscles compared with M group. Excess dietary Se mainly resulted in the upregulation of SelN mRNA level in skeletal muscles compared with the M group. SecS mRNA levels responded to dietary Se concentrations showed a similar change compared with SelN in cardiac muscle. SPS1 mRNA levels responded to dietary Se concentrations showed a downregulation in L group and upregulation in H group. However, SelN mRNA levels displayed a different expression pattern in different skeletal and cardiac muscles. Moreover, Se also regulated the levels of SPS1 and SecS mRNAs. In summary, Se regulated the expression of SelN gene and affected the mRNA levels of SecS and SPS1. The level of Se in the feed may regulate SelN biosynthesis by affecting the levels of SPS1 and SecS mRNA.
    Biological trace element research 02/2014; · 1.92 Impact Factor
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    ABSTRACT: Avermectin (AVM) is a pesticide that can accumulate in the environment through spray-drift, runoff or field drainage. Residues of AVM or its metabolites in livestock feces have toxic effects on non-target aquatic and terrestrial organisms. In this study, changes in oxidative stress and immunity in pigeon spleen tissues were detected after subchronic exposure to AVM for 30, 60, and 90 days. In pigeon spleen, the activities of total anti-oxidation capability (T-AOC), superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) decreased significantly, whereas the levels of malondialdehyde (MDA), protein carbonyl (PCO), and DNA-protein crosslink (DPC) coefficients increased. Additionally, obvious ultrastructure alterations were observed. These results indicated that AVM induced oxidative stress and damaged the normal structure of spleen cells. The exposure to AVM could lead to increases in the mRNA levels of interleukin-1β (IL-1β), tumor necrosis factor-α (TNF-α), and interleukin-4 (IL-4), as well as a decrease in the mRNA level of interferon-γ (IFN-γ), in a dose-time-dependent manner in pigeon spleen. The results imply that AVM induces immunosuppression in the spleen tissue of pigeons. The information presented in this study may be helpful for understanding the mechanism of AVM-induced immunotoxicity in birds.
    Chemico-biological interactions 01/2014; · 2.46 Impact Factor
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    ABSTRACT: Cadmium (Cd), a potent hepatotoxin, has been reported to induce endoplasmic reticulum (ER) stress in various cell types. However, whether such effect exists in bird is still unclear. To delineate the effects of Cd exposure on ER stress response, we examined the expression of 78-kDa glucose-regulated protein (GRP78) and alteration in calcium homeostasis in primary chicken hepatocytes treated with 2–22 µM Cd for 24 h. A significant decrease of cell viability was observed in chicken hepatocytes following Cd administration. In cells treated with Cd, GRP78 protein levels increased in a dose-dependent manner. In addition, GRP78 and GRP94 mRNA levels were elevated in response to Cd exposure. The increase of the intracellular Ca2+ concentration in chicken hepatocytes was found during Cd exposure. Cd significantly decreased the CaM mRNA levels in hepatocytes. These results show that Cd regulates the expression of GRP78 and calcium homeostasis in chicken hepatocytes, suggesting that ER stress induced by Cd plays an important role in the mechanisms of Cd cytotoxicity to the bird hepatocytes.
    Ecotoxicology and Environmental Safety 01/2014; 106:109–114. · 2.20 Impact Factor
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    ABSTRACT: Selenium (Se) plays an important role in the brain development, function, and degeneration, nutritional encephalomalacia is closely related with dietary Se in avian. However, there is little evidence on the relationship between inflammation and encephalomalacia in avian and the mechanism which Se regulates the inflammatory response in brain tissues remains to be unclear. The present paper describes the effects of Se-deficient granulated diet on one transcription factor-nuclear factor kappaB and four pro-inflammatory cytokines-tumor necrosis factor, cyclooxygenase2, inducible nitric oxide synthase and Prostaglandin E synthase mRNA expression in the chicken brain tissues associated encephalomalacia. One hundred male chickens (1 day old; Weiwei Co. Ltd., Harbin, China) were divided into two groups (50 chickens per group). The expression levels in the brain tissues (cerebral gray matter, cerebral white matter, marrowbrain, cerebellum, thalamus and brain stem) were determined by real-time PCR on days 15, 25, 35, 45, and 55, respectively. The results showed the productions of pro-inflammatory mediators were increased following Se-deficiency. These data indicate the correlations between nutritional encephalomalacia and inflammatory response and the activity of inflammatory response in chicken brain may be induced by Se-deficiency.
    Biology of Metals 12/2013; · 2.69 Impact Factor
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    ABSTRACT: Extensive use of avermectin (AVM) can result in environment pollution, and it is important to evaluate the potential impact this antibiotic has on ecological systems. Few published literatures have discussed the liver injury mechanisms induced by AVM on birds. In this study, pigeons were exposed to feed containing AVM (0, 20, 40 and 60mg/kg diet) for 30, 60, 90 days respectively. The results showed that AVM increased the number of apoptosis and the expression level of caspase-3, 8, fas mRNA in the liver of pigeons. Ultrastructural alterations, including mitochondrial damage and chromatin aggregation, become severe with increase exposure dose. Exposure to AVM induced significant changes in antioxidant enzyme {superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px)} activities and malondialdehyde (MDA) content, augmented protein carbonyl (PCO) content and DNA-protein crosslink (DPC) coefficient, in a concentration-dependent manner in the liver of pigeons. Our results show that AVM has toxic effect in pigeon liver, and the mechanism of injury caused by AVM is closely related to apoptosis and oxidative stress.
    Ecotoxicology and Environmental Safety 10/2013; · 2.20 Impact Factor
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    ABSTRACT: Avermectins (AVMs) are the active components of some insecticidal and nematicidal products used in agriculture and veterinary medicine for the prevention of parasitic diseases. Residues of AVM drugs or their metabolites in livestock feces have toxic effects on non-target aquatic and terrestrial organisms. In this study, oxidative stress responses and pathological changes on pigeon brain tissues and serum after subchronic exposure to AVM for 30, 60 and 90 days were investigated. The decrease in antioxidant enzyme (superoxide dismutase, SOD and glutathione peroxidase, GSH-Px) activities and increase in methane dicarboxylic aldehyde content in a dose-time-dependent manner in the brain and serum of pigeon were observed. The protein carbonyl content, an indicator of protein oxidation, and DNA-protein crosslink coefficient were significantly augmented with dose-time-dependent properties. The microscopic structures of the cerebrum, cerebellum and optic lobe altered obviously, the severity of which increased with the concentration of AVM and exposure time. The results imply that AVM could induce oxidative damage to the brain tissue and serum of pigeon. The information presented in this study is helpful to understand the mechanism of AVM-induced oxidative stress in birds.
    Ecotoxicology 08/2013; · 2.50 Impact Factor

Publication Stats

148 Citations
107.58 Total Impact Points

Institutions

  • 2009–2014
    • Northeast Agricultural University
      Charbin, Heilongjiang Sheng, China
  • 2012
    • Harbin University of Commerce
      Charbin, Heilongjiang Sheng, China
    • China Agricultural University
      • College of Veterinary Medicine
      Beijing, Beijing Shi, China