Assessing and mitigating foodborne acetochlor exposure induced ileum toxicity in broiler chicks: The role of omega-3 polyunsaturated fatty acids supplementation and molecular pathways analysis.

Excessive acetochlor residues present ecological and food safety challenges. Here, broiler chicks were exposed to varied acetochlor doses to first assess its effects on the gut. Subsequent dietary supplementation with omega-3 was used to assess its anti-contamination effects. Pathologically, acetochlor induced notable ileal lesions including inflammation, barrier disruption, tight junction loss, and cellular anomalies. Mechanistically, acetochlor stimulated the TNFα/TNFR1 and TLR4/NF-κB/NLRP3 pathways, promoting RIPK1/RIPK3 complex formation, MLKL phosphorylation, NLRP3 inflammasome activation, Caspase-1 activation, and GSDMD shearing with inflammatory factor release. These mechanisms elucidate ileal cell death patterns essential for understanding chicken enteritis. Omega-3 supplementation showed promise in mitigating inflammation, though its precise counteractive role remains unclear. Our findings suggest early omega-3 intervention offered protective benefits against acetochlor's adverse intestinal effects, emphasizing its potential poultry health management role. Harnessing dietary interventions' therapeutic potential will be pivotal in ensuring sustainable poultry production and food safety despite persistent environmental contaminants.

Polystyrene microplastics mediate cell cycle arrest, apoptosis, and autophagy in the G2/M phase through ROS in grass carp kidney cells.

Microplastics (MPs) have attracted widespread worldwide attention as a new pollutant. However, the role of reactive oxygen species (ROS) and cell cycle in nephrotoxicity induced by different concentrations of polystyrene microplastics (PS-MPs) is unknown. This study used grass carp kidney cells (CIK) treated with different concentrations of PS-MPs (0, 0.012, 0.0625, and 0.5 mg L-1 ) as subjects. With the increase of PS-MPs concentration, the levels of ROS and malonaldehyde increased, while the level of total antioxidant capacity, superoxide Dismutase (SOD), and glutathione (GSH) activity decreased. The expression of BUB1 mitotic checkpoint serine/threonine kinase (BUB1), cyclin-dependent kinase (CDK1), CDK2, CyclinB1, cell division cycle 20 homolog (CDC20), and B-cell lymphoma-2, sequestosome 1 decreased significantly. Nevertheless, the expression of Caspase 3, Cleave-Caspase 3, cytochrome c (Cytc), BCL2-associated X, apoptosis regulator, poly ADP-ribose polymerase (PARP), Cleave-PARP, Caspase 9, autophagy immunoblot kit (LC3), and Beclin1 increased. Our research shows that PS-MPs can trigger oxidative stress and induce cell cycle arrest, apoptosis, and autophagy in CIK cells by regulating ROS. This work provides a theoretical basis for cellular biology and toxicology mechanisms and new insights into the potential risks to animals from MPs exposure in the environment.

Polystyrene microplastics induce autophagy and apoptosis in birds lungs via PTEN/PI3K/AKT/mTOR.

Microplastics (MPs) seriously pollute and potentially threaten human health. Birds are sentinels of environmental pollutants, which respond quickly to contamination events and reveal current environmental exposure. Therefore, birds are good bioindicators for monitoring environmental pollutants. However, the mechanism of lung injury in birds and the role of the PTEN/PI3K/AKT axis are unknown. In this study, broilers treated with different polystyrene microplastics (PS-MPs) (0, 1, 10, and 100 mg/L) were exposed to drinking water for 6 weeks to analyze the effect of PS-MPs on lung injury of broilers. The results showed that with the increase of PS-MPs concentration, malonaldehyde (MDA) content increased, and catalase (CAT) and glutathione (GSH) activity decreased, further leading to oxidative stress. PS-MPs caused the PI3K/Akt/mTOR pathway to be inhibited by phosphorylation, and autophagy accelerated formation (LC3) and degradation (p62), causing autophagy. In PS-MPs exposed lung tissues, the expression of Bax/Bcl-2 and Caspase family increased, and MAPK signaling pathways (p38, ERK, and JNK) showed an increase in phosphorylation level, thus leading to cell apoptosis. Our research showed that PS-MPs could activate the antioxidant system. The antioxidant system unbalance-regulated Caspase family, and PTEN/PI3K/AKT pathways initiated apoptosis and autophagy, which in turn led to lung tissue damage in chickens. These results are of great significance to the toxicological study of PS-MPs and the protection of the ecosystem.

Lycopene attenuates oxidative stress, inflammation, and apoptosis by modulating Nrf2/NF-κB balance in sulfamethoxazole-induced neurotoxicity in grass carp (Ctenopharyngodon Idella).

All drugs that can penetrate the blood-brain barrier (BBB) may lead to mental state changes, including the widely used anti-infective drug sulfamethoxazole (SMZ). Herein, we investigated whether lycopene (LYC) could ameliorate SMZ-induced brain injury and the postulated mechanisms involved. A total of 120 grass carps were exposed under SMZ (0.3 µg/L, waterborne) or LYC (10 mg/kg fish weight, diet) or their combination for 30 days. Firstly, brain injury induced by SMZ exposure was suggested by the damage of BBB (decreases of Claudins, Occludin and Zonula Occludens), and the decrease of neurotransmitter activity (AChE). Through inducing oxidative stress (elevations of malondialdehyde and 8-hydroxy-2 deoxyguanosine, inhibition of glutathione), SMZ increased the intra-nuclear level of NF-κB and its target genes (TNF-α and interleukins), creating an inflammatory microenvironment. As a positive feed-back mechanism, apoptosis begins with activation of pro-death proteins (Bax/Bcl-2) and activation of caspases (caspase-9 and caspase-3). Meanwhile, a compensatory upregulation of constitutive Nrf2 and its downstream antioxidative gene expression (NAD(P)H Quinone Dehydrogenase 1 and Heme oxygenase 1) and accelerated autophagy (increases of autophagy-related genes and p62 inhibition) were activated as a defense mechanism. Intriguingly, under SMZ stress, LYC co-administration decreased NF-κB/apoptosis cascades and restored Nrf2/autophagy levels. The neuroprotective roles of LYC make this natural compound a valuable agent for prevention SMZ stress in environment. This study suggests that LYC might be developed as a potential candidate for alleviating environmental SMZ stress in aquaculture.

NLRP3 inflammasome is involved in the mechanism of the mitigative effect of lycopene on sulfamethoxazole-induced inflammatory damage in grass carp kidneys.

Freshwater environmental antibiotic pollution is becoming more severe because of the irregular use of sulfonamide antibiotics. Sulfamethoxazole (SMZ) is a kind of antibiotic that can cause harm to the urinary systems of organisms. However, the toxic impacts of environment-related concentrations of antibiotics in fish have not been thoroughly studied. Lycopene (LYC) has the property of alleviating antibiotic toxicity by diminishing oxidative stress and inflammation. This investigation is intended to examine the instrument of the mitigative part of LYC on SMZ-caused renal inflammatory injury in grass carp. Grass carp were born with SMZ (0. 3 µg L-1) and LYC (10 mg/kg body weight) for 30 days. Serum was used to measure creatinine (CREA) and urea nitrogen (BUN) contents; what is more, kidneys were used to measure histological structure, oxidative stress indicators, relative expressions of cytokines, and inflammatory factors. We found that SMZ exposure significantly increased oxidative stress, characterized by decreased catalase activity (CAT) and superoxide dismutase (SOD). In addition, inflammation-related factors: interleukin (IL-18, IL-6, and IL-1ß), an apoptotic speck-containing protein with a card (ASC), NOD-like receptor protein3 (NLRP3), cysteinyl aspartate specific proteinase-1 (caspase-1), tumor necrosis factor-α (TNF-α), and nuclear factor-activated B cells (NF-κB) expression increased significantly contrasted with those control group. Inflammatory reactions and ultrastructural changes accompany. LYC administration alleviated the changes mentioned above. In conclusion, In conclusion, these results suggest a protective effect of LYC dietary supplements against kidney damage caused by SMZ. LYC is expected to prevent and treat oxidative stress and chronic inflammation caused by antibiotics as a critical component in the fish breeding diet.

ROS-Induced Hepatotoxicity under Cypermethrin: Involvement of the Crosstalk between Nrf2/Keap1 and NF-κB/iκB-α Pathways Regulated by Proteasome.

Cypermethrin (CMN) is a man-made insecticide, and its abuse has led to potential adverse effects, particularly in sensitive populations such as aquatic organisms. The present study was focused on the toxic phenotype and detoxification mechanism in grass carp (Ctenopharyngodon idella) after treatment with waterborne CMN (0.651 µg/L) for 6 weeks in vivo or 6.392 µM for 24 h in vitro. In vivo, we describe the toxic phenotype of the liver of grass carp in terms of pathological changes, serum transaminase levels, oxidative stress indexes, and apoptosis rates. RNA-Seq analysis (2 × 3 cDNA libraries) suggested a compromise of proteasome and oxidative phosphorylation signaling pathways under CMN exposure. Thus, these two pathways were chosen for the in vitro study, which suggested that the CMN intoxication-induced proteasome pathway caused hepatotoxicity in the liver cell line of grass carp (L8824 cells). Moreover, pretreatment with MG132, a proteasome inhibitor, displayed protection against the toxic effects of CMN by enhancing antioxidative and anti-inflammatory capability by directly inhibiting the proteasomal degradation of nuclear factor erythroid-2 related factor (Nrf2) and IκB-α, thus turning on the transcription of downstream genes of Nrf2 and NF-κB, respectively. Taken together, these results suggest proteasome activity as a reason for CMN-induced hepatotoxicity.

Zinc offers splenic protection through suppressing PERK/IRE1-driven apoptosis pathway in common carp (Cyprinus carpio) under arsenic stress.

Arsenic (As) occurs naturally and concentrations in water bodies can reach high levels, leading to accumulation in vital organs like the spleen. Being an important organ in immune response and blood development processes, toxic effects of As on the spleen could compromise immunity and cause associated disorders in affected individuals. Splenic detoxification is key to improving the chances of survival but relatively little is known about the mechanisms involved. Essential trace elements like zinc have shown immune-modulatory effects humans and livestock. This study aimed to investigate the mechanisms involved in As-induced splenic toxicity in the common carp (Cyprinus carpio), and the protective effects of zinc (Zn). Our findings suggest that environmental exposure to As caused severe histological injuries and Ca2+ accumulation in the spleen of common carp. Additionally, transcriptional and translational profiles of endoplasmic reticulum stress, apoptosis and autophagy-related genes of the spleen showed upward trends under As toxicity. Treatment with Zn appears to offer protection against As-induced splenic injury in common carp and the pathologic changes above were alleviated. Our results provide additional insight into the mechanism of As toxicity in common carp while elucidating the role of Zn, a natural immune-modulator, as a potential antidote against As poisoning.

Zinc exerts its renal protection effect on arsenic-exposed common carp: A signaling network comprising Nrf2, NF-κB and MAPK pathways.

Epidemiological and laboratory investigations have extensively indicated that arsenic exposure accounts for several kidney diseases. Zinc has been suggested as a possible natural preventive and therapeutic agent. This study is designed to explore the beneficial effect of zinc supplementation against arsenic-induced renal toxicity in common carp, and the results point to signaling pathway possibly compromised. In the present study, renal injury was induced in common carp by waterborne exposure to arsenic (2.83 mg/L) for 30 days, and zinc (1 mg/L) was simultaneously supplemented. First, the arsenic-exposed fish showed histological and functional renal alterations (indicated by hematoxylin-eosin staining, biochemical indexes and a TUNEL assay). Moreover, as a reactive oxygen species (ROS) stimulant, arsenic was found to induce oxidative toxicity as determined by increased renal ROS, malondialdehyde, protein carbonyl and 8-hydroxydeoxyguanosine levels. When antioxidant-mediation attempts (through superoxide dismutase and glutathione)-mediated to restore homeostasis failed and ROS increased to extreme levels, inflammation (indicated by elevated inducible nitric oxide synthetase, tumor necrosis factor-alpha and interleukins levels) and apoptosis (through both mitochondrial- and death receptor-dependent pathways) were triggered. However, abnormalities in the upstream mediators Nrf2, NF-κB and MAPK were significantly ameliorated and blocked by treatment with zinc. In conclusion, zinc exerts a substantial protective effect against arsenic-triggered subchronic renal injury in common carp via the amelioration of oxidative stress, suppression of apoptosis and reduced inflammation through Nrf2, NF-κB and MAPK signaling.

Zinc application alleviates the adverse renal effects of arsenic stress in a protein quality control way in common carp.

The potential antagonistic mechanism between zinc (Zn) and arsenic (As) on renal toxicity was investigated in common carp. The results showed that by increased Zn efflux and retention (as reflected by zinc transporter 1 (ZnT-1), Zrt- and Irt- 1ike protein (ZIP) and metallothionein (MT) expression), Zn co-administration significantly recovered the antioxidant function (catalase, CAT) and the level of renal barrier function (Occludin, Claudins and Zonula Occludens) in comparison to As treatment. Interestingly, Zn co-administration with As resulted in carps undergoing reduction of heat shock response (HSPs), a low induction of autophagy flux (Beclin-1, microtubule-associated protein 1 light chain 3 (LC3) and sequestosome 1 (P62)) and decreased endoplasmic reticulum (ER) stress (activating transcription factor 6 (ATF-6), inositol requiring-1α (IRE1) and PKR-like ER kinase (PERK)) in the aspect of mRNA or protein levels. All these alleviated protein quality control processes induced by Zn under As stress was correlated with the no longer loosen tight connection, less swollen endoplasmic reticulum as well as reduced formation of autophagosomes and autophagic vesicles. Mechanically, post-transcriptional regulated protein quantities compromising phosphatidylinositol-3-kinase (PI3K)/protein kinase B (AKT)/mammalian target of rapamycin (mTOR) pathway was demonstrated true causative forces inside the cell for Zn against As poisoning. In conclusion, we suggested the potential renal protective effect of Zn supplementation against As exposure by the modulation of protein quality control processes.

As3+ or/and Cu2+ exposure triggers oxidative stress imbalance, induces inflammatory response and apoptosis in chicken brain.

Arsenic (As) and copper (Cu) are common environmental pollutants in nature. When they are excessively present in living organisms, they can cause heavy metal poisoning. There were relatively few studies of the toxicological concentrations of As and Cu in the brain using chicken as a model. Therefore, in this study, arsenic trioxide or/and copper sulfate were added to chicken diets for a 12-week toxicity test. The test results showed that excessive intake of As or/and Cu led to a significant reduction in the total antioxidant capacity (T-AOC), catalase (CAT) and hydroxyl radicals. And significant increase in nitric oxide synthase (NOS) indicates an imbalanced oxidation reaction. In addition, the increase in heat shock protein (HSPs), the increase of NF-κB pathway-related pro-inflammatory mediators, the change of apoptosis factors on the death receptor and mitochondrial apoptosis pathway show that, As or/and Cu exposure induced chicken brain has heat shock response (HSP), tissue inflammation and apoptosis. This damage is inseparable from the oxidative imbalance. It is worth noting that these injury changes are time-dependent, and the combined effect of these two metals is more severe than that of a single group of injuries. Our findings can inform the regulation of animal feed additives and avoid agricultural economic losses or biological health damage.

Arsenic (III) or/and copper (II) exposure induce immunotoxicity through trigger oxidative stress, inflammation and immune imbalance in the bursa of chicken.

The environmental hazards of arsenic (As) and copper (Cu) contamination have swept through quite a few districts worldwide. Whereas, molecular mechanisms involved in As- and Cu-induced immunotoxicity in Gallus gallus bursa of Fabricius (BF) are complex and elusive. Male Hy-line chickens were exposed to arsenic trioxide (As2O3; 30 mg/kg) and copper sulfate (CuSO4; 300 mg/kg) alone or in combination, respectively, to examine the potential ecotoxicity of them. The ions homeostasis and BF index of chicken had distinct changes after As or/and Cu exposure. Moreover, As or/and Cu treatment significantly increased the MDA content and NOS activity, and simultaneously resulted in reductions in CAT and AHR activities. Subsequently, it was further exhibited up-regulations of nuclear factor-κB (NF-κB), inflammatory mediators and pro-inflammation cytokines accompanied by depletion of anti-inflammatory cytokines and severe pathological conditions. Moreover, decreased ratio of IFN-γ/IL-4 and increased level of IL-17 illustrated an imbalance of the immune response. Meanwhile, incremental mRNA transcription and protein levels of heat shock proteins (HSPs) alleviated toxicity caused by As or/and Cu. Importantly, exposure to both contaminants significantly soared the BF injury in comparison with exposure to As or Cu alone. All these results illustrated that exposure to As2O3 or/and CuSO4 elicited BF tissue damage and ions changes, and its severity was associated with prolonged persistence of oxidative damage, accompanied by a dysregulated immune response which played a vital role in inflammatory injury. Additionally, combined management of As2O3 and CuSO4 could exacerbate BF injury.

Zinc alleviates arsenism in common carp: Varied change profiles of cytokines and tight junction proteins among two intestinal segments.

This study was designed to evaluate the effects of zinc on inflammation and tight junction (TJ) in different intestinal regions of common carp under sub-chronic arsenic insult. Fish were exposed to zinc (0, 1 mg/L) and arsenic trioxide (0, 2.83 mg/L) in individual or combination for a month. Inflammatory infiltration and TJ structure changes were displayed by H&E staining and transmission electron microscope. To further explore these changes, biochemical indicator (SOD), gene or protein expressions of inflammatory responses (NF-κB, IL-1ß, IL-6 and IL-8) and TJ proteins (Occludin, Claudins and ZOs) were determined. In the anterior intestine, arsenic decreased activity of SOD, mRNA levels of Occludin, Claudins and ZOs, increased mRNA levels of ILs. However, unlike the anterior intestine, arsenic has an upregulation effects of Occludin and Claudin-4 in the mid intestine. These anomalies induced by arsenic, except IL-8, were completely or partially recovered by zinc co-administration. Furthermore, transcription factor (NF-κB) nuclear translocation paralleled with its downstream genes in both intestinal regions. In conclusion, our results unambiguously suggested that under arsenic stress, zinc can partly relieve intestinal inflammation and disruption of tight junction segment-dependently.

Arsenic trioxide or/and copper sulfate co-exposure induce glandular stomach of chicken injury via destruction of the mitochondrial dynamics and activation of apoptosis as well as autophagy.

Arsenic and copper are naturally occurring element. Contamination from natural processes and anthropogenic activities can be discovered all over the world and their unique interactions with the environment lead to widespread toxicity. When the content was excessive, the organism would be hurt seriously. The glandular stomach is an important organ of the poultry gastrointestinal tract. This study was aimed to investigate the toxicity of arsenic trioxide or/and copper sulfate (As or/and Cu) on chicken glandular stomach. Seventy-two 1-day-old Hy-Line chickens were randomly divided into control (C) group, arsenic trioxide (As) group, copper sulfate (Cu) group and arsenic trioxide and copper sulfate (AsCu) group, and exposed to 30 mg/kg arsenic trioxide or/and 300 mg/kg copper sulphates for 12 weeks. The indicators of mitochondrial dynamics, apoptosis and autophagy were tested in the glandular stomach. The results showed that exposure to As or/and Cu caused mitochondrial dynamic imbalance. Additionally, the levels of pro-apoptosis and autophagy indicators were increased and the levels of anti-apoptosis indicators were decreased in the treatment groups. Beyond that, in the treatment groups, we could clearly see karyopyknosis and chromatin condensation were associated with increased apoptosis rate, as well as the disappearance of the nuclear membrane, the swelling of mitochondria and the accumulation of autophagosomes were involved in the death of cells. It was worth noting that the glandular stomach lesions were time-dependent, and the combination of As and Cu were worse than the As and Cu alone. Collectively, our results suggest that As or/and Cu aggravate mitochondrial dysfunction, apoptosis and autophagy in a time-dependent manner, and the combined toxicity of As and Cu was higher.

Discrepant effects of copper (II) stress on different types of skeletal muscles in chicken: Elements and amino acids.

Different distributions of 28 elements and 17 amino acids in pectoralis, wing biceps brachii and leg gastrocnemius of chicken upon CuSO4 (300 mg/kg) exposure for 90 days were investigated. Accompanied by copper accumulation, pathological injuries were observed in those three kinds of skeletal muscles using histological and ultrastructural methods. Based on data obtained, we analyzed leg gastrocnemius displayed the most increases (P < 0.000) in all three kinds of elements detected, including macroelements (131%), essential microelements (129%) and toxic microelements (179%) than the other two skeletal muscles. Furthermore, decreased total amino acids (P = 0.006), a susceptibility of lipid peroxidation/oxidative stress and a disequilibrium of nutrition and taste were analyzed in the leg gastrocnemius, indicating an unsuitability for human consumption. Intriguingly, these anomalies were scarce in pectoralis and wing biceps brachii. Combined with multivariate analysis we may conclude that leg gastrocnemius are more vulnerable to copper stress than pectoralis and wing biceps brachii in chicken.

Destruction of redox and mitochondrial dynamics co-contributes to programmed cell death in chicken kidney under arsenite or/and copper (II) exposure.

BACKGROUND: Sub-chronic arsenic (arsenite) exposure-induced oxidative toxicity leads to adverse effects in various organ systems, especially the kidney. Copper sulphate (Cu2+), known for its extensive uses in agriculture, has also been reported to have pro-oxidation properties. Both of these two potential toxic elements can bio-accumulate through food chain, thus endangering human health. However, their interaction study in the kidney is scanty. AIM: To investigate the synergism effects of Cu2+ in arseniasis-elicited oxidative stress and cascaded renal injury in chickens. RESULTS: Arsenite intoxication decreased renal antioxidant system along with ATPases. Arsenite exposure also significantly elicited disequilibrium of mitochondrial homeostasis, accompanying by elevated apoptotic and autophagic cell death. The disturbed morphological and ultrastructural changes further corroborated arsenite nephrotoxicity. These anomalies aligned with the findings in Cu2+ groups, which co-administrated with arsenic further deteriorated these pathological changes. This synergism was achieved partially via the inactivation of phosphoinositide-3-kinase/protein kinase b/mammalian target of rapamycin (PI3K/AKT/mTOR) pathway through the activation of P53. CONCLUSIONS: Copper excess and arsenic exposure can function independently or cooperatively to affect oxidative stress, mitochondrial dynamics and programmed cell death. These results highlighted the need to take precautions against copper and arsenic co-exposure when considering their impact in susceptible animals/populations.

Regulation of autophagy factors by oxidative stress and cardiac enzymes imbalance during arsenic or/and copper induced cardiotoxicity in Gallus gallus.

Basal autophagy has an indispensable role in the functioning and maintenance of cardiac geometry under physiological conditions. Recently, increasing evidence has demonstrated that arsenic (As)/copper (Cu) play important roles in the autophagy of the heart. The current study was to evaluate whether oxidative damage by As or/and Cu was correlated with autophagy through the phosphatidylinositol 3-kinase (PI3K)/protein kinase B (AKT)/mammalian target of rapamycin (mTOR) pathway in the heart of birds. Arsenic trioxide (30mg/kg) or/and cupric sulfate (300mg/kg) were administered in a basal diet to male Hy-line chickens (one-day-old) for 12 weeks. The results showed that heart weight/body weight ratio decreased in the As + Cu group only at 4, 8 and 12 weeks. Moreover, we observed that As or/and Cu decreased high-density lipoprotein cholesterol (HDL-C) concentrations, increased total cholesterol (T-CHO) concentrations and cardiac enzymes activities in the serum. On the other hand, As or/and Cu significantly reduced the activities of total antioxidant (T-AOC), superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GSH-Px)) along with decreased nonenzymic antioxidant (glutathione (GSH)) concentrations and increased malondialdehyde (MDA) concentrations in the heart. Furthermore, As or/and Cu could induce autophagy in the heart of chickens through decreased mRNA levels of TORC1, TORC2, microtubule associated light chains 3-I (LC3-I) and increased PI3K, AKT1, Beclin1, autophagy associated gene 4B (Atg4B), microtubule associated light chains 3-II (LC3-II), autophagy associated gene 5 (Atg5) and Dynein. Meanwhile, ultrastructural examinations showed that As/Cu could result in the appearance of autolygosomes, autophagic vacuoles and double-membrane structures in the heart. In conclusion, As or/and Cu induced cardiac damage and autophagy via elevating cardiac enzymes activities, inducing oxidative stress and activating the PI3K/AKT/mTORC pathway in heart of chickens. Moreover, As and Cu had a possible synergistic relationship in the heart of chickens.

Complete genome sequence and evolution analysis of a columbid herpesvirus type 1 from feral pigeon in China.

Here, we report the genome sequence of a feral pigeon alphaherpesvirus (columbid herpesvirus type 1, CoHV-1), strain HLJ, and compare it with other avian alphaherpesviruses. The CoHV-1 strain HLJ genome is 204,237 bp in length and encodes approximately 130 putative protein-coding genes. Phylogenetically, CoHV-1 complete genome resides in a monophyletic group with the falconid herpesvirus type 1 (FaHV-1) genome, distant from other alphaherpesviruses. Interestingly, the evolutionary analysis of partial genes of CoHV-1 isolated from different organisms and areas (currently accessible on GenBank) indicates that the CoHV-1 HLJ strain isolated from pigeon (Columba livia) is closely related to the strains isolated from peregrine falcon (Falco peregrinus) in Poland and owl (Bubo virginianus) in USA. These results may suggest possible transmission of the virus between different organisms and different geographic areas.

Arsenic affects inflammatory cytokine expression in Gallus gallus brain tissues.

BACKGROUND: The heavy metal arsenic is widely distributed in nature and posses a serious threat to organism's health. However, little is known about the arsenic-induced inflammatory response in the brain tissues of birds and the relationship and mechanism of the inflammatory response. The purpose of this study was to explore the effects of dietary arsenic on the expression of inflammatory cytokines in the brains of Gallus gallus. RESULTS: Seventy-two 1-day-old male Hy-line chickens were divided into a control group, a low arsenic trioxide (As2O3)-treated (7.5 mg/kg) group, a middle As2O3-treated (15 mg/kg) group, and a high As2O3-treated (30 mg/kg) group. Arsenic exposure caused obvious ultrastructural changes. The mRNA levels of the transcription factor nuclear factor-κB (NF-κB) and of pro-inflammatory cytokines, including inducible NO synthase (iNOS), cyclooxygenase-2 (COX-2), and prostaglandin E synthase (PTGEs), in chicken brain tissues (cerebrum, cerebellum, thalamus, brainstem and myelencephalon) on days 30, 60 and 90, respectively, were measured by real-time PCR. The protein expression of iNOS was detected by western blot. The results showed that after being treated with As2O3, the levels of inflammatory-related factor NF-κB and pro-inflammatory cytokines in chicken brain tissues increased (P < 0.05). CONCLUSIONS: Arsenic exposure in the chickens triggered host defence and induced an inflammatory response by regulating the expression of inflammatory-related genes in the cerebrum, cerebellum, thalamus, brainstem and myelencephalon. These data form a foundation for further research on arsenic-induced neurotoxicity in Gallus gallus.

Assessment of 28 trace elements and 17 amino acid levels in muscular tissues of broiler chicken (Gallus gallus) suffering from arsenic trioxide.

The contents of 28 trace elements, 17 amino acid were evaluated in muscular tissues (wings, crureus and pectoralis) of chickens in response to arsenic trioxide (As2O3). A total of 200 one-day-old male Hy-line chickens were fed either a commercial diet (C-group) or an As2O3 supplement diet containing 7.5mg/kg (L-group), 15mg/kg (M-group) or 30mg/kg (H-group) As2O3 for 90 days. The elements content was analyzed by inductively coupled plasma mass spectrometry (ICP-MS). Under As2O3 exposure, the concentration of As were elevated 8.87-15.76 fold, 7.93-15.63 fold and 5.94-12.45 fold in wings, crureus and pectoralis compared to the corresponding C-group, respectively. 19 element levels (lithium (Li), magnesium (Mg), aluminum (Al), silicon (Si), kalium (K), vanadium (V), chromium (Cr), manganese (Mn), nickel (Ni), copper (Cu), selenium (Se), strontium (Sr), molybdenum (Mo), cadmium (Cd), tin (Sn), antimony (Sb), barium (Ba), mercury (Hg) and lead (Pb), 9 element levels (K, Co, Ni, Cu, As, Se, Sr, Sn, Ba and Hg) and 4 element levels (Mn, cobalt (Co), As, Sr and Ba) were significantly increased (P < 0.05) in wing, crureus and pectoralis, respectively. 2 element levels (sodium (Na) and zinc (Zn)), 5 element levels (Li, Na, Si, titanium (Ti and Cr), 13 element levels (Li, Na, Mg, K, V, Cr, iron (Fe), Cu, Zn, Mo, Sn, Hg and Pb) were significantly decreased (P < 0.05) in wing muscle, crureus and pectoralis, respectively. Additionally, in crureus and pectoralis, the content of total amino acids (TAA) was no significant alterations in L and M-group and then increased approximately 10.2% and 7.6% in H-group, respectively (P < 0.05). In wings, the level of total amino acids increased approximately 10% in L-group, whereas it showed unchanged in M and H-group compared to the corresponding C-group. We also observed that significantly increased levels of proline, cysteine, aspartic acid, methionine along with decrease in the tyrosine levels in muscular tissues compared to the corresponding C-group. In conclusion, the residual of As in the muscular tissues of chickens were dose-dependent and disrupts trace element homeostasis, amino acids level in muscular tissues of chickens under As2O3 exposure. Additionally, the response (trace elements and amino acids) were different in wing, thigh and pectoral of chick under As2O3 exposure. This study provided references for further study of heavy metal poisoning and may be helpful to understanding the toxicological mechanism of As2O3 exposure in muscular tissues of chickens.

Assessment of arsenic trioxide toxicity on cock muscular tissue: alterations of oxidative damage parameters, inflammatory cytokines and heat shock proteins.

To evaluate the toxicity of arsenic trioxide (As2O3) in the muscular tissues (wing, thigh and pectoral) of birds, 72 one-day-old Hy-line cocks were selected and randomly divided into four groups. They were fed either a commercial diet or an arsenic-supplemented diet containing 7.5, 15 or 30 mg/kg As2O3. The experiment lasted for 90 days and the samples of muscular tissues were collected at 30, 60 and 90 days. The results showed that As2O3 exposure significantly lowered the activities of antioxidant enzymes (catalase (CAT), glutathione peroxidase (GSH-Px)) and inhibition ability of hydroxyl radicals (OH) and increased the malondialdehyde (MDA) contents. Furthermore, the mRNA levels of inflammatory cytokines (tumor necrosis factor-α (TNF-α), nuclear factor-kappa B (NF-κB), cyclooxygenase-2 (COX-2), inducible NO synthase (iNOS), prostaglandin E synthase (PTGEs)) and heat shock proteins (HSPs) in muscular tissue were significantly upregulated in the As2O3 exposure groups. The results indicated that As2O3 exposure resulted in oxidative damage, induced the inflammatory response, and influenced the mRNA levels of HSPs in muscular tissue of cocks. Additionally, the results suggested that HSPs possibly resisted due to the As2O3 exposure-induced oxidative stress and inflammatory response, which provided a favorable environment and played protective roles in the muscular tissues of cocks. The information presented in this study is helpful to understand the mechanism of As2O3 toxicity in bird muscular tissues.