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Lighting in poultry production holds notable importance with the advancement and modernization of the industry, as it plays a significant role in the physiology and growth of broiler chickens. Increasing attention has been paid to the impacts of lighting management on growth performance, immune status, and welfare of meat-type chickens. It is essential to have an appropriate lighting regimen that includes the light source, intensity, duration, and wavelength of light to improve broilers' growth and behavior. By manipulating various physiological, immunological, and behavioral activities, altering the color of light has been acknowledged as a potent managerial strategy capable of mitigating an array of stressors in broiler chickens. Assessing animal welfare is necessary for animal behavior and product quality perspectives. Birds have a unique visual system, and their behavior is primarily mediated by vision. Different monochromatic light regimes can affect feed conversion ratio, modulating broiler chickens' systematic immune response and aggressive behavior. With the advancement of lighting technology, new possibilities have emerged to enhance traditional lighting programs in poultry houses. This review integrates recent findings on the use of monochromatic light and its impact on broilers' welfare, growth, and physiological response. [ABSTRACT FROM AUTHOR]

Lead (Pb), a heavy metal environmental pollutant, poses a threat to the health of humans and birds. Inflammation is one of the most common pathological phenomena in the case of illness and poisoning. However, the underlying mechanisms of inflammation remain unclear. The cerebellum and the thalamus are important parts of the nervous system. To date, there have been no reports of Pb inducing inflammation in animal cerebellums or thalami. Selenium (Se) can relieve Pb poisoning. Therefore, we aimed to explore the mechanism by which Se alleviates Pb toxicity to the cerebellums and thalami of chickens by establishing a chicken Pb or/and Se treatment model. Our results demonstrated that exposure to Pb caused inflammatory damage in cerebellums and thalami, evidenced by the characteristics of inflammation, the decrease in anti-inflammatory factors (interleukin (IL)-2 and interferon-γ (INF-γ)), and the increase in pro-inflammatory factors (IL-4, IL-6, IL-12β, IL-17, and nitric oxide (NO)). Moreover, we found that the IL-2/IL-17–NO pathway took part in Pb-caused inflammatory injury. The above findings were reversed by the supplementation of dietary Se, meaning that Se relieved inflammatory damage caused by Pb via the IL-2/IL-17–NO pathway. In addition, an up-regulated oxidative index malondialdehyde (MDA) and two down-regulated antioxidant indices (glutathione (GSH) and total antioxidant capacity (TAC)) were recorded after the chickens received Pb stimulation, indicating that excess Pb caused an oxidant/antioxidant imbalance and oxidative stress, and the oxidative stress mediated inflammatory damage via the GSH–IL-2 axis. Interestingly, exposure to Pb inhibited four glutathione peroxidase (GPx) family members (GPx1, GPx2, GPx3, and GPx4), three deiodinase (Dio) family members (Dio1, Dio2, and Dio3), and fifteen other selenoproteins (selenophosphate synthetase 2 (SPS2), selenoprotein (Sel)H, SelI, SelK, SelM, SelO, SelP1, SelPb, SelS, SelT, SelU, and selenoprotein (Sep)n1, Sepw1, Sepx1, and Sep15), suggesting that Pb reduced antioxidant capacity and resulted in oxidative stress involving the SPS2–GPx1–GSH pathway. Se supplementation, as expected, reversed the changes mentioned above, indicating that Se supplementation improved antioxidant capacity and mitigated oxidative stress in chickens. For the first time, we discovered that the SPS2–GPx1–GSH–IL-2/IL-17–NO pathway is involved in the complex inflammatory damage mechanism caused by Pb in chickens. In conclusion, this study demonstrated that Se relieved Pb-induced oxidative stress and inflammatory damage via the SPS2–GPx1–GSH–IL-2/IL-17–NO pathway in the chicken nervous system. This study offers novel insights into environmental pollutant-caused animal poisoning and provides a novel theoretical basis for the detoxification effect of Se against oxidative stress and inflammation caused by toxic pollutants. [ABSTRACT FROM AUTHOR]

Lead (Pb), a toxic environmental pollutant, is hazardous to the health of humans and birds. Bursa of Fabricius (BF) is a unique organ of birds. Toxic substances can attack BF and induce proteotoxicity. Increased heat shock proteins (HSPs) can induce oxidative damage. Selenium (Se) can alleviate harmful substance-caused oxidative damage. This study aimed to investigate whether Pb can cause oxidative damage and proteotoxicity, as well as Se reverse Pb-caused chicken BF toxicity. A model of chickens treated with Se and Pb alone and in combination was established. BFs were collected on days 30, 60, and 90. H&E and qRT-PCR were performed to observe the microstructure and to detect HSP27, HSP40, HSP60, HSP70, and HSP90 mRNA levels, respectively, in BFs. Multivariate correlation analysis and principal component analysis were conducted to explore the correlation among the five HSPs. In our results, Pb caused BF damage and up-regulated the five HSPs at three time points, causing oxidative damage and proteotoxicity via HSP27–HSP40–HSP70–HSP90 pathway. Furthermore, Pb caused time-dependent stress on HSP27, HSP40, HSP60, and HSP70. In addition, Se relieved Pb-caused damage and up-regulation of HSPs. Taken together, we concluded that Se alleviated Pb-caused oxidative injury and proteotoxicity in chicken BFs via the HSP27–HSP40–HSP70–HSP90 pathway. [ABSTRACT FROM AUTHOR]

Manganese (Mn) poisoning can happen in the case of environmental pollution and occupational exposure. However, the underlying mechanisms of Mn-induced teste toxicity and whether mitochondrion and heat shock proteins (HSPs) are involved in toxic effect of Mn on chicken testes remain poorly understood. To investigate this, MnCl2·4H2O was administered in the diet (600, 900, and 1800 mg/kg Mn) of chickens for 30, 60, and 90 days. Electron microscopy and qPCR were performed. Results showed that Mn exposure suppressed dose- and time-dependently HSP40 and HSP60 mRNA levels, meanwhile increased does-dependently HSP27, HSP70, and HSP90 mRNA levels at all three time points under three Mn exposure concentrations. Furthermore, Mn treatment damaged myoid cells, spermatocytes, and Sertoli cells through electron microscopic observation, indicating that Mn treatment damaged chicken testes. In addition, abnormal shapes of mitochondria were found, and mitochondria displayed extensive vacuolation. The increase of HSP90 and HSP70 induced by Mn exposure inhibited HSP40 and stimulated HSP27, respectively, in chicken testes, which needs further to be explored. Taken together, our study suggested that there was toxic effect in excess Mn on chickens, and HSPs and mitochondria were involved in the mechanism of dose-dependent injury caused by Mn in chicken testes. This study provided new insights for Mn toxicity identification in animal husbandry production practice. [ABSTRACT FROM AUTHOR]

Manganese (Mn) is a ubiquitous heavy metal pollutant in environment, and excess Mn can damage nervous system of humans and animals. However, molecular mechanism of Mn-induced poultry neurotoxicity on inflammatory injury is still not fully clear. Thus, the purpose of the conducted research was to explore molecular mechanism of inflammatory injury caused by Mn in chicken nervous system. Two Mn poisoning models were established in vivo and in vitro. One hundred and eighty chickens were randomly separated into four groups. One control group was raised drinking water and standard diet. Three Mn groups were raised drinking water, and the standard diet supplemented with three different concentrations of MnCl2 ∙ 4H2O. There were 45 birds and 3 replicates in each group. Neurocytes from chicken embryos were cultured in mediums without and with six different concentrations of MnCl2 ∙ 4H2O in vitro. Our experiments showed that excess Mn caused cerebral histomorphological structure alternations and damage, and increased the expressions (P < 0.05) of inflammation-related factor NF-κB, TNF-α, iNOS, COX-2, and PTGEs in vivo and in vitro, meaning that excess Mn caused inflammatory damage and inflammatory response in chicken nervous system. Moreover, there were an upregulated IFN-γ mRNA expression and a downregulated IL-4 mRNA expression (P < 0.05) in bird cerebra and embryonic neurocytes after exposure to Mn, indicating that Mn exposure caused Th1/Th2 imbalance and immunosuppression. Additionally, in our research, the elevation (P < 0.05) of five HSPs (HSP27, HSP40, HSP60, HSP70, and HSP90) was found, suggesting that HSPs participated molecular mechanism of Mn stress. In addition, the inflammatory toxicity of Mn to chicken nervous system was time- and dose-dependent. Taken all together, our findings indicated that Th1/Th2 imbalance and HSPs mediated Mn-caused inflammatory injury via NF-κB pathway in chicken nervous system in vivo and in vitro. [ABSTRACT FROM AUTHOR]

Lead (Pb) is a kind of widespread toxic environmental pollutant which can cause harm to organisms. Selenium (Se) has the property of mitigating Pb toxicity through decreasing oxidative stress and inflammation caused by Pb. Nucleotide-binding domain, leucine-rich-containing family, and pyrin-domain containing-3 (NLRP3) inflammasome involve in inflammation process. However, the effect of NLRP3 inflammasome in heavy metal-caused animal damage remains unknown. This research aimed to explore the mechanism of mitigative role of Se on Pb-caused renal inflammatory injury in chickens. One-week-old male chickens were provided a standard diet and drinking water, a standard diet added with 1 mg kg−1 of Se and drinking water, a standard diet and drinking water added with 350 mg L−1 Pb, and a standard diet added with 1 mg kg−1 Se and drinking water added with 350 mg L−1 Pb. On the 4th, 8th, and 12th weeks, serum was used to measure creatinine (CREA) and uric acid (UA) contents, and kidneys were used to measure Se and Pb concentrations, histological structure, oxidative stress indicators, relative expressions of cytokines, and inflammatory factors. The results showed that Pb accumulated, Se concentration decreased, CREA and UA contents increased, and renal injury occurred in Pb-treated chicken kidneys. Excess Pb increased MDA content and the expressions of IL-1β, IL-6, IL-17, NLRP3, caspase-1, NF-κB, COX-2, TNF-α, and PTGEs and decreased GSH content, GPx and SOD activities, and IFN-γ expression in the chicken kidneys. Se administration alleviated the aforementioned changes. In addition, toxic effect of Pb on the chicken kidneys was time-dependent. NLRP3 inflammasome, caspase-1, and IL-1β may be sensitive indicators in Pb-induced chicken kidney inflammatory damage. In conclusion, NLRP3 inflammasome took part in antagonistic role of Se against Pb-caused inflammation via changing oxidative stress indicators, cytokines, and inflammation-related genes in the chicken kidneys. [ABSTRACT FROM AUTHOR]

Ammonia (NH3) is a toxic, environmental pollutant, and irritant gas. Previous studies reported the toxic effects of NH3 which led to inflammation in various organs of chicken. However, the exact mechanism of NH3-induced inflammation in chicken lymphoid organs bursa of fabricius (BF) and thymus is still elusive. Thus, this study was designed to investigate NH3-induced inflammation in chicken BF and thymus. Experimental chickens were divided into low (5.0 mg/m3), middle (10.0–15.0 mg/m3), and high (20.0–45.0 mg/m3) NH3-treated groups. To investigate NH3-induced inflammation in chicken's BF and thymus, histological observation, NO content and iNOS activity, inflammatory cytokine contents, and mRNA levels were performed by light microscopy, microplate spectrophotometer, ELISA assay, and qRT-PCR. The finding of the present study showed that NH3 exposure reduced BF and thymus index, increased nitric oxide (NO) content and inducible nitric oxide synthase (iNOS) activity, inflammatory cytokine contents and mRNA levels of nuclear factor-kappa B (NF-κB), cyclooxygenase-2 (Cox-2), tumor necrosis factor alpha (TNF-α), interleukin 6 (IL-6), IL-10, IL-1β, IL-18, toll-like receptor 2A (TLR-2A), and iNOS. Histopathological examination revealed signs of inflammation including increased nuclear debris and vacuoles in the cortex and medulla of thymus and bursal follicles. Conclusively, our findings displayed that NH3 exposure affects the normal function of BF and thymus and led inflammation. The data provided a new ground for NH3-induced toxicity and risk assessment in chicken production. [ABSTRACT FROM AUTHOR]

Ordinary planar waveguide cannot support electromagnetic (EM) wave propagating at frequency below the cut-off frequency of the waveguide, due to the evanescent wave nature of the EM wave in such waveguide. We have found by theoretical analysis that extraordinary EM wave transmission could occur for transverse-electric modes at frequency below the cut-off frequency of the hollow waveguide by inserting different kinds of anisotropic metamaterials (AMMs) in the hollow waveguide. Such transmission of EM energy has no lower cut-off frequency and is due to the conversion of the evanescent wave into propagating mode inside the AMMs, which is quite different from that in the case of waveguide loaded with an isotropic left-handed material slab. We have verified the extraordinary phenomenon by performing circuit analog of the planar waveguide loaded with different kinds of AMMs through realization with transmission line metamaterials. [ABSTRACT FROM AUTHOR]

We analyze the subwavelength imaging using compensated bilayer of anisotropic metamaterials and study the material loss and retardation effect on the image properties. Through rigorous analysis of the electromagnetic wave transmission and numerical calculations of the electromagnetic field distribution, we demonstrate that the anisotropic bilayer lens exhibits a decreased sensitivity to material loss and retardation, therefore has a better image with subwavelength resolution than that of the isotropic perfect lens configuration. We find that this is due to the fact that the inhomogeneous evanescent waves that are responsible for image resolution beyond the diffraction limit have been converted to propagating waves in the anisotropic bilayer, resulting in less sensitive to material loss and retardation. [ABSTRACT FROM AUTHOR]

We have studied the electromagnetic wave propagation in two-dimensional anisotropic metamaterial (AMM) by realizing the AMM through periodic structure composed of anisotropically loaded transmission line (TL) network. The dispersion relation of the TL metamaterial is analyzed by rigorous periodic TL theory, which shows hyperbolic dispersion surface in phase space below certain critical frequency. Utilizing microstrip line technique, we have constructed an interface between isotropic normal medium and a particular type of AMM with properly designed normal TL mesh and the loaded TL network, respectively. The electromagnetic wave propagation in such system has been analyzed with the consideration of circuit losses using microwave circuit simulations. We directly demonstrate interesting phenomena including the total reflection with inversion of the critical angle at small incident angle as well as the oblique total transmission at large incident angle at the interface, which have good agreement with the theoretical prediction. [ABSTRACT FROM AUTHOR]

Cadmium (Cd) is a heavy metal in natural environment and has extreme toxicity. Selenium (Se) has protective effect against heavy metal-induced injury or oxidative stress. Cytochrome P450 (CYP450) enzymes are a family of hemoproteins primarily responsible for detoxification functions. In order to investigate whether CYP450 is related to the damage of livers caused by Cd exposure, we chose forty-eight 28-day-old healthy Hailan cocks for four groups: control group, Se group, Cd group, and Se + Cd group. After 90-day treatment, euthanized for experiment. Based on an established subchronic Cd poisoning model in chicken, this experiment was designed to detect mitochondrial structure, malondialdehyde (MDA), glutathione (GSH), DNA and protein crosslink (DPC) and protein carbonyl (PCO) content, the CYP450 and b5 contents, the aminopyrine-N-demethylase (AND), erythromycin N-demethylase (ERND), aniline 4-hydroxylase (AH) and NADPH-cytochrome C reducatase (CR) activities, and mRNA expression level in the livers. The present results indicated that the MDA content, PCO content, and DPC index in Cd group were higher than those observed in other three groups. Most of the mitochondrial structure is incomplete in Cd group. The contents of CYP450 and b5 were decreased in Cd group. The activities of AND, ERND, AH, and CR got reduced after Cd exposure, as observed in CYP450 gene expression. Our results showed that CYP450 system was involved in the entire process of injury and protection. This research provides a comprehensive evaluation of the oxidative stress effects of Cd related to CYP450 in chicken. [ABSTRACT FROM AUTHOR]

The evolution and driving factors underlying dust activity in central Asia remain controversial, particularly in its effects on downwind regions. We present a Holocene dust storm activity record retrieved from the Tarim Basin (TB) and perform linear and nonlinear analyses on dust records from the TB and the Greenland areas. The results indicate a similar response of dust activities to total solar irradiance in both areas, and an outbreak of dust storms in the TB at ~3.5 kyr BP. We suggest that decreasing temperature in high northern latitudes, aided by solar activity change, reached a critical threshold near ~3.5 kyr BP. The resulting steepening of the meridional temperature gradient would have facilitated strengthening and southward shift of the Northern Hemisphere westerly jet, leading to the outbreak of dust storms through intensification of low level wind intensity and prolonged spring conditions in the Asian interior. Key Points: A possible tipping point of dust activity in central Asia at ~3.5 kyr BP was indicated by intensity and regime changes of dust recordWe identify similar response of dust activities in both central Asia and Greenland areas to solar activity changeInsolation and solar activity change drive dust storm outbreak in Asia by increased wind intensity and prolonged spring conditions [ABSTRACT FROM AUTHOR]

Lead (Pb) is an environmental pollutant and can damage organisms. Selenium (Se) can alleviate Pb poisoning. The present study aimed to investigate the alleviative effect of Se on Pb-induced immune toxicity in chicken hearts. One-hundred-and-eighty Hy-line male chickens were randomly divided into four groups at 7 days of age. The control group was offered a standard commercial diet (SD) and drinking water (DW); the Se group was offered SD supplemented with sodium selenite (SeSD) and DW; the Pb + Se group was offered SeSD and DW supplemented with lead acetate (PbDW); and the Pb group was offered SD and PbDW. Relative mRNA expression of inducible nitric oxide synthase (iNOS), interleukins (IL-2, IL-4, IL-6, IL-12β, IL-17 and IFN-γ), and heat shock proteins (HSP27, HSP40, HSP60, HSP70, and HSP90) were determined by means of quantitative real-time PCR. Relative protein expression of iNOS, HSP60, HSP70, and HSP90 was assessed, as well as nitric oxide (NO) content and iNOS activity in heart tissue. The results indicated a down-regulation of interleukin (IL)-2 and IFN-γ and an up-regulation of NO, iNOS, interleukins (IL-4, IL-6, IL-12β, IL-17), and heat shock proteins (HSP27, HSP40, HSP60, HSP70, and HSP90) in Pb-damaged hearts. Se alleviated all of the above Pb-induced changes. There were time-dependent effects on NO content, iNOS activity, and mRNA levels of iNOS, IL-2, IL-4, IL-6, IL-17, HSP27, HSP40, HSP60, HSP70, and HSP90 after Pb treatment in the chicken hearts. Se alleviated Pb-induced immune toxicity in the chicken hearts. [ABSTRACT FROM AUTHOR]

Se is an important bioelement essential for a healthy immune system. Dietary Se influences both innate and adaptive immune responses. However, the effects of Se deficiency in chicken spleen are still unknown; thus, we designed an experiment to study the role of Se in chicken spleen. A total of 180 one-day-old sea blue white laying hens were randomly allocated into two groups (a control group and a Se-deficient group). The control group was fed a diet supplemented with sodium selenite with a final Se content of 0.15 mg/kg, and the Se-deficient group was fed a Se-deficient diet with a Se content of 0.033 mg/kg. Twenty selenoproteins and ten cytokines were investigated in detail. The expression levels of selenoproteins in spleen were determined via real-time qPCR at 15, 35, and 55 days, and cytokine levels were determined using ELISA at 15, 35, and 55 days. Protein-protein interaction predictions and principal component analysis were performed. We found that the selenoprotein mRNA levels were significantly lower (P < 0.05) in the Se-deficient group compared with the control group. The expression levels of IL-2, IL-1β, IL-6, IFN-α, and IL-17 were significantly lower (P < 0.05), and the levels of IL-8, IL-10, IFN-γ, IFN-β, and TNF-α were significantly higher (P < 0.05) in the Se-deficient group. These selenoproteins were positively correlated with component 1 and component 2 of the PCA, but the relationship between cytokines and principal components in spleens was very complex. The investigation showed that Se deficiency caused a reduction in selenoprotein gene expression and further affected certain cytokines levels. Our results provide some compensatory data about selenoproteins and cytokines in spleens of Se-deficient chickens and provide clues for further research on the relationship between selenoproteins and cytokines. [ABSTRACT FROM AUTHOR]

Lead (Pb) is an environmental pollutant. Selenium (Se) has alleviative effect on Pb poisoning. However, mitigative effect of Se on Pb-induced apoptosis has not been unclear via endoplasmic reticulum (ER) pathway in chicken testes. The aim of this study was to investigate mitigative effect of Se on apoptosis induced by Pb poisoning via ER pathway in chicken testes. Sixty male chickens (7-day-old) were randomly divided into the control group offered drinking water (DW) and basic diet (BD) (0.49 mg/kg Se), the Se group offered DW and BD containing Na2SeO3 (SeBD) (1.00 mg/kg Se), the Pb group offered DW containing (CH3OO)2Pb (PbDW) (350.00 mg/L Pb) and BD, and the Pb + Se group offered PbDW and SeBD; and were fed for 90 days. The following contents were performed as follows: histology; antioxidant indexes (reduced glutathione (GSH), malondialdehyde (MDA), glutathione peroxidase (GPx), glutathione S-transferase (GST), and superoxide dismutase (SOD)); mRNA expressions of ER-related genes (glucose-related protein 78 (GRP78), protein kinase-like ER kinase (PERK), eukaryotic initiation factor 2α (eIF2α), activating transcription factor 4 (ATF4), and enhancer-binding protein homologous protein (CHOP)); and apoptosis-related genes (cysteine-aspartic protease (caspase)-3 and caspase-12) in chicken testes. The results indicated that Pb poisoning caused histological changes; increased MDA content; decreased the content of GSH and the activities of GPx, GST, and SOD; and upregulated mRNA expressions of the above five ER-related genes and two apoptosis-related genes in the chicken testes. Se alleviated Pb-induced oxidative stress, ER stress, and apoptosis via CHOP/caspase-3 signal pathway in the chicken testes. [ABSTRACT FROM AUTHOR]

Lead (Pb) is a toxic heavy metal and can harm organisms by inducing apoptosis. Selenium (Se), an essential trace element for humans and animals, can alleviate heavy metal toxicity. The aim of our study is to investigate alleviative effect of Se on Pb-induced apoptosis via endoplasmic reticulum (ER) stress in chicken kidneys. One hundred and eighty male chickens were randomly divided into four groups at 7 days of age and were fed with commercial diet (containing 0.49 mg/kg Se) and drinking water, Na2SeO3-added commercial diet (containing 1 mg/kg Se) and drinking water, the commercial diet and (CH3OO)2Pb-added drinking water (containing 350 mg/L Pb), and Na2SeO3-added commercial diet (containing 1 mg/kg Se) and (CH3OO)2Pb-added drinking water (containing 350 mg/L Pb), respectively. On the 30th, 60th, and 90th days of the experiment period, 15 chickens in each group were euthanized and the kidneys were collected. Following contents were performed: kidney ultrastructure; nitric oxide (NO) content; inducible nitric oxide synthase (iNOS) activity; relative messenger RNA (mRNA) and protein expression of iNOS, ER-related genes (glucose-regulated protein (GRP)78, GRP94, activating transcription factor (ATF)4, ATF6, and iron-responsive element (IRE)), and apoptosis-related genes (caspase-3 and B cell lymphoma-2 (Bcl-2)); and caspase-12 protein expression. The results indicated that Pb changed kidney ultrastructural structure; decreased Bcl-2 mRNA and protein expression; and increased NO content, iNOS activity, relative mRNA and protein expression of iNOS, ER-related genes, and caspase-3 and caspase-12 protein expression. Se attenuated above changes caused by Pb. Pb had time-dependent manners on NO content, GRP78, GRP94, ATF4, IRE, and caspase-3 mRNA expression. Se attenuated Pb-induced apoptosis via ER stress in the chicken kidneys. [ABSTRACT FROM AUTHOR]

There were many studies about the effect of excess manganese (Mn) on nervous system apoptosis; however, Mn-induced apoptosis in chicken cerebrums and embryonic neurocytes was unclear. The purpose of this study was to investigate the effect of excess Mn on chicken cerebrum and embryonic neurocyte apoptosis. Seven-day-old Hyline male chickens were fed either a commercial diet or three levels of manganese chloride (MnCl)-added commercial diets containing 600-, 900-, and 1800-mg/kg-Mn diet, respectively. On the 30th, 60th, and 90th days, cerebrums were collected. Fertilized Hyline chicken eggs were hatched for 6-8 days and were selected. Embryonic neurocytes with 0, 0.5, 1, 1.5, 2, 2.5, and 3 mM Mn were collected and were cultured for 12, 24, 36, and 48 h, respectively. The following research contents were performed: superoxide dismutase (SOD) and total antioxidant capacity (T-AOC) activities; tumor protein p53 (p53), B cell lymphoma-2 (Bcl-2), B cell lymphoma extra large (Bcl-x), Bcl-2-associated X protein (Bax), Bcl-2 homologous antagonist/killer (Bak), fas, and caspase-3 messenger RNA (mRNA) expression; and morphologic observation. The results indicated that excess Mn inhibited SOD and T-AOC activities; induced p53, Bax, Bak, fas, and caspase-3 mRNA expression; and inhibited Bcl-2 and Bcl-x mRNA expression in chicken cerebrums and embryonic neurocytes. There were dose-dependent manners on all the above factors at all the time points and time-dependent manners on SOD activity of 1800-mg/kg-Mn group, T-AOC activity, and apoptosis-related gene mRNA expression in all the treatment groups in chicken cerebrums. Excess Mn induced chicken cerebrum and embryonic neurocyte apoptosis. [ABSTRACT FROM AUTHOR]

Lead (Pb) is a toxic element and environmental pollutant. Pb toxicity and antagonistic effect of selenium (Se) on Pb have been deeply studied in mammals. The testis is one of the target organs of Pb in birds. The aim of this study was to investigate the mitigating effect of Se on Pb toxicity in chicken testes by determining messenger RNA (mRNA) expressions of 5 heat shock proteins (HSPs) and 25 selenoproteins. Sixty male chickens (7-day-old) were randomly divided into the control group, the Se group, the Pb group, and the Pb + Se group, and were fed for 90 days. The feeding methods of chickens were as follows: The control group was fed drinking water and commercial diet (0.49 mg/kg Se). Lead acetate was added into the drinking water (350 mg/L Pb). Sodium selenite was added into the commercial diet (1 mg/kg Se). Multivariate correlation analysis and principal component analysis (PCA) were used to define the relationships among all the measured factors and the most important parameters that could be used as key factors, respectively. The results indicated that Se decreased the increase of mRNA expressions of all the HSPs and increased the decrease of mRNA expressions of all the selenoproteins induced by Pb in the chicken testes. HSP70 may be a biomarker of Pb poisoning in the chicken testes. Se alleviated Pb-induced toxicity in the chicken testes through regulating mRNA expressions of HSPs and selenoproteins. [ABSTRACT FROM AUTHOR]

The aim of this study was to investigate ameliorative effect of selenium (Se) on lead (Pb)-induced inflammatory damage in chicken testes. One hundred eighty 7-day-old male chickens were randomly assigned into the control group, the Se group, the Pb group, and the Pb/Se group. Lead acetate was added in drinking water (350 mg/L Pb). Sodium selenite was added in the standard commercial diet (1 mg/kg Se). On the 30th, 60th, and 90th days of the experiment, 15 chickens of each group were euthanized. Inductively coupled plasma mass spectrometry, hematoxylin and eosin staining, real-time quantitative PCR, and Western blot were used. The results indicated that excess Pb increased nitric oxide content; inducible nitric oxide synthase (iNOS) activity; nuclear factor-kappa B (NF-κB), tumor necrosis factor-α, cyclooxygenase-2, prostaglandin E synthases, and iNOS mRNA levels in a time-dependent manner; NF-κB, iNOS, heat shock protein (HSP) 60, HSP70, and HSP90 protein levels; and Pb concentration. Excess Pb decreased Se concentration and induced histological changes. Se-alleviated Pb caused all of the above changes. Se improved Pb-caused inflammatory damage by decreasing the expression of inflammatory factors and heat shock proteins in the chicken testes. Our results provided theoretical basis of an alleviative effect of Se on Pb-induced bird testis damage. [ABSTRACT FROM AUTHOR]

We investigated lead (Pb)-induced oxidative stress and immune damage in the chicken bursa of Fabricius (BF) and the ameliorative effect of selenium (Se). Seven-day-old male chickens were randomly divided into four groups and were provided standard diet and drinking water, NaSeO added to the standard diet and drinking water, standard diet and (CHCOO)Pb added to drinking water, and NaSeO added to the standard diet and (CHCOO)Pb added to drinking water for 30, 60, and 90 days. The presence of Pb inhibited total antioxidant capacity (T-AOC), glutathione peroxidase (GPx), glutathione S-transferase (GST), superoxide dismutase (SOD), and catalase (CAT) activities; decreased glutathione (GSH) content; increased malondialdehyde (MDA) and hydrogen peroxide (HO) contents; inhibited interleukin (IL)-2 and interferon-γ (IFN-γ) messenger RNA (mRNA) expression; and increased IL-4, IL-6, IL-10, IL-12β, and IL-17 mRNA expression. The presence of Se relieved all of the above Pb-induced changes. There were close correlations among GSH, CAT, T-AOC, SOD, GPx, MDA, and HO and among IL-2, IL-4, IL-6, IL-12β, IL-17, and IFN-γ. Our data showed that Pb caused oxidative stress and immune damage in the chicken BF. Se alleviated Pb-induced oxidative stress and immune damage in the chicken BF. [ABSTRACT FROM AUTHOR]

Selenoprotein has many functions in chicken, and the expression of selenoproteins is closely associated with the selenium (Se) level. However, little is known about the expression patterns of selenoproteins in chicken immune organs. Here, we investigated the effect of dietary Se deficiency on the expressions of 23 selenoproteins in broiler immune organs. In this study, 150 broilers were randomly divided into two groups (75 chickens per group). The chickens were maintained either on a diet supplemented with Se through the addition of 0.2 mg/kg of Se (C group) via sodium selenite or on a Se-deficient granulated diet (L group) until the broilers exhibited an onset of exudative diathesis (ED). Following euthanasia, the samples from the immune tissues (including the spleen, thymus, and bursa of Fabricius) were quickly collected, and the messenger RNA (mRNA) expression levels of 23 selenoproteins were examined by real-time quantitative PCR and analyzed using principal component analysis. The results showed that Se deficiency decreased the mRNA levels of 23 selenoproteins in the thymus, spleen, and bursa of the Fabricius tissues of broiler chickens. Furthermore, we found that among 23 selenoproteins, the mRNA levels of Dio1 in the thymus, Txnrd2 in the spleen, and Txnrd3 in the bursa of Fabricius decreased significantly (90.9 %, 83.3 %, and 96.8 %, respectively). In addition, the principal component analysis (PCA) results suggested that Se deficiency mainly influenced the expression of antioxidative selenoproteins, especially glutathione peroxidases (Gpxs), thioredoxin reductases (Txnrds), and iodothyronine deiodinases (Dios) in chicken immune organs. The results of this study are valuable for understanding the relevance of selenoprotein activity in vivo. [ABSTRACT FROM AUTHOR]

The aim of this study was to investigate the effect of lead (Pb) poisoning on nitric oxide (NO) content, inducible nitric oxide synthase (iNOS) activity, the messenger RNA (mRNA) levels of inflammatory factors (nuclear factor-kappa B (NF-κB), tumor necrosis factor-α (TNF-α), cyclooxygenase-2 (COX-2), prostaglandin E synthases (PTGEs), and iNOS), heat shock proteins (HSPs) (HSP27, HSP40, HSP60, HSP70, and HSP90), and the antagonistic effect of selenium (Se) on Pb in chicken livers. One hundred eighty 7-day-old male chickens were randomly divided into four groups and were fed commercial diet and drinking water, NaSeO-added commercial diet and drinking water, commercial diet and (CH3OO)Pb-added drinking water, and NaSeO-added commercial diet and (CH3OO)Pb-added drinking water, respectively, for 30, 60, and 90 days. Then, NO content, iNOS activity, and the mRNA levels of NF-κB, TNF-α, COX-2, PTGEs, iNOS, HSP27, HSP40, HSP60, HSP70, and HSP90 were examined in chicken livers. The results showed that Pb poisoning induced NO content, iNOS activity, and mRNA expression of inflammation factors and HSPs in chicken livers. In addition, Se alleviated Pb-induced increase of inflammation factor and HSP expression in chicken livers. [ABSTRACT FROM AUTHOR]

Despite increasing evidence indicating the essential involvement of selenium (Se) in the immune system, the effect of Se deficiency on the regulation of oxidative stress and heat shock proteins (Hsps) in broiler chickens is still unclear. In the present study, we established an exudative diathesis (ED) broiler chicken model caused by Se deficiency. We then analyzed histological observations and detected the expression levels of Hsps and antioxidant indexes in immune tissues. The antioxidant function declined remarkably, and most of the Hsp expression levels increased significantly in the spleen, thymus, and bursa of Fabricius of the broiler chicks with ED (except the messenger RNA (mRNA) levels of Hsp27, Hsp40, and Hsp70, which decreased in thymus tissues from the treatment groups); therefore, constitutive oxidation resistance and higher Hsps in broiler chicks with ED caused defects in immune organ morphology and function, as evidenced by abnormal histological structures: red pulp broadening and lymphocytes in the cortex and medulla of the thymic lobule decreased distinctly and distributed loosely. These results underscore the importance of Se in establishing an immune organ microenvironment conducive to normal function. [ABSTRACT FROM AUTHOR]

Nasal olfactory mucosa mesenchymal stem cells (OM-MSCs) have the ability to promote regeneration in the nervous system in vivo. Moreover, with view to the potential for clinical application, OM-MSCs have the advantage of being easily accessible from patients and transplantable in an autologous manner, thus eliminating immune rejection and contentious ethical issues. So far, most studies have been focused on the role of OM-MSCs in central nervous system replacement. However, the secreted proteomics of OM-MSCs have not been reported yet. Here, proteins secreted by OM-MSCs cultured in serum-free conditions were separated on SDS-PAGE and identified by LC-MS/MS. As a result, a total of 274 secreted proteins were identified. These molecules are known to be important in neurotrophy, angiogenesis, cell growth, differentiation, and apoptosis, and inflammation which were highly correlated with the repair of central nervous system. The proteomic profiling of the OM-MSCs secretome might provide new insights into their nature in the neural recovery. However, proteomic analysis for clinical biomarkers of OM-MSCs needs to be further studied. [ABSTRACT FROM AUTHOR]

Nasal olfactory mucosa mesenchymal stem cells (OM-MSCs) have the ability to promote regeneration in the nervous system in vivo. Moreover, with view to the potential for clinical application, OM-MSCs have the advantage of being easily accessible from patients and transplantable in an autologous manner, thus eliminating immune rejection and contentious ethical issues. So far, most studies have been focused on the role of OM-MSCs in central nervous system replacement. However, the secreted proteomics of OM-MSCs have not been reported yet. Here, proteins secreted by OM-MSCs cultured in serum-free conditions were separated on SDS-PAGE and identified by LC-MS/MS. As a result, a total of 274 secreted proteins were identified. These molecules are known to be important in neurotrophy, angiogenesis, cell growth, differentiation, and apoptosis, and inflammation which were highly correlated with the repair of central nervous system. The proteomic profiling of the OM-MSCs secretome might provide new insights into their nature in the neural recovery. However, proteomic analysis for clinical biomarkers of OM-MSCs needs to be further studied. [ABSTRACT FROM AUTHOR]

Manganese (Mn) pollution can cause tissue and organ dysfunction and structural damage. The toxicity of Mn in poultry was reported, but inflammatory damage that Mn induced in the testicular tissue has not been reported. The aim of this study was to investigate the effect of Mn poisoning on NF-κB/iNOS-COX-2 signaling pathway in chicken testes. One hundred eighty Hyline male chickens at 7 days of age were fed either commercial diet or MnCl-added commercial diet containing 600, 900, and 1800 mg/kg Mn for 30, 60, and 90 days, respectively. The messenger RNA (mRNA) expression of nuclear factor-κB (NF-κB), tumor necrosis factor-α (TNF-α), cyclooxygenase-2 (COX-2), and inducible nitric oxide synthase (iNOS), nitric oxide (NO) content, iNOS activity, and histopathology were examined in chicken testes. The results showed that excess Mn upregulated mRNA expression of NF-κB, COX-2, TNF-α, and iNOS, NO content, and iNOS activity at 60th and 90th day. Mn had a time-dependent effect on NF-κB and TNF-α mRNA expression. Mn had a dose- and time-dependent effect on NO content and iNOS activity. Mn exposure induced chicken testis histological changes in dose- and time-dependent manner. It indicated that Mn exposure resulted in inflammatory injury of chicken testis tissue through NF-κB/iNOS-COX-2 signaling pathway. [ABSTRACT FROM AUTHOR]

The purpose of this study was to investigate the effect of manganese (Mn)-induced cytotoxicity on heat shock proteins in chicken spleen lymphocytes. Lymphocytes were cultured in medium in the absence and presence of MnCl 2 (2 × 10 −4, 4 × 10 −4, 6 × 10 −4, 8 × 10 −4, 10 × 10 −4, and 12 × 10 −4 mmol/L) for 12, 24, 36, and 48 h in vitro. Then, the mRNA levels of HSP27, HSP40, HSP60, HSP70, and HSP90 were examined by real-time quantitative PCR. The results showed that the mRNA levels of HSP27, HSP40, HSP60, HSP70, and HSP90 in all treatment groups at all time points, except mRNA levels of HSP27 at 48 h, had the same tendency. As manganese concentration increased, the mRNA expression of the heat shock proteins first increased and then decreased. In other words, we demonstrated that the mRNA expression of the heat shock proteins was induced at lower concentrations of manganese and was inhibited at higher concentrations. Mn had a dosage-dependent effect on HSP27, HSP40, HSP60, HSP70, and HSP90 mRNA expression in chicken spleen lymphocytes in vitro. [ABSTRACT FROM AUTHOR]

Highlights: [•] Trigger expression of HIF-1α provides profound protection against hostile environments. [•] Over-expression of HIF-1α improve the survival of transplanted NSCs. [•] HIF-1α-expressing stable NSC enhance angiogenesis in the injured site and promote differentiation of neurons. [•] Transplanted HIF-1α expressing NSCs will bring a promising therapy method for the people who afflicted with SCI. [ABSTRACT FROM AUTHOR]