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Selenium nanoparticle (Nano-Se) is a new type of selenium supplement, which can improve the deficiency of traditional selenium supplements and maintain its physiological activity. Due to industrial pollution and irrational use in agriculture, Cu overexposure often occurs in animals and humans. In this study, Nano-Se alleviated CuSO4-induced testicular Cu accumulation, serum testosterone level decrease, testicular structural damage, and decrease in sperm quality. Meanwhile, Nano-Se reduced the ROS content in mice testis and enhanced the activities of T-AOC, GSH, SOD, and CAT compared with CuSO4 group. Furthermore, Nano-Se alleviated CuSO4-induced apoptosis by increasing the protein expression of Cleaved-Caspase-3, Cleaved-Caspase-9, Cleaved-Caspase-12, and Bax/Bcl-2 compared with CuSO4 group. At the same time, Nano-Se reversed CuSO4-induced increase of γ-H2AX protein expression in mice testis. In conclusion, this study confirmed that Nano-Se could alleviate oxidative stress, apoptosis, and DNA damage in the testis of mice with Cu excess, thereby protecting the spermatogenesis disorder induced by Cu. [ABSTRACT FROM AUTHOR]

Inflammation is a complex physiological process that enables the clearance of pathogens and repairing damaged tissues. Elevated serum copper concentration has been reported in cases of inflammation, but the role of copper in inflammatory responses remains unclear. This study used bovine macrophages to establish lipopolysaccharide (LPS)-induced inflammation model. There were five groups in the study: a group treated with LPS (100 ng/ml), a group treated with either copper chelator (tetrathiomolybdate, TTM) (20 μmol) or CuSO4 (25 μmol or 50 μmol) after LPS stimulation, and a control group. Copper concentrations increased in macrophages after the LPS treatment. TTM decreased mRNA expression of pro-inflammatory factors (IL-1β, TNF-α, IL-6, iNOS, and COX-2), whereas copper supplement increased them. Compared to the control group, TLP4 and MyD88 protein levels were increased in the TTM and copper groups. However, TTM treatment decreased p-p65 and increased IкB-α while the copper supplement showed reversed results. In addition, the phagocytosis and migration of bovine macrophages decreased in the TTM treatment group while increased in the copper treatment groups. Results mentioned above indicated that copper could promote the LPS-induced inflammatory response in bovine macrophages, promote pro-inflammatory factors by activating the NF-кB pathway, and increase phagocytosis capacity and migration. Our study provides a possible targeted therapy for bovine inflammation. [ABSTRACT FROM AUTHOR]

Background: The immunomodulatory function of mesenchymal stem cells (MSCs) has been considered to be vital for MSC-based therapies. Many works have been devoted to excavate effective strategies for enhancing the immunomodulation effect of MSCs. Nonetheless, canine MSC-mediated immunomodulation is still poorly understood. Methods and results: The inflammatory microenvironment was simulated through the employment of interferon-γ (IFN-γ) in a culture system. Compared with unstimulated cBMSCs, IFN-γ stimulation increased the mRNA levels of Toll-like receptor 3 (TLR3) and indoleamine 2, 3-dioxygenase 1 (IDO-1), and simultaneously enhanced the secretion of immunosuppressive molecules, including interleukin (IL)-10, hepatocyte growth factor (HGF), and kynurenine in cBMSCs. IFN-γ stimulation significantly enhanced the ability of cBMSCs and their supernatant to suppress the proliferation of murine spleen lymphocytes. Lymphocyte subtyping evaluation revealed that cBMSCs and their supernatant diminished the percentage of CD3+CD4+ and CD3+CD8+ lymphocytes compared with the control group, with a decreasing CD4+/CD8+ ratio. Notably, exposure to IFN-γ decreased the CD4+/CD8+ ratio more effectively than unstimulated cells or supernatant. Additionally, IFN-γ-stimulation increased the mRNA levels of the Th1 cytokines TNF-α, and remarkably decreased the mRNA level of the Th2 cytokine IL-4 and IL-10. Conclusion: Our findings substantiate that IFN-γ stimulation can enhance the immunomodulatory properties of cBMSCs by promoting TLR3-dependent activation of the IDO/kynurenine pathway, increasing the secretion of immunoregulatory molecules and strengthening interactions with T lymphocytes, which may provide a meaningful strategy for the clinical application of cBMSCs in immune-related diseases. [ABSTRACT FROM AUTHOR]

Cadmium (Cd), a heavy metal element, cumulates in the testis and can cause male reproductive toxicity. Although vitamin E (VE) as one of potential antioxidants protects the testis against toxicity of Cd, the underlying mechanism remained uncompleted clear. The aim of this study was to investigate whether the Nrf-2 pathway is involved with the protective effect of VE on testicular damages caused by sub-chronic Cd exposure. Thirty-two SD rats were divided into four groups and orally administrated with VE and/or Cd for 28 consecutive days: control group, VE group (100 mg VE/kg), Cd group (5 mg CdCl2/kg), and VE + Cd group (100 mg VE/kg + 5 mg CdCl2/kg). The results showed that 28-day exposure of Cd caused accumulation of Cd, histopathological lesions, and alternations of sperm parameters (elevated rate of abnormal sperm, decreased count of sperm, declined motility, and viability of sperm). Moreover, the rats exposed to Cd showed significant oxidative stress (increased contents of MDA and decreased levels or activities of T-AOC, GSH, CAT, SOD and GSH-Px) and inhibition of Nrf-2 signaling pathway (downregulation of Nrf-2, HO-1, NQO-1, GCLC, GCLM and GST) of the testes. In contrast, VE treatment significantly reduced the Cd accumulation, alleviated histopathological lesions and dysfunctions, activated Nrf-2 pathway, and attenuated the oxidative stress caused by Cd in the testes of rats. In conclusion, VE, through upregulating Nrf-2 pathway, could protect testis against oxidative damages induced by sub-chronic Cd exposure. [ABSTRACT FROM AUTHOR]

The aim of this study was to investigate the effects of different doses of selenium (Se) on oxidative damage and neurotransmitter-related parameters in arsenic (As)-induced broiler brain tissue damage. Two hundred 1-day-old avian broilers were randomly divided into five groups and fed the following diets: control group (As 0.1 mg/kg + Se 0.2 mg/kg), As group (As 3 mg/kg + Se 0.2 mg/kg), low-Se group (As 3 mg/kg + Se 5 mg/kg), medium-Se group (As 3 mg/kg + Se 10 mg/kg), and high-Se group (As 3 mg/kg + Se 15 mg/kg). Glutathione (GSH), glutathione peroxidase (GSH-PX), nitric oxide (NO), nitric oxide synthase (NOS) activity, glutamate (Glu) concentration, glutamine synthetase (GS) activity, acetylcholinesterase (TchE) activity, and the apoptosis rate of brain cells were measured. The results showed that 3 mg/kg dietary As could induce oxidative damage and neurotransmitter disorder of brain tissue, increase the apoptosis rate of brain cells and cause damage to brain tissue, decrease activities of GSH and GSH-PX, decrease the contents of NO, decrease the activities of iNOS and tNOS, increase contents of Glu, and decrease activities of Gs and TchE. Compared with the As group, the Se addition of the low-Se and medium-Se groups protected against As-induced oxidative damage, neurotransmitter disorders, and the apoptosis rate of brain cells, with the addition of 10 mg/kg Se having the best effect. However, 15 mg/kg Se not only did not produce a protective effect against As damage but actually caused similar or severe damage. [ABSTRACT FROM AUTHOR]

Sichuan, located in the upper reaches of the Yangtze River, is the gathering place of many rivers and plays an important role in sturgeon aquaculture and wild sturgeon protection in China, where it suffered the severe influence of Streptococcus iniae infection in sturgeon. However, the annual thousands of tons of antibiotic usage in Sichuan may accumulate in water and cause obstacles to the prevention of S. iniae infection. In contrast, the regional antibiotic resistance characteristics have been rarely unknown. Seventeen S. iniae strains were collected from the major sturgeon culture areas in Sichuan, and the genotyping and the distribution of antibiotic resistance profiles (ARPs) and genes (ARGs) of S. iniae were established in this study. The results showed that the isolates could be divided into four subtypes by pulsed-field gel electrophoresis analysis. Besides, most isolates showed multiple resistance to the antibiotic such as amikacin, neomycin, enrofloxacin, lincomycin, and sulfamethoxazole. Also, sturgeon-derived S. iniae has a relatively low similarity with other fish-derived S. iniae in the world but high similarity with three animal-derived pathogens from Sichuan in previous studies. Moreover, a total of 37 ARGs were detected positively based on 95 ARGs detection, in which aac(6')-Ib(aka aacA4)-01, aac(6')-Ib(aka aacA4)-02, aadA1, floR, blaTEM, sulA/folP-03, and tetA-02 were most prevalent. Our study indicated that the ARGs of sturgeon-derived S. iniae were significantly enhanced compared with the ATCC29178 strains and have a risk of accessing more ARGs from other bacteria in water in Sichuan. This study claimed that sturgeon has a potential risk in the prevention and control of Streptococcosis in Sichuan, the upper reaches of Yangtze River, based on the antibiotic resistance analysis of S. iniae, and it may also increase the risk of highly resistant S. iniae transmission into the middle and lower reaches. [ABSTRACT FROM AUTHOR]

Cadmium (Cd), a widely distributed heavy metal, is extremely toxic to the kidney. Vitamin E (VE) is an important antioxidant in the body. It is known that VE exerts a protective effect on renal oxidative damage caused by Cd, but the effect and mechanism of VE on apoptosis are not fully understood. Thus, we conducted this study to explore the protective effect of VE on Cd-induced renal apoptosis and to elucidate its potential mechanism. Thirty-two 9-week-old male Sprague-Dawley rats were randomly divided into four groups, namely control, VE (100 mg/kg VE), Cd (5 mg/kg CdCl2), and VE + Cd (100 mg/kg VE + 5 mg/kg CdCl2), and received intragastric administration of Cd and/or VE for 4 weeks. The results showed that Cd exposure significantly reduced the weight of the body and kidney, elevated the accumulation of Cd in the kidney as well as the levels of BUN and Scr in serum, caused renal histological alterations, decreased the GSH and T-AOC contents and antioxidant enzyme (SOD, CAT, GSH-PX) activities, and increased renal MDA content. And the increased number of TUNEL-positive cells by Cd was accompanied by upregulated mRNA and protein expressions of apoptotic regulatory molecules (Bax, Caspase-3, GRP94, GRP78, Caspase-8) and downregulated Bcl-2 expressions. However, the combined treatment of Cd and VE could restore the above parameters to be close to those in the control rats. In conclusion, VE supplement could alleviate Cd-induced rat renal damage and oxidative stress through enhancing the antioxidant defense system and inhibiting apoptosis of renal cells. [ABSTRACT FROM AUTHOR]

The destruction of biological activity such as senescence and apoptosis caused by oxidative stress could play a pivotal role in the poor therapeutic efficiency of bone marrow mesenchymal stem cells (BMSCs) transplantation. Mitoquinone (MitoQ) has a highly effective mitochondrial antioxidant effect, and has been widely used in many oxidative damage models. This study aimed to investigate the protective effect of MitoQ on the oxidative stress-mediated senescence of canine BMSCs and the underlying mechanism. The senescence of BMSCs was determined by senescence-associated β-galactosidase staining and quantitative real-time PCR. The expression of p-Nrf2 protein was detected by Western blotting. The results demonstrated that, as BMSCs were expanded in vitro, the senescent phenotype appeared. And the senescence of BMSCs may be caused by oxidative stress, manifested by increasing the level of ROS and decreasing the activity of antioxidant enzymes. Treatment of MitoQ down-regulated the mRNA levels of senescence-related and apoptosis-related genes, but up-regulated the mRNA levels of proliferation-related genes. Meanwhile, ROS generation and senescent activity were reduced in MitoQ-treated BMSCs. Further mechanism studies showed that MitoQ obviously promoted Nrf2 phosphorylation, and also facilitated the translocation of Nrf2 into the nucleus. Moreover, treatment of MitoQ increased the mRNA levels of downstream antioxidant genes and enhanced the activities of superoxide dismutase, catalase, and glutathione peroxidase. Thus, our study revealed that MitoQ, via the Nrf2/ARE signaling pathway, exerts an antioxidant effect as well as potentially delays OS-mediated senescence during BMSCs that were expanded in vitro, which may serve as a novel strategy to optimize the clinical application of BMSCs. [ABSTRACT FROM AUTHOR]

In 2019, diarrhea cases occurred on cattle farms in Qionglai and Guang'an, Sichuan Province. Two out of 20 (10%) serum and nasal swab samples were positive when tested using a bovine viral diarrhea virus (BVDV) antigen-capture ELISA kit. Two non-cytopathic strains of BVDV were isolated and named QL1903 and GA190608, respectively. The nucleotide sequences of the genomes of the two isolates were 89.52% identical. Phylogenetic analysis based on the 5'-UTR sequence revealed that the BVDV isolate QL1903 belonged to BVDV subtype 1b, whereas isolate GA190608 clustered with strains HN1814, EN-19, and BJ09_26 in a separate branch, which has tentatively been classified as a new genetic subtype, "1v". [ABSTRACT FROM AUTHOR]

The aim of the present study was to investigate the abilities of selenium to counteract the toxic damage of arsenic (As). Two hundred 1-day-old healthy male broilers were randomly divided into five groups and fed the following diets: control group (0.1 mg/kg As + 0.2 mg/kg Se), As group (3 mg/kg As + 0.2 mg/kg Se), As + Se group I (3 mg/kg As + 5 mg/kg Se), As + Se group II (3 mg/kg As + 10 mg/kg Se), and As + Se group III (3 mg/kg As + 15 mg/kg Se), respectively. The relative weight of the liver, hepatic protein content, GSH-Px levels, SOD activities, NO contents, iNOS and tNOS activities, and increased malondialdehyde contents, ALT and AST activities, and the apoptotic hepatocytes were analyzed. Adding 3 mg/kg arsenic to the diet caused the growth and development of chicken liver to be blocked, resulting in decrease of protein contents in liver tissue, decrease of SOD and GSH-Px activities, increase of MDA contents, decrease of NO contents, decrease of iNOS and TNOs activities, increase of ALT and AST activities, increase of apoptosis rates of liver cells. Compared to the 3-mg/kg arsenic group, adding 5 mg/kg and 10 mg/kg selenium, respectively, could repair the liver growth retardation and steatosis caused by arsenic, increase the protein contents in liver tissue, increase the activities of SOD and GSH-Px, reduce the contents of MDA, increase the contents of NO, enhance the activities of iNOS and TNOs, reduce the activities of ALT and AST, and reduce the rates of apoptosis of liver cells, in which the best effects are to add 10 mg/kg selenium. While 15 mg/kg of sodium selenite may induce progression of As-induced hepatic lesions, the results indicated that 5 and 10 mg/kg of sodium selenite supplied in the diet, through mechanisms of oxidative stress and apoptosis regulation, may ameliorate As-induced hepatic lesions in a dose-dependent manner. [ABSTRACT FROM AUTHOR]

Nickel (Ni) is a widely distributed metal in the environment and an important pollutant due to its widespread industrial applications. Ni has various toxicity in humans and experimental animals, including carcinogenicity. However, the carcinogenic effects of Ni remain troublesome. Cell cycle dysregulation may be an important carcinogenic mechanism and is also a potential molecular mechanism for Ni complexes anti-cancerous effects. Therefore, we conducted a literature review to summarize the effects of Ni on cell cycle. Up to now, there were three different reports on Ni-induced cell cycle arrest: (i) Ni can induce cell cycle arrest in G0/G1 phase, phosphorylation and degradation of IkappaB kinase-alpha (IKKα)–dependent cyclin D1 and phosphoinositide-3-kinase (PI3K)/serine-threonine kinase (Akt) pathway–mediated down-regulation of expressions of cyclin-dependent kinases 4 (CDK4) play important role in it; (ii) Ni can induce cell cycle arrest in S phase, but the molecular mechanism is not known; (iii) G2/M phase is the target of Ni toxicity, and Ni compounds cause G2/M cell cycle phase arrest by reducing cyclinB1/Cdc2 interaction through the activation of the ataxia telangiectasia mutated (ATM)-p53-p21 and ATM-checkpoint kinase inhibitor 1 (Chk1)/Chk2-cell division cycle 25 (Cdc25) pathways. Revealing the mechanisms of cell cycle dysregulation associated with Ni exposure may help in the prevention and treatment of Ni-related carcinogenicity and toxicology. [ABSTRACT FROM AUTHOR]

Cladosporium cladosporioides causes asthma and superficial and deep infections, mostly in immunodeficient individuals and animals. This study aimed to investigate whether C. cladosporioides spores can enter the lungs through pulmonary circulation and influence pulmonary immune response. We intravenously injected mice with C. cladosporioides spore suspension and conducted several assays on the lungs. Pulmonary hemorrhage symptoms and congestion were most severe on days 1, 2, and 3 post-inoculation (PI). Extensive inflammatory cell infiltration occurred throughout the period of infection. More spores and hyphae colonizing the lungs were detected on days 1, 2, and 3 PI, and fewer spores and hyphae were observed within 21 d of infection. Numerous macrophages, dendritic cells, and neutrophils were observed on day 5 PI, along with upregulation of CD54, an intercellular adhesion molecule. Th1 and Th2 cells increased after infection; specifically, Th2 cells increased considerably on day 5 PI. These results suggest that days 2 and 5 PI represent the inflammatory peak in the lungs and that the Th2 and Th1 signaling pathways are potentially involved in pulmonary immune responses. In conclusion, the further adaptive immune responses played important roles in establishing effective pulmonary immunity against C. cladosporioides systemic infections based on innate immune responses. [ABSTRACT FROM AUTHOR]

Splenic immune function was enhanced in diet-induced-obese (DIO) mice caused by Escherichia coli. The changes in spleen function on apoptosis were still unknown. Two hundred mice in groups Lean-E. coli and DIO-E. coli were intranasal instillation of E. coli. And another two hundred mice in groups Lean-PBS and DIO-PBS were given phosphate-buffered saline (PBS). Subsequently, spleen histology was analyzed. Then the rates of spleen cell (SC) apoptosis, and expression of the genes and proteins of Bcl-2, Bax, caspase-3 and caspase-9 were quantified in each group at 0 h (uninfected), 12 h, 24 h, and 72 h postinfection. The SC apoptosis rates of the DIO-E. coli groups were lower than those of the DIO-PBS groups at 12, 24 and 72 h (p < 0.05). Anti-apoptotic Bcl-2 expression gene and protein of the DIO-E. coli groups were higher than those of the DIO-PBS groups (p < 0.05). Gene expressions of pro-apoptotic Bax, caspase-3 and caspase-9 of the DIO-E. coli groups were lower than those of DIO-PBS groups at 12, 24 and 72 h (p < 0.05). The SC apoptosis rates of the Lean-E. coli groups were higher than those of the Lean- PBS groups at 12 h and 24 h (p < 0.05). Interestingly, the SC apoptosis rates in the DIO-E. coli groups were lower than those of the Lean-E. coli groups at 12 h (p < 0.05). In conclusion, our results suggested that the DIO mice presented stronger anti-apoptotic abilities than Lean mice in non-fatal acute pneumonia induced by E. coli infection, which is more conducive to protecting the spleen and improving the immune defense ability of the body. [ABSTRACT FROM AUTHOR]

Animal feed is prone to becoming infected with molds during production and storage, resulting in secondary metabolite mycotoxins, such as aflatoxin B1 (AFB1), T-2 toxins, deoxynivalenol (DON), and ochratoxin A (OTA), which are harmful to humans and animals. Selenium is an essential trace element for humans and animals, and it is also an effective antioxidant. Many studies have shown that selenium can reduce the damage caused by mycotoxins in animals. This article reviews the current literature on the antagonistic effects of selenium on AFB1, T-2, DON, and OTA toxicity. [ABSTRACT FROM AUTHOR]

This research was designed to explore the protective effects of sodium selenite on G0/G1 phase arrest induced by AFB1 in thymocytes of broilers. Two hundred eighty-eight Cobb broilers were divided into control group, + Se group (0.4 mg/kg Se), AFB1 group (0.6 mg/kg AFB1), and AFB1 + Se group (0.6 mg/kg AFB1 + 0.4 mg/kg Se). The results revealed that 0.4 mg/kg Se supplement in diets could improve the AFB1-induced histological lesions in the thymus consisting of the more vacuoles and nuclear debris in thymic cortical area. The results of flow cytometric detect showed that 0.4 mg/kg Se relieved the G0/G1 phase arrest caused by AFB1 in thymocytes. The results of transcription levels of ATM, p53, p21, p27, p15, p16, CyclinD1, CyclinE, Cdk6, Cdk2, and PCNA genes by qRT-PC, and protein expression level of PCNA by immunohistochemistry demonstrated that 0.4 mg/kg Se could reduce the adverse effects of AFB1 on these parameters. In conclusion, Se could relieve AFB1-induced G0/G1 phase arrest by p15 (or p16)-CyclinD1/Cdk6, ATM-p53-p21-CyclinE/Cdk2, p27-CyclinE/Cdk2 pathways. [ABSTRACT FROM AUTHOR]

At present, no reports are focused on fluoride-induced hepatic inflammatory responses in human beings and animals. This study aimed to investigate the mRNA and protein levels of inflammatory cytokines and signaling molecules for evaluating the effect of different doses (0, 12, 24, and 48 mg/kg) of sodium fluoride (NaF) on inflammatory reaction in the mouse liver by using methods of experimental pathology, quantitative real-time polymerase chain reaction (qRT-PCR), and western blot analysis. We found that NaF in excess of 12 mg/kg caused the hepatic inflammatory responses, and the results showed that NaF activated the mitogen-activated protein kinases (MAPKs) signaling pathway by markedly increasing (p < 0.01 or p < 0.05) mRNA and protein levels of apoptosis signal-regulating kinase 1 (ASK1), mitogen-activated protein kinase kinases 1/2 (MEK1/2), extracellular signal-regulated protein kinases 1/2 (Erk1/2), mitogen-activated protein kinase kinases 4/7 (MEK4/7), c-Jun N-terminal kinase (JNK), p38 mitogen-activated protein kinase (p38) and mitogen-activated protein kinase kinases 3/6 (MEK3/6), and the nuclear factor-kappa B (NF-κB) signaling pathway by increasing (p < 0.01 or p < 0.05) the production of NF-κB and inhibitor of nuclear factor kappa-B kinase subunit beta (IKK-β) and reducing (p < 0.01 or p < 0.05) the production of the inhibitory kappa B (IκB). Thus, NaF that caused the hepatic inflammatory responses was characterized by increasing (p < 0.01 or p < 0.05) the production of pro-inflammatory mediators such as interleukin-1β (IL-1β), interleukin-6 (IL-6), interleukin-8 (IL-8), monocyte chemotactic protein 1 (MCP-1), and cyclooxygenase-2 (COX-2) via the activation of MAPKs and NF-κB pathways, and by significantly inhibiting (p < 0.01 or p < 0.05) the production of anti-inflammatory mediators including interleukin-4 (IL-4) and transforming growth factor beta (TGF-β). [ABSTRACT FROM AUTHOR]

Cecal tonsil is the largest peripheral lymphoid organ of the gut-associated lymphoid tissue executing immune function. To evaluate the protective effect of selenium (Se) on the cecal tonsil of chicken exposed to aflatoxin B1 (AFB1), 144 1-day-old healthy Cobb chickens were randomly divided into four groups, and fed with basal diet (control group), 0.6 mg/kg AFB1 (AFB1 group), 0.4 mg/kg Se supplement (+Se group), and 0.6 mg/kg AFB1 + 0.4 mg/kg Se supplement (AFB1 + Se group) for 21 days, respectively. The results showed that AFB1 significantly decreased the percentages of CD3+, CD3+CD4+, CD3+CD8+ T cells, and the CD4+/CD8+ ratio, and suppressed the expressions of IL-2, IL-4, TNF-α, and IFN-γ mRNA in the cecal tonsil. However, Selenium (Se) supplied in the diets restored the percentages of T cell subsets, the CD4+/CD8+ ratio, and mRNA expressions of cytokines in the AFB1 group to be close to those in the control group, and did not exhibit obvious toxicity to the cecal tonsil. These results indicated that Se exerted protective effect against AFB1 on the functions of cecal tonsil, and also partially uncovered a new role of Se that could protect cecal tonsil of chickens from immunotoxicity of AFB1. [ABSTRACT FROM AUTHOR]

This document is a retraction note from the journal Scientific Reports. The article titled "Effect of intranasal instillation of Escherichia coli on apoptosis of spleen cells in diet-induced-obese mice" has been retracted at the request of the corresponding authors. Concerns were raised about the images presented in Figure 3, and the authors were unable to provide the raw data upon request. As a result, the editors no longer have confidence in the data presented in the article. All authors agree with the retraction. [Extracted from the article]

Aflatoxin B1 (AFB1) can cause hepatotoxicity, genotoxicity, and immunosuppressive effects for a variety of organisms. Selenium (Se), as an essential nutrient element, plays important protective effects against cell apoptosis induced by AFB1. This research aimed to reveal the ameliorative effects of selenium on AFB1-induced excess apoptosis in chicken splenocytes through death receptor and endoplasmic reticulum pathways in vivo. Two hundred sixteen neonatal chickens, randomized into four treatments, were fed with basal diet (control treatment), 0.4 mg/kg Se supplement (+Se treatment), 0.6 mg/kg AFB1 (AFB1 treatment), and 0.6 mg/kg AFB1 + 0.4 mg/kg Se (AFB1 + Se treatment) during 21 days of experiment, respectively. Compared with the AFB1 treatment, the levels of splenocyte apoptosis in the AFB1 + Se treatment were obviously dropped by flow cytometry and TUNEL assays although they were still significantly higher than those in the control or + Se treatments. Furthermore, the mRNA expressions of CASP-3, CASP-8 and CASP-10, GRP78, GRP94, TNF-α, TNF-R1, FAS, and FASL of splenocytes in the AFB1 + Se treatment by qRT-PCR assay were significantly decreased compared with the AFB1 treatment. These results indicate that Se could partially ameliorate the AFB1-caused excessive apoptosis of chicken splenocytes through downregulation of endoplasmic reticulum and death receptor pathway molecules. This research may rich the knowledge of the detoxification mechanism of Se on AFB1-induced apoptosis. [ABSTRACT FROM AUTHOR]

Fluorine or fluoride can have toxic effects on bone tissue and soft tissue at high concentrations. These negative effects include but not limited to cytotoxicity, immunotoxicity, blood toxicity, and oxidative damage. Apoptosis plays an important role in fluoride-induced toxicity of kidney, liver, spleen, thymus, bursa of Fabricius, cecal tonsil, and cultured cells. Here, apoptosis activated by high level of fluoride has been systematically reviewed, focusing on three pathways: mitochondrion-mediated, endoplasmic reticulum (ER) stress-mediated, and death receptor-mediated pathways. However, very limited reports are focused on the death receptor-mediated apoptosis pathways in the fluoride-induced apoptosis. Therefore, understanding and discovery of more pathways and molecular mechanisms of fluoride-induced apoptosis may contribute to designing measures for preventing fluoride toxicity. [ABSTRACT FROM AUTHOR]

Aflatoxin B1 (AFB1) is a naturally occurring secondary metabolites of Aspergillus flavus and Aspergillus parasiticus, and is the most toxic form of aflatoxins. Selenium (Se) with antioxidant and detoxification functions is one of the essential trace elements for human beings and animals. This study aims to evaluate the protective effects of Se on AFB1-induced tissue damage and cell cycle arrest in bursa of Fabricius (BF) of chickens. The results showed that a dietary supplement of 0.4 mg·kg−1 Se alleviated the histological lesions induced by AFB1, as demonstrated by decreasing vacuoles and nuclear debris, and relieving oxidative stress. Furthermore, flow cytometry studies showed that a Se supplement protected AFB1-induced G2M phase arrest at 7 days and G0G1 phase arrest at 14 and 21 days. Moreover, the mRNA expression results of ATM, Chk2, p53, p21, cdc25, PCNA, cyclin D1, cyclin E1, cyclin B3, CDK6, CDK2, and cdc2 indicated that Se supplement could restore these parameters to be close to those in the control group. It is concluded that a dietary supplement of 0.4 mg kg−1 Se could diminish AFB1-induced immune toxicity in chicken’s BF by alleviating oxidative damage and cell cycle arrest through an ATM-Chk2-cdc25 route and the ATM-Chk2-p21 pathway. [ABSTRACT FROM AUTHOR]

Deoxynivalenol (DON) is a mycotoxin that causes immunosuppression, especially in swine. Selenium (Se) is essential for proper functioning of the immune system in animals. However, little is known about the effects of DON and Se on cytokine or immunoglobulin production in piglets. Here, we addressed this gap by examining piglet splenic lymphocyte responses in vitro. Cells were stimulated with concanavalin A, a T cell stimulatory lectin, in the absence or presence of DON (0.1, 0.2, 0.4, and 0.8 μg/mL), Se (Na2SeO3, 2 μM), or combinations of Se 2 μM and DON 0.1-0.8 μg/mL for 12, 24, or 48 h. At each time point, supernatants and cells were collected and the expression of cytokine and immunoglobulin protein and mRNA was examined. Compared with control and Se-alone treatments, DON exposure significantly and dose dependently decreased the expression levels of IL-2, IL-4, IL-6, IL-10, IFN-γ, IgG, and IgM mRNA and protein. By contrast, co-treatment with DON + Se significantly increased the mRNA and protein levels of all factors examined, except IL-4 and IL-6, compared with DON treatment alone. The results of this investigation demonstrate that Se has the potential to counteract DON-induced immunosuppression in piglets and is a promising treatment for DON-mediated toxicity. [ABSTRACT FROM AUTHOR]

Aflatoxin B (AFB) is the most toxic among the mycotoxins and causes detrimental health effects on human and animals. Selenium (Se) plays an important role in chemopreventive, antioxidant, anticarcinogen, and detoxification and involved in cell cycle regulation. The aim of this study was to explore the molecular mechanisms of selenium involved in inhibition of G/M cell cycle arrest of broiler's jejunum. A total of 240 one-day-old healthy Cobb broilers were randomly divided into four groups and fed with basal diet (control group), 0.6 mg/kg AFB (AFB group), 0.4 mg/kg Se (+Se group), and 0.6 mg/kg AFB + 0.4 mg/kg Se (AFB + Se group) for 21 days, respectively. The histological observation and morphological analysis revealed that 0.4 mg/kg Se prevented the AFB-associated lesions of jejunum including the shedding of the apical region of villi, the decreased villus height, and villus height/crypt ratio. The cell cycle analysis by flow cytometry showed that 0.4 mg/kg Se ameliorated the AFB-induced G/M phase arrest in jejunal cells. Moreover, the expressions of ATM, Chk2, p53, Mdm2, p21, PCNA, Cdc25, cyclin B, and Cdc2 analyzed by immunohistochemistry and qRT-PCR demonstrated that 0.4 mg/kg Se restored these parameters to be close to those in the control group. In conclusion, Se promoted cell cycle recovery from the AFB-induced G/M phase arrest by the molecular regulation of ATM pathway in the jejunum of broilers. The outcomes from the present study may lead to a better understanding of the nature of selenium's essentiality and its protective roles against AFB. [ABSTRACT FROM AUTHOR]

The present research was conducted to study the morphology, histology and enzymatic activities of the digestive tract of Gymnocypris eckloni by light and transmission electron microscopes as well as by enzyme assays. The digestive tract of G. eckloni consisted of the oropharyngeal cavity, oesophagus and intestine. The wall of the digestive tract was composed of mucosa, submucosa, muscularis and serosa but lacked muscularis mucosa and glands. The stratified epithelium of the oropharyngeal cavity and oesophagus contained numerous mucous cells. Taste buds were found in the epithelium of the oropharyngeal cavity. A large number of isolated longitudinal striated muscular bundles were present in the submucosa of the oesophagus. The mucosal epithelium of the intestine was composed of simple columnar cells containing absorptive, goblet and endocrine cells. Numerous mitochondria and endoplasmic reticulum were observed in the absorptive cells, especially in the anterior intestine. From the anterior to the posterior intestine, the number and length of mucosal folds and microvilli decreased, but the number of goblet cells increased. The intestinal coefficient was 2.38. Maximum trypsin activity was measured in the anterior intestine, while the lowest lipase and amylase activities were tested in the middle and posterior intestines, respectively. The results provided experimental evidence for evaluating physiological condition of G. eckloni digestive tract, which will be useful for improving current rearing practices and diagnoses of digestive tract diseases. [ABSTRACT FROM AUTHOR]

This study investigated the effects of dietary high fluorine on ileal and cecal microbiota in broiler chickens. Two hundred eighty 1-day-old broiler chickens were randomly assigned to four groups and raised for 42 days. The control group was fed a corn-soybean basal diet (fluorine 22.6 mg/kg). The other three groups were fed the same basal diet, but supplemented with 400, 800, and 1200 mg/kg fluorine (high fluorine groups I, II, and III), administered in the form of sodium fluoride. The microbiota of ileal and cecal digesta was assessed with plate counts and polymerase chain reaction-based denaturing gradient gel electrophoresis (PCR-DGGE). It was found that, compared with those in the control group, the counts of Lactobacillus spp . and Bifidobacterium spp . were markedly decreased ( P < 0.01 or P < 0.05), whereas the counts of Escherichia coli and Enterococcus spp . were significantly increased ( P < 0.01 or P < 0.05) in the high fluorine groups II and III. PCR-DGGE analysis showed that the number of DGGE bands, similarity, and Shannon index of ileal and cecal bacteria were markedly reduced in the high fluorine groups II and III from 21 to 42 days. Sequencing analysis revealed that the composition of the intestinal microbiota was altered in the high fluorine groups. In conclusion, dietary fluorine in the range of 800-1200 mg/kg obviously altered the bacterial counts, and the diversity and composition of intestinal microbiota in broiler chickens, a finding which implies that dietary high fluorine can disrupt the natural balance and structure of the intestinal microbiota. [ABSTRACT FROM AUTHOR]

The purpose of this study was to investigate the histopathological lesions, oxidative damage, changes of immunoglobulin G (IgG), immunoglobulin M (IgM), and immunoglobulin A (IgA) contents in the bursa of Fabricius and serum immunoglobulins (IgG, IgM, IgA) induced by dietary nickel chloride (NiCl). Two hundred and eighty-one-day-old broilers were randomly divided into four groups and fed on a control diet and three experimental diets supplemented with 300, 600, and 900 mg/kg of NiCl for 42 days. Lesions were observed in the NiCl-treated groups. Histopathologically, lymphocytes were decreased in lymphoid follicles with thinner cortices and wider medullae. Concurrently, the activities of superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GSH-Px), and the ability to inhibit hydroxyl radical and glutathione (GSH) contents were significantly ( p < 0.05 or p < 0.01) decreased, while malondialdehyde (MDA) contents were increased in the NiCl-treated groups. The serum IgG, IgM, and bursa IgG and IgM contents were significantly ( p < 0.05 or p < 0.01) lower in the NiCl-treated groups than those in the control group. The above-mentioned results show that dietary NiCl in excess of 300 mg/kg can cause histopathological lesions via oxidative damage, which finally impairs the function of the bursa of Fabricius and reduces IgG and IgM contents of the serum and the bursa of Fabricius. The study is aimed to provide helpful materials for studies on Ni- or Ni compounds-induced B cell toxicity in both human and other animals in the future. [ABSTRACT FROM AUTHOR]

The purpose of this study was to define the inhibitive effects of dietary nickel chloride (NiCl) on thymocytes in broilers fed on diets supplemented with 0, 300, 600, and 900 mg/kg of NiCl for 42 days. We examined the changes of cell cycle phase, percentages of apoptotic cells, T cell subsets, cytokines, and mRNA expression of apoptotic proteins (bcl-2, bax, and caspase-3) in thymocytes by flow cytometry and quantitative real-time polymerase chain reaction (qRT-PCR). In the NiCl-treated broilers, the percentages of thymocytes in G/G phase were increased, whereas thymocytes in the S phase and the proliferation index were decreased. The percentages of apoptotic thymocytes were increased. Also, the mRNA expression levels of bax and caspase-3 were increased, and mRNA expression levels of bcl-2 were decreased. The percentages of CD3, CD3CD4, and CD3CD8 T lymphocytes in the thymus and peripheral blood were diminished. Concurrently, thymic cytokine (interleukin-1 beta (IL-1β), interleukin-2 (IL-2), interleukin-10 (IL-10), interleukin-12 p35 subunit (IL-12p35), interleukin-12 p40 subunit (IL-12p40), interleukin-21 (IL-21), interferon gamma (IFN-γ), tumor necrosis factor alpha (TNF-α), thymosin β4, thymosin β10, and thymosin β15) mRNA expression levels were decreased. The abovementioned results showed that dietary NiCl in excess of 300 mg/kg inhibited thymocyte growth by arresting cell cycle, increasing apoptosis percentage, altering apoptotic protein mRNA expression levels, and downregulating cytokine expression levels. [ABSTRACT FROM AUTHOR]

While taxol yields of fungi from non-animal sources are still low, whether Pestalotiopsis hainanensis isolated from the scurf of a dermatitic giant panda, Ailuropoda melanoleuca, provides a greater taxol yield remains unknown. The objective of the study was to determine the corresponding taxol yield. The structure of the taxol produced by the fungus was evaluated by thin layer chromatography (TLC), ultraviolet (UV) spectroscopy, high-performance liquid chromatography (HPLC), H and C nuclear magnetic resonance spectroscopy (H-NMR and C-NMR), and time-of-flight mass spectrometry (TOF-MS), with standard taxol as a control. The results demonstrated that the P. hainanensis fungus produced taxol, which had the same structure as the standard taxol and yield of 1,466.87 μg/L. This fungal taxol yield from the dermatitic giant panda was significantly greater than those of fungus from non-animal sources. The taxol-producing fungus may be a potential candidate for the production of taxol on an industrial scale. [ABSTRACT FROM AUTHOR]

The kidney serves as a major organ of nickel (Ni) excretion and is a target organ for acute Ni toxicity due to Ni accumulation. There are no studies on the Ni or Ni compound-regulated antioxidant enzyme mRNA expression in animals and human beings at present. This study was conducted to investigate the pathway of nickel chloride (NiCl)-caused renal oxidative damage by the methods of biochemistry, quantitative real-time polymerase chain reaction, and enzyme-linked immunosorbent assay. Two hundred and eighty one-day-old broilers were randomly divided into four groups and fed on a control diet and three experimental diets supplemented with 300, 600, and 900 mg/kg of NiCl for 42 days. Dietary NiCl elevated the malondialdehyde (MDA), nitric oxide (NO), 8-hydroxy-2'-deoxyguanosine (8-OHdG) contents, and reduced the ability to inhibit hydroxy radical in the NiCl-treated groups. Also, the renal inducible nitric oxide synthase (iNOS) activity and mRNA expression levels were increased. The total antioxidant (T-AOC) and activities of antioxidant enzymes including copper zinc superoxide dismutase (CuZn-SOD), manganese superoxide dismutase (Mn-SOD), catalase (CAT), glutathione peroxidase (GSH-Px), glutathione reductase (GR), and glutathione- s-transferase (GST) were decreased, and the glutathione (GSH) contents as well were decreased in the kidney. Concurrently, the renal CuZn-SOD, Mn-SOD, CAT, GSH-Px, GST, and GR mRNA expression levels were decreased. The above-mentioned results showed that dietary NiCl in excess of 300 mg/kg caused renal oxidative damage by reducing mRNA expression levels and activities of antioxidant enzymes, and then enhancing free radicals generation, lipid peroxidation, and DNA oxidation. [ABSTRACT FROM AUTHOR]

This study describes the screening of soil bacteria for their capability to degrade zearalenone (ZEN), employing an enrichment technique in which ZEN is used as the sole carbon source. Two isolates that were able to degrade ZEN belonged to the genus Pseudomonas according to biochemical characterization and 16S rRNA gene sequence and were named as Pseudomonas alcaliphila TH-C1 and Pseudomonas plecoglossicida TH-L1, respectively. The results showed that the degradation rates of P. alcaliphila TH-C1 and P. plecoglossicida TH-L1 for ZEN (2 μg/ml) were 68 ± 0.85 % and 57 ± 0.73 %, when incubated for 72 h at 30 °C in a rotary shaker (160 rpm) and detected by high-performance liquid chromatograms (HPLC). These results suggest that the two Pseudomonas strains are new bacterial resource for degrading ZEN and can provide a new approach for the detoxification of ZEN. [ABSTRACT FROM AUTHOR]

This study was conducted to investigate the immune adherence function of erythrocytes and erythrocyte induced by dietary nickel chloride (NiCl) in broilers fed on a control diet and three experimental diets supplemented with 300, 600, and 900 mg/kg NiCl for 42 days. Blood samples were collected from five broilers in each group at 14, 28, and 42 days of age. Changes of erythrocyte parameters showed that total erythrocyte count (TEC), hemoglobin (Hb) contents, and packed cell volume (PCV) were significantly lower ( p < 0.05 or p < 0.01) and erythrocyte osmotic fragility (EOF) was higher ( p < 0.05 or p < 0.01) in the 600 and 900 mg/kg groups at 28 and 42 days of age than those in the control group, and the sodium-potassium adenosine triphosphatase (Na/K-ATPase) and calcium adenosine triphosphatase (Ca-ATPase) activities were significantly decreased ( p < 0.05 or p < 0.01) in the NiCl-treated groups. The results of erythrocyte immune adherence function indicated that erythrocyte C receptor rosette rate (E-CRR) was significantly decreased ( p < 0.05 or p < 0.01) in the 600 and 900 mg/kg groups and in the 300 mg/kg group at 42 days of age, whereas the erythrocyte immune complex rosette rate (E-ICRR) was markedly increased ( p < 0.05 or p < 0.01) in the 300, 600, and 900 mg/kg groups at 28 and 42 days of age. It was concluded that dietary NiCl in excess of 300 mg/kg caused anemia and impaired the erythrocytic integrity, erythrocytic ability to transport oxygen, and erythrocyte immune adherence function in broilers. Impairment of the erythrocytes and erythrocyte immune adherence function was one of main effect mechanisms of NiCl on the blood function. [ABSTRACT FROM AUTHOR]

The aim of this study was to investigate the effects of aflatoxin B (AFB) exposure and sodium selenite supplementation on the histology, cell proliferation and cell cycle of jejunum in broilers. A total of 240 1-day-old male AA broilers were divided into four groups of 60 each, fed with basal diet (control group), 0.3 mg/kg AFB (AFB group), 0.4 mg/kg supplement Se (Se group), and 0.3 mg/kg AFB + 0.4 mg/kg supplement Se (AFB + Se group) for 21 days, respectively. Compared with the control group, decreased jejunal villus height, villus height/crypt ratio, and proliferation cell nuclear antigen (PCNA)-positive cells, and G/M phase arrest and shedded epithelial cells on the tip of jejunal villus were observed in AFB groups at 7 and 14 days of age. However, the villus/crypt ratio, PCNA-positive cells and cell percentage of G/G, S, and G/M phases had no significant differences between AFB group and control group at 21 days. Simultaneous supplementation with sodium selenite restored these parameters to be close to those in control group. In conclusion, 0.3 mg/kg AFB in the diet inhibits the development of broiler's jejunum by reducing cellular proliferation and inducing G/M arrest during only the first 2 weeks after hatching. Supplementation of dietary sodium selenite at the concentration of 0.4 mg/kg Se had protective action against these toxic effects of AFB. [ABSTRACT FROM AUTHOR]

This study was aimed to assess the protective effect of sodium selenite on the ileum mucosal immunologic injury induced by AFB. One hundred eighty-one-day-old healthy male Avian broilers were divided into four groups of three replicates and 15 birds per replicate and fed with basal diet (control group), 0.3 mg/kg AFB (AFB group), 0.4 mg/kg Se (+Se group), and 0.3 mg/kg AFB + 0.4 mg/kg Se (AFB + Se group) respectively. The numbers of IgA cells of ileum were determined by immunohistochemistry as well as the contents of sIgA, IgA, IgG, and IgM in the mucosa of ileum by ELISA. Compared with those in the control group, the numbers of IgA cells as well as the sIgA, IgA, IgG, and IgM contents were decreased in the AFB group. However, compared with those in the AFB group, the numbers of IgA cells as well as the sIgA, IgA, IgG, and IgM contents were increased in the AFB + Se group, and these data had no difference between AFB + Se group and control group. It was concluded that 0.3 mg/kg AFB could reduce the humoral immune function of the ileum mucosa, but 0.4 mg/kg supplemented dietary selenium could protect the mucosal humoral immune function from AFB-induced impairment. [ABSTRACT FROM AUTHOR]

This study was designed to evaluate the effects of dietary nickel chloride (NiCl) on the splenic immunity in broilers by observing changes of cytokine mRNA expression and protein levels, immunoglobulin (IgA, IgG, and IgM) contents, and IgA B cell and T-cell numbers using the methods of qRT-PCR, flow cytometry (FCM), and ELISA. A total of 240 1-day-old avian broilers were equally allocated into four groups and fed on a corn-soybean basal diet as the control diet or the same diet supplemented with 300, 600, and 900 mg/kg NiCl for 42 days. The mRNA expression and protein levels of IL-2, IL-6, IL-10, IL-12, TNF-α/LITAF, IFN-γ, and IgA, IgG, and IgM contents were significantly decreased ( p < 0.05 or p < 0.01) in the 300-, 600-, and 900-mg/kg NiCl groups when compared with those of the control group, which was consistent with the reduction of T-cell subset percentages and IgA B cell numbers in the 300-, 600-, and 900-mg/kg NiCl groups. The abovementioned results showed that dietary NiCl in excess of 300 mg/kg caused damage on splenocytes and splenic immune function. The results of the present study provided new experimental evidences for further study on the effect mechanism of NiCl on splenic immunity. [ABSTRACT FROM AUTHOR]

The aim of this work was to assess the protective effect of sodium selenite on the ileum mucosal immunologic toxicity induced by aflatoxin B (AFB). One hundred and eighty one-day-old healthy male avian broilers were divided into four groups of three replicates and 15 birds per replicate and fed with basal diet (control group), 0.3 mg/kg AFB (AFB group), 0.4 mg/kg Se (+Se group), and 0.3 mg/kg AFB + 0.4 mg/kg Se (AFB+Se group), respectively. The ileac T-cell subsets were determined by the methods of flow cytometry (FCM), and the mRNA contents of interleukin-2 (IL-2), interleukin-6(IL-6), and tumor necrosis factor-alpha (TNF-α) by quantitative real-time PCR. Compared with those in control group, the percentages of CD, CDCD, CDCD intraepithelial lymphocytes (IELs) and LPLs, the CD4/CD8 ratio of IELs, and the mRNA contents of IL-2, IL-6, and TNF-α were decreased in AFB group. However, compared with those in AFB group, these parameters of AFB+Se group were increased to be close to those in control group. It was concluded that 0.3 mg/kg AFB could reduce the cellular immune function of the ileum mucosa, but 0.4 mg/kg supplemented dietary selenium showed protective effects on AFB-induced immunologic injury. [ABSTRACT FROM AUTHOR]

Fecal specimens from two Bactrian camels were collected in the Ya'an city zoo of China and were examined for Cryptosporidium by centrifugal flotation. One specimen was found to be parasitized by Cryptosporidium via microscopy, and the oocysts were measured to have an average size of 7.03 × 5.50 μm ( n > 50). The isolate was genotyped by polymerase chain reaction (PCR) amplification and DNA sequence analysis of the partial 18S rRNA, COWP, and A135 genes, and was confirmed to be Cryptosporidium andersoni with minor nucleotide differences. Multilocus sequence typing (MLST) analysis indicated that the subtype of the camel-derived C. andersoni isolate was A4, A4, A4, and A1 at the four minisatellite loci ( MS1, MS2, MS3, and MS16, respectively). Therefore, this isolate belongs to the most common MLST subtype reported in cattle in China and is distinct from two other known camel C. andersoni MLST subtypes (A6, A4, A2, A1 and A6, A5, A2, A1). Animal transmission experiments demonstrated that the C. andersoni isolate was not infectious to immunosuppressed or immunocompetent Kun-ming mice, Sprague-Dawley rats, and hamsters but was biologically similar to most bovine C. andersoni isolates characterized so far. Therefore, transmission of this camel-derived C. andersoni isolate is very likely to occur between camels and bovine. [ABSTRACT FROM AUTHOR]

Toll-like receptors (TLRs) are important immune receptors in discriminating self from nonself and in initiating the innate and adaptive immune response. TLR4 and TLR7 have been proven to be highly expressed in chicken's spleen. Thus, this study was to evaluate the TLR4 and TLR7 messenger RNA (mRNA) expression levels in the spleen of broilers fed diets supplemented with nickel chloride (NiCl) using the methods of quantitative real-time PCR (qRT-PCR). Two hundred forty-one-day-old avian broilers were equally divided into 4 groups and fed on a corn-soybean basal diet as control diet or the same basal diet supplemented with 300, 600, and 900 mg/kg of NiCl for 42 days. Results showed that TLR4 and TLR7 mRNA expression levels in the spleen were lower ( P < 0.05 or P < 0.01) in the 300, 600, and 900 mg/kg groups than those in the control group. It was concluded that dietary NiCl in excess of 300 mg/kg could lower TLR4 and TLR7 mRNA expression levels in the spleen of broilers, implying that NiCl could impair the innate and adaptive immunity in spleen by injuring immunocytes and/or decreasing the content of cytokines through TLRs. [ABSTRACT FROM AUTHOR]

Fluoride (F) is a well-recognized hazardous substance. Ingested F initially acts locally on the intestines. The small intestine plays a critical role in the digestion, absorption, and defense. In this study, therefore, we investigated the effects of fluorine on the intestinal development by light microscopy, transmission electron microscopy, and histochemistry. A total of 280 one-day-old avian broilers were randomly divided into four groups and fed on a corn-soybean basal diet as control diet (fluorine, 22.6 mg/kg) or the same basal diet supplemented with 400, 800, and 1,200 mg/kg fluorine (high fluorine groups I, II, and III) in the form of sodium fluoride for 42 days. The results showed that the intestinal gross, histological, and ultrastructural changes were observed in the high fluorine groups II and III. Meanwhile, the intestinal length, weight, viscera index, villus height, crypt depth, villus height to crypt depth ratio, diameter, muscle layer thickness, and goblet cell numbers were significantly lower ( p < 0.01 or p < 0.05), and the intestinal diameter to villus height ratio was markedly higher ( p < 0.01 or p < 0.05) in the high fluorine groups II and III than those in control group. In conclusion, dietary fluorine in the range of 800–1,200 mg/kg obviously altered the aforementioned parameters of the intestines, implying that the intestinal development was suppressed and the intestinal functions, such as digestion, absorption, defense, or osmoregulation were impaired in broilers. [ABSTRACT FROM AUTHOR]

The aim of this study was to determine the effects of dietary NiCl on the development of the small intestine in broilers by the methods of light microscopy, histochemistry and enzyme-linked immunosorbent assay. A total of 240 one-day-old avian broilers were divided into four groups and fed on a corn-soybean basal diet or the same basal diet supplemented with 300, 600 and 900 mg/kg of nickel chloride (NiCl) for 42 days. Results showed that the small intestinal villus height, crypt depth and villus/crypt ratio were significantly decreased, and also the small intestinal goblet cells numbers and insulin-like growth factor-1 (IGF-1) and epidermal growth factor (EGF) contents were significantly decreased in the 300-, 600- and 900-mg/kg groups when compared with those of the control group. In conclusion, dietary NiCl in excess of 300 mg/kg reduced the villus height, crypt depth, the goblet cells population and the IGF-1 and EGF contents in the small intestine, indicating that the normal development and function of the small intestine were finally impaired in broilers. This study firstly provided the new experimental information for future studies on the effects of NiCl on the intestinal function in humans and other animals. [ABSTRACT FROM AUTHOR]

Fluoride can exert toxic effects on soft tissues, giving rise to a broad array of symptoms and pathological changes. The aim of this study was to investigate on erythrocytes and erythrocyte immune adherence function in broiler chickens fed with high fluorine (F) diets by measuring the total erythrocyte count (TEC), the contents of hemoglobin (Hb), packed cell volumn (PCV), erythrocyte osmotic fragility (EOF), erythrocyte C receptor rosette rate (E-CRR), and erythrocyte immune complex rosette rate (E-ICRR). A total of 280 1-day-old healthy avian broiler chickens were randomly allotted into four equal groups of 70 birds each and fed with a corn-soybean basal diet containing 22.6 mg F/kg (control group) or same basal diets supplemented with 400, 800, and 1,200 mg F/kg (high F groups I, II, and III) in the form of sodium fluoride for 42 days. Blood samples were collected for the abovementioned parameters analysis at 14, 28, and 42 days of age during the experiment. The experimental results indicated that TEC, Hb, and PCV were significantly lower ( p < 0.05 or p < 0.01), and EOF was higher ( p < 0.05 or p < 0.01) in the high F groups II and III than that in the control group from 14 to 42 days of age. The E-CRR was significantly decreased ( p < 0.01) in the three high F groups, whereas the E-ICRR was markedly increased ( p < 0.01) in the high F groups II and III from 14 to 42 days of age. It was concluded that dietary F in the range of 800 to 1, 200 mg/kg could significantly cause anemia and impair the integrity of erythrocyte membrane, the transport capacity of oxygen and carbon dioxide, and erythrocyte immune adherence function in broiler chickens. [ABSTRACT FROM AUTHOR]

Fluoride (F), a well-recognized harmful substance, is easily absorbed by the intestinal mucosa. The intestinal mucosal immune system is equipped with unique innate and adaptive defense mechanisms that provide a first line of protection against infectious agents. Meanwhile, immunoglobulins are the major secretory products of the adaptive immune system and their levels can be a strong indicator of a disease or condition. In this study, therefore, we investigated the effects of high dietary fluorine on the numbers of immunoglobulin A-positive (IgA) cells in the lamina propria of intestines (duodenum, jejunum and ileum) by immunohistochemistry as well as on the contents of immunoglobulin A (IgA), immunoglobulin G (IgG), and immunoglobulin M (IgM) in the mucosa of intestines (duodenum, jejunum, and ileum) by enzyme-linked immunosorbent assay (ELISA). A total of 280 1-day-old healthy avian broilers were randomly divided into four groups and fed on a corn-soybean basal diet as control diet (fluorine 22.6 mg/kg) or the same basal diet supplemented with 400, 800, and 1,200 mg/kg fluorine (high fluorine groups I, II, and III) in the form of sodium fluoride (NaF) for 42 days. The experimental data showed that the numbers of IgA cells as well as the IgA, IgG, and IgM contents were significantly decreased ( P < 0.01 or P < 0.05) in the high fluorine groups II and III when compared with those of the control group. It was concluded that dietary fluorine in the range of 800-1,200 mg/kg significantly reduced the numbers of the IgA cells and the contents of aforementioned immunoglobulins in the intestines (duodenum, jejunum, and ileum) of broilers, which could finally impact the mucosal humoral immune function in the intestines by a way that reduces the lymphocyte population and/or lymphocyte activation. [ABSTRACT FROM AUTHOR]

Fluorine (F) bioaccumulation has been reported in the organs and tissues of organisms, including intestine. The intestinal mucosa is very important to the immune development. Meanwhile, cytokines are present in the normal intestinal mucosal and play an important role in the immune function. Thus, changes of the cytokine contents are related to the state of intestinal mucosal immunity. In this study, we investigated the changes in contents of cytokines such as interleukin-2 (IL-2), interleukin-4 (IL-4), interleukin-6 (IL-6), interferon gamma (IFN-γ), and tumor necrosis factor-alpha (TNF-α) induced by dietary high F in the mucosa of different parts of intestines (duodenum, jejunum, and ileum) by enzyme-linked immunosorbent assay. A total of 280 one-day-old healthy avian broilers were randomly divided into four groups and fed on a corn-soybean basal diet as control diet (F 22.6 mg/kg) or the same basal diet supplemented with 400, 800, and 1,200 mg F/kg (high F groups I, II, and III) in the form of sodium fluoride for 42 days. The experimental data showed that the contents of IL-2, IL-4, IL-6, IFN-γ, and TNF-α in the intestinal mucosa were significantly decreased in the high F groups II and III when compared with those of the control group from 14 to 42 days of age. It was concluded that dietary F in the range of 800-1,200 mg/kg significantly reduced the contents of aforementioned cytokines in the intestinal mucosa of broilers, which could impact the function of intestinal mucosal immunity through the pathways that decreased the lymphocyte population and/or lymphocyte activation. [ABSTRACT FROM AUTHOR]

Long-term excessive fluoride intake is known to be toxic and can lead to fluorosis and bone pathologies. However, the cellular mechanisms underlying sodium fluoride-induced cytotoxicity in the cecal tonsil lymphocytes are not well understood. The aims of this study were to investigate the effects of high dietary fluorine on apoptosis and the expression of the Bcl-2, Bax, and caspase-3 in the cecal tonsil lymphocytes of broilers. The broilers were fed on high-fluorine diets containing 0, 400, 800, and 1,200 mg/kg fluorine. As measured by flow cytometry, the percentage of apoptotic lymphocytes was significantly increased in the high-fluorine groups II and III when compared with those in the control group. Meanwhile, immunohistochemical tests showed that the Bcl-2 protein expression decreased, and the Bax and caspase-3 protein expression increased in the high-fluorine groups II and III. In conclusion, dietary fluorine in the range of 800-1,200 mg/kg increased lymphocyte apoptosis in the cecal tonsil of broilers, suggesting that the lymphocyte apoptosis in the cecal tonsil was mediated by direct effects of fluoride on the expression of Bcl-2, Bax, and caspase-3. [ABSTRACT FROM AUTHOR]

Cytokines are immunoregulatory proteins which play an important role in the immune system. The purpose of this study was to examine the serum cytokine contents including interleukin-2 (IL-2), interleukin-4 (IL-4), interleukin-6 (IL-6), interleukin-10 (IL-10), interferon gamma (IFN-γ), and tumor necrosis factor-alpha (TNF-α) induced by dietary nickel chloride in broilers by enzyme-linked immunospecific assay. A total of 240 one-day-old avian broilers were divided into four groups and fed on a corn-soybean basal diet as control diet or the same basal diet supplemented with 300, 600, and 900 mg/kg of nickel chloride. During the experimental period of 42 days, the results showed that the serum IL-2, IL-4, IL-6, IL-10, IFN-γ and TNF-α contents were lower ( p < 0.05 or p < 0.01) in the 300, 600, 900 mg/kg groups than those in the control group. It was concluded that dietary nickel chloride in the range of 300 to 900 mg/kg could reduce the serum cytokine contents, which could finally impact the immune function in broilers. [ABSTRACT FROM AUTHOR]

The purpose of this 42-day study was to examine the effect of dietary vanadium on intestinal microorganism diversity in the duodenum, ileum, cecum, and rectum segments of broilers by the plate count and polymerase chain reaction-denaturing gradient gel electrophoresis (DGGE). A total of 420 1-day-old avian broilers were divided into six groups and fed on a control diet or the same diet supplemented with vanadium at the doses of 5, 15, 30, 45, and 60 mg/kg in the form of ammonium metavanadate. In comparison with control group, the dietary vanadium at the doses of 45 and 60 mg/kg could decrease the counts of Bifidobacterium spp. in the intestinal tract at 21 and 42 days of age. With increasing level in dietary vanadium, the counts of Escherichia coli were significantly increased in the ileum, cecum, and rectum and were decreased in the duodenum at 21 and 42 days of age. However, the counts of Lactobacilli were decreased in the cecum and rectum and increased in the ileum of 45 and 60 mg/kg groups. The colonization of these three bacteria could be affected by dietary vanadium. DGGE analysis showed that the number of bands in duodenum, ileum, cecum, and rectum were obviously decreased in the 30, 45, and 60 mg/kg groups at 21 and 42 days of age. In conclusion, the dietary vanadium in excess of 30 mg/kg could alter the amount and diversity of intestinal bacteria in broilers, implying that the structure and initial balance in the intestinal microbiota were disrupted. [ABSTRACT FROM AUTHOR]

The purpose of this 42-day study was to investigate the effects of low selenium (Se) on histopathological changes of spleen, cell cycle and apoptosis of splenocytes, and oxidative status of the spleen. One hundred twenty 1-day-old avian broilers were randomly divided into two groups of 60 each and were fed on a low Se diet (0.0342 mg/kg Se) or a control diet (0.2 mg/kg Se), respectively. The weight and relative weight of the spleen were significantly decreased in the low Se group when compared with those of the control group. Histopathologically, splenic lesions in low-Se chicken were characterized by lymphocyte depletion and congestion of red pulp. As measured by flow cytometry, splenocytes in G/G phase were significantly increased, while splenocytes in S phase and G + M phase were obviously decreased in the low Se group. The percentage of apoptotic splenocytes was greatly increased in the low Se group when compared with that of control group. At the same time, the occurrence frequencies of apoptotic splenocytes was markedly increased in the low Se group with the appearance of condensed nucleus ultrastructurally. Oxidative stress in the spleens of the low Se group was evidenced by decrease in glutathione peroxidase and catalase activities and increase in malondialdehyde contents. The results showed that low Se diet intake caused increased apoptosis, arrested cell cycle, and obvious oxidative stress, which provided a possible pathway for the injured structure and immune function of the spleen in chickens. [ABSTRACT FROM AUTHOR]

The purpose of this 42-day study was to examine the effect of dietary vanadium on the ileac T cells and contents of cytokines including interleukin-2 (IL-2), interleukin-6 (IL-6), and interferon-gamma (IFN-γ) in broilers by flow cytometry and enzyme-linked immunosorbent assay. A total of 420 one-day-old avian broilers were divided into six groups (seven replicates in each group and ten broilers in each replicate) and fed on control diet or the same diet supplemented with 5, 15, 30, 45, and 60 mg/kg vanadium in the form of ammonium metavanadate. The results showed that the percentages of CD3, CD3CD4, and CD3CD8 T cells in both ileac lamina propria lymphocytes (LPLs) and intraepithelial lymphocytes (IELs) were significantly lower ( P < 0.05 or P < 0.01) in the 45- and 60-mg/kg groups than in the control group from 14 to 42 days of age. The CD4/CD8 ratio was increased in ileac LPLs in the 60-mg/kg group at 28 days of age, and in ileac IELs in the 60-mg/kg group at 28 days of age and in the 45-mg/kg group at 42 days of age. Meanwhile, the ileac IL-2, IL-6 contents were decreased ( P < 0.05 or P < 0.01) in the 60-mg/kg group from 14 to 42 days of age and in the 45-mg/kg group from 28 to 42 days of age in comparison with those of the control group. It was concluded that dietary vanadium in excess of 30 mg/kg reduced the ileac T cell population and percentages of T cell subsets, and IL-2, IL-6, and IFN-γ contents, implying that the immune function of local intestinal mucosa in broilers could be affected by the dietary vanadium. [ABSTRACT FROM AUTHOR]

The cecal tonsil of broiler is known as a secondary lymphoid tissue, which is involved in antigen-specific humoral immune responses. The purpose of this study was to investigate the effects of dietary vanadium on the tissue distribution and quantity of immunoglobulin A-positive (IgA) cell in the cecal tonsil by immunohistochemistry. Simultaneously, the changes in interleukin-6 (IL-6), interleukin-10 (IL-10), interferon gamma (IFN-γ) and tumor necrosis factor-alpha (TNF-α) contents in the cecal tonsil were also quantified by enzyme-linked immunosorbent assay (ELISA). A total of 420 one-day-old avian broilers were divided into six groups and fed on a corn-soybean basal diet (control diet) or the same diet supplemented respectively with 5, 15, 30, 45, and 60 mg/kg of vanadium in the form of ammonium metavanadate for 42 days. The results showed that the population of the IgA cells in the cecal tonsil were significantly lower ( p < 0.05 or p < 0.01) in the 45 and 60 mg/kg groups than that in the control group. Meanwhile, IL-10, IFN-γ and TNF-α contents in the cecal tonsil were significantly decreased ( p < 0.05 or p < 0.01) in the 30, 45 and 60 mg/kg groups in comparison with those of the control group. However, IL-6 content in the cecal tonsil was only decreased ( p < 0.05 or p < 0.01) in 60 mg/kg at 14 and 28 days of age. In conclusion, dietary vanadium in excess of 30 mg/kg reduced the numbers of the IgA cells and changed the contents of the abovementioned cytokines in the cecal tonsil, which may finally impact the function of local mucosal humoral immunity in broilers. [ABSTRACT FROM AUTHOR]

The purpose of this 42-day study was to investigate the apoptosis in the bursa of Fabricius induced by different levels of dietary vanadium. A total of 420 1-day-old avian broilers were divided into 6 groups in which there were 7 replicates in each group and 10 broilers in each replicate and fed on a corn-soybean basal diet as control diet (vanadium 0.073 mg/kg) or the same diet amended to contain 5, 15, 30, 45, and 60 mg/kg vanadium supplied as ammonium metavanadate (NHVO). Ultrastructurally, mitochondrial injury and increased numbers of apoptotic cells with condensed nuclei were observed in the 30, 45, and 60 mg/kg groups. As measured by flow cytometry, the percentages of apoptotic lymphocytes were significantly increased in the 15-, 30-, 45-, and 60-mg/kg groups when compared with those of control group. Meanwhile, the terminal deoxynucleotidyl transferase 2′-deoxyuridine 5′-triphosphate nick end-labeling assay showed that there were increased numbers of apoptotic cells in the 30-, 45-, and 60-mg/kg groups. Immunohistochemical tests showed increased numbers of positive cells under Bax and caspase-3 protein detection and decreased Bcl-2 protein in the 15-, 30-, 45-, and 60-mg/kg groups. The vanadium content of the bursa was found to be significantly increased in the 30-, 45-, and 60-mg/kg groups. These results suggested that dietary vanadium in excess of 15 mg/kg could cause lymphocyte apoptosis in the bursa of Fabricius and impact humoral immunity in broilers. Lymphocyte apoptosis in the bursa induced by high levels of dietary vanadium is associated with mitochondrial injury and changes in levels of apoptogenic proteins, such as Bcl-2, Bax, and caspase-3. [ABSTRACT FROM AUTHOR]

The purpose of this study was to investigate the renal and hepatic oxidative damage and toxicity caused by dietary high vanadium in broilers. A total of 420 one-day-old avian broilers were divided into six groups and fed on a corn-soybean basal diet as control diet (vanadium 0.073 mg/kg), and five high vanadium diets (vanadium 5 mg/kg, high vanadium group I; 15 mg/kg, high vanadium group II; 30 mg/kg, high vanadium group III; 45 mg/kg, high vanadium group IV; and 60 mg/kg, high vanadium group V) throughout the experimental period of 42 days. The results showed that the renal and hepatic superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) activities, ability to inhibit hydroxy radical, and malondialdehyde (MDA), glutathione, and vanadium contents were not significantly changed in high vanadium group I and II when compared with those of the control groups. However, the SOD and GSH-Px activities, ability to inhibit hydroxy radical, and GSH content were significantly decreased, and the MDA and vanadium contents were markedly increased in high vanadium groups III, IV, and V. At the same time, the lesions were also observed in the kidney and liver of high vanadium groups III, IV, and V. The renal tubular epithelial cells showed granular degeneration and vacuolar degeneration, and hepatocytes showed granular degeneration, vacuolar degeneration, and fatty degeneration. It was concluded that dietary vanadium in the range of 30-60 mg/kg could cause oxidative damage and vanadium accumulation, which induced renal and hepatic toxicity and lesions. The renal and hepatic function was finally impaired in boilers. [ABSTRACT FROM AUTHOR]