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In October 2020, an avian paramyxovirus serotype 14 (APMV-14)-designated chicken/Fujian/2160/2020 (FJ2160) was isolated from tracheal and cloacal swab sample of chicken collected from live bird market in Fujian province in China during the active surveillance program. The complete genome of FJ2160 comprised 15,444 nucleotides (nt) complying with the paramyxovirus "rule of six" and encoded six non-overlapping structural proteins in the order of 3′-NP-P-M-F-HN-L-′5. The complete genome sequence analysis showed that FJ2160 had the highest identity (90.0%) with the APMV-14 isolated from Japan, while the nucleotide sequence identities of FJ2160 and other APMVs ranged from 42.4 to 51.1%. The F protein cleavage site was TREGR↓L, which resembled a lentogenic strain of APMV-1. Phylogenetic analysis revealed that the FJ2160 closest relative was APMV-14. The intracerebral pathogenicity index (ICPI) tests indicated that the virus was lentogenic. This is the first report of APMV-14 in China. These results provide evidence that APMV-14 could infect chickens and reveal the genetic characteristics and biological properties of the virus, which can help to better understand this new emerging APMV-14. [ABSTRACT FROM AUTHOR]

Twelve Kunming mice were randomly divided into two groups (n = 6), and administered with distilled water containing 0 mg/L and 160 mg/L HgCl2 respectively, with an experimental period of 3 days. Our results showed that mercury exposure significantly reduced weight gain in mice (P < 0.01). Through pathological observation of cecum tissues, significant pathological changes were observed in cecum tissues of mice exposed to mercury. Furthermore, mercury exposure not only significantly increased malondialdehyde (MDA) content in mice (P < 0.01) but also significantly decreased superoxide dismutase (SOD) activity (P < 0.01) and glutathione peroxidase (GSH) level in mice (P < 0.01). Furthermore, high-throughput sequencing analysis showed that at the genus level some microbial populations including Clostridiales, Lactobacillus, Treponema, Oscillospira, and Desulfovibrio were significantly increased whereas some microbial populations including S24-7, Acinetobacter, and Staphylococcus were significantly decreased. Moreover, correlation analysis indicated that microorganisms were not correlated with biomarkers of oxidative stress. In summary, mercury exposure reduced the growth performance of mice, resulting in gut microbiota alterations, and led to oxidative stress by increasing the concentration of malondialdehyde (MDA) and decreasing the concentration of superoxide dismutase (SOD) and glutathione peroxidase (GSH). [ABSTRACT FROM AUTHOR]

The aim of the present study was to investigate the effects of high concentrations of copper (Cu) on the cecum and rectum of intestinal microbiota in female mice. Twenty-four Kunming mice were weighed and randomly divided into two groups (n = 12 per group) including the control group and Cu group. Cu group was given drinking water with 5 mg/kg-bw copper chloride (CuCl2), while the control group was treated with drinking water without CuCl2. At the 90th day, results showed that compared with the control group, mice in the treatment group had a lower body weight, and the feces turned yellow and had a lower pH value. Histopathological lesions showed that the intestinal tissue from the treatment group had increased thickness of outer muscularis and smoothed muscle fiber, widened submucosa, decreased goblet cells, and showed blunting of intestinal villi and severe atrophy of central lacteal. In addition, at the genus level, 16S rRNA gene sequencing from the Cu group showed that Corynebacterium were significantly increased whereas Staphylococcaceae, Odoribacter, Rikenella, and Jeotgalicoccus were significantly decreased in the cecum. Dehalobacterium, Coprococcus, and Spirochaetales increased significantly whereas Salinicoccus, Bacillales, Staphylococcus, and Lactobacillales decreased sharply in the rectum. This study demonstrated that high concentrations of Cu could induce tissue injury and interrupt the homeostasis of microbiota. [ABSTRACT FROM AUTHOR]

The aim of the present study was to investigate the effects of high doses of copper (Cu) and mercury (Hg) on the cecal microbiota in female mice. Forty-eight Kunming mice were randomly divided into the control group (CCk group), the Cu group (CCu group), the Hg group (CHg group), and the Cu + Hg group (CCH group). At the 90th day, cecal tissues were prepared for histopathological analysis and cecal contents for analysis by 16S rRNA sequencing method. Cecal tissues from treatment groups had histopathological lesions including increased thickness of inner muscularis and outer muscularis, widened submucosa, decreased goblet cells, mild to moderate necrosis of enterocytes, blunting of intestinal villi, and severe atrophy of central lacteal. Furthermore, compared to the CCk group, the abundance of bacteria genera Rikenella, Jeotgailcoccus, and Staphylococcus were significantly decreased, whereas the bacteria genus Corynebacterium was significantly increased in the CCu group. The abundance of bacteria genera of Sporosarcina, Jeotgailcoccus, and Staphylococcus were significantly decreased in the CHg group and CCH group. The bacteria genus Anaeroplasma was significantly increased in the CCH group. The results indicated that high doses of Cu and Hg caused histopathological lesions and changed the diversity of microbiota in the cecum of female mice, which provide a theoretical basis for more accurate assessment of the risk in intestinal diseases caused by Cu and Hg. [ABSTRACT FROM AUTHOR]

To investigate the effects of co-exposure to molybdenum (Mo) and cadmium (Cd) on oxidative stress and cell apoptosis in caprine livers, 36 Boer goats were randomly divided into four groups with nine goats in each group. Three groups were randomly assigned with one of three oral treatments of CdCl (0.5 mg Cd kg·BW) and [(NH)MoO·4HO] (15 mg Mo kg·BW, 30 mg Mo kg·BW, 45 mg Mo kg·BW), while the control group received deionized water. Liver tissues on days 0, 25, and 50 were subjected to determine antioxidant activity indexes and the messenger RNA (mRNA) expression levels of ceruloplasmin ( CP), cysteinyl aspartate-specific proteinase-3 ( caspase-3), second mitochondria-derived activator of caspases ( Smac), and cytochrome-C ( Cyt-C) genes. The results showed that significant reductions were observed in total antioxidant capacity (T-AOC) and total superoxide dismutase (T-SOD) activities ( P < 0.05), while activities or contents of malondialdehyde (MDA), nitric oxide (NO), and nitric oxide synthase (NOS) were increased ( P < 0.05). The mRNA expression levels of CP, caspase-3, Smac, and Cyt-C genes were upregulated ( P < 0.05). In addition, histopathological lesions showed different degrees of vacuolar degeneration and edematous and mitochondrial swelling. The results suggest that co-exposure to Mo and Cd could induce oxidative stress and cell apoptosis possibly associated with mitochondrial intrinsic pathway in goat liver and show possible synergistic effects between the two elements. [ABSTRACT FROM AUTHOR]

Molybdenum (Mo) is an essential element for human beings and animals; however, high dietary intake of Mo can lead to adverse reactions. Cadmium (Cd) is one of the major transitional metals which have toxic effects in animals. The toxicity of simple Cd or Mo has been researched frequently. However, the toxicity of Mo combined with Cd was rarely studied. To investigate the toxicity of Mo combined with Cd in liver of goats, 36 Boer goats were randomly divided into four groups and assigned with one of the three oral treatments of CdCl (0.5 mg kg Cd) and [(NH)MoO·4HO] (15 mg kg Mo, group I; 30 mg kg Mo, group II; 45 mg kg Mo, group III), while the control group received deionized water. Blood samples were collected on days 0, 10, 20, 30, 40, and 50 to determine antioxidant indices in serum. In addition, liver tissues were collected on days 0, 25, and 50 for detecting the messenger RNA (mRNA) expression levels of Bcl-2 and Bax. Moreover, liver tissues at 50 days were subjected to histopathological analysis with the optical microscope. The results revealed a significant increase ( P < 0.05 or P < 0.01) in the levels of nitric oxide (NO), malonaldehyde (MDA), and the activity of nitrix oxide synthase (NOS) and a significant decline ( P < 0.05) in the activities of total superoxide dismutase (T-SOD) and total antioxidative capacity (T-AOC). The mRNA expression level of Bcl-2 was suppressed ( P < 0.05), while the expression of Bax was increased ( P < 0.05) in liver. The histopathological changes were observed in the liver of goats including a small amount of erythrocyte, the unclear structure of hepatic cord and hepatic sinusoid, granular degeneration, vacuolar degeneration, and steatosis. In conclusion, combined chronic toxicity of Cd with different levels of Mo might induce goat liver cell apoptosis and cause oxidative stress in serum, and it showed a possible synergistic relationship between the two elements. [ABSTRACT FROM AUTHOR]

The present experiment aims at evaluating chronic toxic effects of the combination of cadmium (Cd) and molybdenum (Mo) according to residual element contents, apoptosis gene expression, and ultrastructure and histopathology changes of caprine spleen. In total, 36 Boer goats were randomly divided into four groups with the equal number in each group. The control group was orally administered with deionized water while the experimental groups I, II, and III were administered with the equal quantity of CdCl (1 mg kg BW) and (NH4)·MoO·4HO including 15, 30, and 45 mg·Mo kg BW, respectively. Three individuals from each group were treated with euthanasia on days 0, 25, and 50. The data showed that the content of splenic residual Mo and Cd increased ( P < 0.05) in the experimental groups on days 25 and 50, while no significant difference was observed in the content of Cu. The apoptosis-related gene expression levels including Bcl-2, Bax, Caspase-3, Smac, and ceruloplasmin ( CP) were also determined. Results showed that significant reductions were observed in Bcl-2 and CP expressions ( P < 0.01), while Caspase-3 gene was up-regulated ( P < 0.05). However, no significant difference was observed in Smac and Bax expressions. Furthermore, on day 50, spleen tissues were presented to observe ultrastructural changes in lesions by means of transmission electron microscopy, with fragmentized nucleus, vesiculation of cytoplasm, mitochondria hyperplasia, and increasing lysosomes included. In addition, histopathology results corroborated the toxicity by showing cell hemorrhage, thickening central arteries, and enhanced capsule thickness. To sum up, our study revealed that the combination of Cd and Mo could induce remarkable damage to the spleen of goats by promoting cell apoptosis in the mitochondrial pathway and affecting the deposition of Mo and Cd. [ABSTRACT FROM AUTHOR]

Molybdenum (Mo) is an essential trace element for animals and humans. However, the high dietary intake of Mo leads to disease conditions in heavy metal pollution areas. To the best of our knowledge, the effect of high levels of Mo on the apoptosis of hepatocyte in goats has not been investigated. Therefore, the aim of the present in vivo study was to investigate the impact of Mo on mitochondrial oxidative stress and apoptosis genes in the liver using real-time quantitative polymerase chain reaction (RT-qPCR) and transmission electron microscopy, respectively. Thirty-six healthy goats were randomly divided into three groups: two groups treated with ammonium molybdate [(NH)·MoO·HO] at 15 and 45 mg Mo kg BW, respectively, and a control group without treatment. Liver samples were collected from individual goats at different time intervals. The levels of oxidative stress in the mitochondrial membrane and expression of liver-related apoptosis genes, including Bcl-2, Cyt c, caspase-3, and Smac, were examined. The results demonstrated that the levels of superoxide dismutase (SOD) and catalase (CAT) expression were significantly down-regulated in liver cells, whereas malondialdehyde (MDA), nitric oxide (NO), and total nitric oxide synthase (T-NOS) expression was up-regulated ( P < 0.01). The expression of Smac, Cyt c, and caspase-3 was significantly up-regulated, whereas Bcl-2 expression was down-regulated in liver cells ( P < 0.01). In addition, histopathological examination revealed varying degrees of vacuolization, irregularity, nuclear fission, and mitochondrial swelling and high-density electrons in the cytoplasm of hepatocytes in groups treated with 15 and 45 mg Mo kg BW. Thus, these results suggested that high molybdenum induced hepatocyte apoptosis and might involve a mitochondrial pathway. [ABSTRACT FROM AUTHOR]

Molybdenum (Mo) is an essential element for human beings and animals; however, high dietary intake of Mo can lead to adverse reactions. Cadmium (Cd) is harmful to health. To investigate the toxicity of Mo combined with Cd in duck kidneys, 240 ducks were randomly divided into six groups and treated with a commercial diet containing Mo, Cd or Mo combined with Cd. Kidneys were collected on days 30, 60, 90 and 120 for determining the expression of heat shock proteins (HSPs), including HSP60, HSP70 and HSP90 in the kidney through quantitative RT-PCR. We also determined the antioxidant activity indexes in the kidney mitochondria. Moreover, kidney tissues at 120 days were subjected to histopathological analysis with the optical microscope. The results indicated that the expression of HSPs was highly significantly ( P < 0.01) upregulated in the kidneys of the combination groups and the Cd group. Exposure to Cd and a high dose of Mo decreased the total antioxidative capacity and the activity of xanthine oxidase, while malondialdehyde levels and the activity of nitric oxide synthase increased compared with those of the control groups in the kidney mitochondria. This was particularly evident at 90 and 120 days. Histopathological lesions included congestion and bleeding in the renal interstitium, swelling of the distal convoluted tubule epithelial cells, granular degeneration and blister degeneration in the renal tubular epithelial cells. These results suggest that a combination of Mo and Cd leads to greater tissue damage and has a synergistic effect on kidney damage. Oxidative damage of kidney mitochondria may be a potential nephrotoxicity mechanism of molybdenum and cadmium, and the high expression of HSPs may play a role in the resistance of kidney toxicity induced by Mo and Cd. [ABSTRACT FROM AUTHOR]

Fatty liver haemorrhagic syndrome (FLHS) is a widespread metabolic disease in laying hens that causes a decrease in egg production and even death. Insulin resistance is a major contributor to the pathogenesis of nonalcoholic fatty liver disease. However, the relationship between FLHS and the insulin resistance mechanisms underlying FLHS is not well elucidated. Therefore, we established an FLHS model induced by feeding a high-energy low-protein diet. In the current study, we found that the fasting glucose and insulin concentrations were elevated in the FLHS group compared with the control group during the experimental period. The results of the oral glucose tolerance test (OGTT) and insulin sensitivity test (IST) showed a high level of insulin resistance in the FLHS model. InsR, 4EBP-1, Glut-1 and Glut-3 mRNA expression were decreased, and TOR, S6K1, and FOXO1 were elevated (P < 0.05). Metabolomic analysis with GC/MS identified 46 differentially expressed metabolites between these two groups, and of these, 14 kinds of metabolism molecules and 32 kinds of small metabolism molecules were decreased (P < 0.05). Further investigation showed that glucose, lipid and amino acid metabolism blocks in the progression of FLHS by GO functional and pathway analysis. Overall, these results suggest that insulin resistance participated in FLHS; comprehensively, metabolites participated in the dysregulated biological process. [ABSTRACT FROM AUTHOR]