Alterations in antioxidant function and cell apoptosis in duck spleen exposed to molybdenum and/or cadmium

Zhang, Mengmeng; Luo, Junrong; Zhang, Caiying; Xia, Bing; Hu, Guoliang

doi:10.4142/jvs.2017.18.2.193

Cited by 18 publications

(10 citation statements)

References 40 publications

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“…Excess Mo is mainly related to occupational activities or contaminated nutrients, whose consequences are not well characterized. It has been reported in ducks that spleen Mo accumulation decreases antioxidant capacity, favors cell apoptosis, and increases heat shock proteins and TNF-a in spleen (38,39). Similar data have been found in chickens fed with a high-Mo diet (40).…”

Section: Discussionsupporting

confidence: 79%

Spleen iron, molybdenum, and manganese concentrations are coregulated in hepcidin‐deficient and secondary iron overload models in mice

et al. 2019

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Iron excess increases the hepatic expression of hepcidin, the systemic iron metabolism regulator that favors iron sequestration in the spleen. Genetic iron overload related to hepcidin insufficiency decreases the spleen iron concentration and increases hepatic iron concentration, whereas during secondary iron overload, the hepcidin expression increases together with spleen iron concentration in addition to hepatic iron concentrations increase. Links between iron metabolism and other metals being suggested, our aim was to investigate, during iron overload, the relationships between the hepatic hepcidin expression level and the hepatic and splenic concentrations of iron, manganese, copper, zinc, and molybdenum, determined using inductively coupled plasma mass spectrometry. Hepcidin‐deficient mice, secondary iron overload mice models, and their respective controls were studied. Spleen molybdenum and manganese concentrations paralleled the modulation of both spleen iron concentrations, increasing in secondary iron overload and decreasing in hepcidin deficiency related iron overload, as well as hepatic hepcidin mRNA expression. Our data suggest that iron, manganese, and molybdenum metabolisms could share mechanisms controlling their distribution that are associated to hepcidin modulation. In diseases with abnormal hepcidin levels, including chronic inflammation, special attention should be paid to those metals that can participate with the phenotype.—Cavey, T., Latour, C., Island, M.‐L., Leroyer, P., Guggenbuhl, P., Coppin, H., Roth, M.‐P., Bendavid, C., Brissot, P., Ropert, M., Loréal, O. Spleen iron, molybdenum, and manganese concentrations are coregulated in hepcidin‐deficient and secondary iron overload models in mice. FASEB J. 33, 11072–11081 (2019). http://www.fasebj.org

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Section: Discussionsupporting

confidence: 79%

Spleen iron, molybdenum, and manganese concentrations are coregulated in hepcidin‐deficient and secondary iron overload models in mice

et al. 2019

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“…Molybdenum is a critical component of several enzymes, including sulfite oxidase, XOD, and aldehyde oxidase [36]. High dietary MO levels decreased serum XOD activity in agreement with the result of Zhang et al [37]. Moreover, in this study, high dietary MO levels resulted in decreased activities of antioxidant enzymes (T-AOC, XOD, GSH-ST) and GSH concentration while MDA levels were increased.…”

Section: Discussionsupporting

confidence: 89%

“…Studies in rabbits have shown that high MO accumulation generates free radical processes or reactive intermediates, resulting in the alteration of MDA and GSH-Px levels [44,45]. In ducks exposed to high levels of MO, an increase in MDA levels and a decrease in XOD and CAT activities in serum and spleen tissue has also been observed [28,37]. Therefore, the toxic effect of exposure to high MO levels can result in oxidative damage.…”

Section: Discussionmentioning

confidence: 99%

Alteration of the Antioxidant Capacity and Gut Microbiota under High Levels of Molybdenum and Green Tea Polyphenols in Laying Hens

et al. 2019

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High dietary levels of molybdenum (MO) can negatively affect productive performances and health status of laying hens, while tea polyphenol (TP) can mitigate the negative impact of high MO exposure. However, our understanding of the changes induced by TP on MO challenged layers performances and oxidative status, and on the microbiota, remains limited. The aim of the present study was to better understand host (performances and redox balance) and microbiota responses in MO-challenged layers with dietary TP. In this study, 200 Lohmann laying hens (65-week-old) were randomly allocated in a 2 × 2 factorial design to receive a diet with or without MO (0 or 100 mg/kg), and supplemented with either 0 or 600 mg/kg TP. The results indicate that 100 mg/kg MO decreased egg production (p = 0.03), while dietary TP increased egg production in MO challenged layers (p < 0.01). Egg yolk color was decreased by high MO (p < 0.01), while dietary TP had no effect on yolk color (p > 0.05). Serum alanine transaminase (ALT), aspartate aminotransferase (AST), and malonaldehyde (MDA) concentration were increased by high MO, while total antioxidant capacity (T-AOC), xanthine oxidase (XOD) activity, glutathione s-transferase (GSH-ST), and glutathione concentration in serum were decreased (p < 0.05). Dietary TP was able to reverse the increasing effect of MO on ALT and AST (p < 0.05). High MO resulted in higher MO levels in serum, liver, kidney, and egg, but it decreased Cu and Se content in serum, liver, and egg (p < 0.05). The Fe concentration in liver, kidney, and eggs was significantly lower in MO supplementation groups (p < 0.05). High MO levels in the diet led to lower Firmicutes and higher Proteobacteria abundance, whereas dietary TP alone and/or in high MO treatment increased the Firmicutes abundance and the Firmicutes/Bacteroidetes ratio at phylum level. High MO increased the abundance of Proteobacteria (phylum), Deltaproteobacteria (class), Mytococcales (order), and Nanocystaceae (family), whereas dietary TP promoted the enrichment of Lactobacillus agilis (species). Dietary TP also enhanced the enrichment of Bacilli (class), Lactobacillates (order), Lactobacillus (family), and Lactobacillus gasseri (species). Microbiota analysis revealed differentially enriched microbial compositions in the cecum caused by MO and TP, which might be responsible for the protective effect of dietary TP during a MO challenge.

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“…Liu et al [ 11 ] found that Pb caused ultrastructural changes and apoptosis in rat proximal tubular cells. Zhang et al [ 47 ] found that molybdenum and Cd changed ultrastructural structure and induced apoptosis in duck spleens. Nickel chloride decreased Bcl-2 mRNA expression, increased Bax, Cyt c, and Caspase-3 mRNA expression, and induced apoptosis via mitochondrial pathway in chicken bursa of Fabricius [ 48 ].…”

Section: Discussionmentioning

confidence: 99%

Selenium against lead-induced apoptosis in chicken nervous tissues via mitochondrial pathway

Zhu

Jiao

et al. 2017

Oncotarget

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To investigate alleviative effect of selenium (Se) on lead (Pb)-induced apoptosis in chicken nervous tissues, 7-day-old chickens were randomly divided into four groups. The control group was fed a standard diet and drinking water. In the Pb and Se/Pb groups, (CH3OO)2Pb was dissolved in drinking water. In the Se and Se/Pb groups, Na2SeO3 was put into the standard diet. Embryonic neurocytes were divided into the control, Se (containing Na2SeO3), Pb (containing (CH3COO)2Pb), and Se/Pb (containing Na2SeO3 and (CH3COO)2Pb) groups. The following contents were performed: Morphologic observation for 90 days in brain tissues and for 12, 24, 36, and 48 hours in embryonic neurocytes; and antioxidant indexes, messenger RNA (mRNA) expression of twenty-five selenoproteins, and mRNA and protein expression of five apoptosis-related genes for 30, 60, and 90 days in brain tissues and for 12, 24, 36, and 48 hours in embryonic neurocytes. The results indicated that Se alleviated Pb-caused morphological changes; the decrease of superoxide dismutase, glutathione peroxidase (GPx), GPx1, GPx2, GPx3, GPx4, thioredoxin reductases (Txnrd)1, Txnrd2, Txnrd3, iodothyronine deiodinases (Dio)1, Dio2, Dio3, selenoprotein (Sel)T, SelK, SelS, SelH, SelM, SelU, SelI, SelO, Selpb, selenoprotein (Sep)n1, Sepp1, Sepx1, Sepw1, 15-kDa selenoprotein, and selenophosphate synthetases 2, and B-cell lymphoma-2 (Bcl-2); the increase of malondialdehyde, p53, Bcl-2 associated X protein, cytochrome c, and Caspase-3. Pb had time-dependent effects on GPx4, SelM, and malondialdehyde in the brain tissues; and on SelU in the embryonic neurocytes. Our data demonstrated that Se alleviated Pb-induced apoptosis in the chicken nervous tissues via mitochondrial pathway.

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Alterations in antioxidant function and cell apoptosis in duck spleen exposed to molybdenum and/or cadmium

Cited by 18 publications

References 40 publications

Spleen iron, molybdenum, and manganese concentrations are coregulated in hepcidin‐deficient and secondary iron overload models in mice

Spleen iron, molybdenum, and manganese concentrations are coregulated in hepcidin‐deficient and secondary iron overload models in mice

Alteration of the Antioxidant Capacity and Gut Microbiota under High Levels of Molybdenum and Green Tea Polyphenols in Laying Hens

Selenium against lead-induced apoptosis in chicken nervous tissues via mitochondrial pathway

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