Pathology of Selenium Deficiency in the Chick

Gries, Christian L.; Scott, M. L.

doi:10.1093/jn/102.10.1287

Cited by 77 publications

(20 citation statements)

References 13 publications

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“…This indicated that the forms and quantity of Se was only one of the factors improving the DWG and FCR of avian broilers. Poultry diets deficient in selenium result in poor growth and development, increased mortality, reduced egg production, decreased hatchability, pancreatic fibrosis, and muscle myopathies [22][23][24]. The present research result proved this point, and the control groups fed with basal diet unsupplemented with any forms of Se showed the symptoms of selenium deficiency such as lower survival rate, DWG, and higher FCR.…”

Section: Discussionsupporting

confidence: 73%

Differential Effects of Sodium Selenite and Nano-Se on Growth Performance, Tissue Se Distribution, and Glutathione Peroxidase Activity of Avian Broiler

2008

Biol Trace Elem Res

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The present research evaluated differential effects of sodium selenite and nano-Se on growth performance, tissue Se distribution, and glutathione peroxidase (GSH-Px) activity of avian broiler. Broilers were randomly segregated into 12 groups so that three replicates were available for each of the three treatments (T-1, T-2, and T-3) and control groups. The control groups were fed basal diets without Se addition. T-1, T-2, and T-3 were fed with diets containing 0.2 mg kg(-1) sodium selenite, 0.2 mg kg(-1) nano-Se, and 0.5 mg kg(-1) nano-Se, respectively. Compared with the control, Se supplementation remarkably improved daily weight gain and survival rate and decreased feed conversion ratio (P < 0.05). However, no significant difference was observed between T-1, T-2, and T-3. The tissue Se content was significantly higher (P < 0.05) in Se-supplemented groups than the control, and T-3 showed the highest. Furthermore, higher Se content was observed in liver, and there was a significant difference (P < 0.05) compared with that in muscle. As for serum and hepatic GSH-Px activities, Se supplementation remarkably improved GSH-Px activity (P < 0.05), and there was no significant difference (P > 0.05) between treatments (T-1, T-2, and T-3).

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Section: Discussionsupporting

confidence: 73%

Differential Effects of Sodium Selenite and Nano-Se on Growth Performance, Tissue Se Distribution, and Glutathione Peroxidase Activity of Avian Broiler

2008

Biol Trace Elem Res

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“…Se-vitamin E deficiency caused various lesions, which include encephalomalacia and exudative diathesis in chick. However, chicks required Se for growth and pancreatic function [2,3,23]. Our study demonstrated that retarded growth and lesions of pancreas were caused by low Se, but exudative diathesis was not observed because there was enough vitamin E in the diet.…”

Section: Discussionmentioning

confidence: 67%

The Cell Cycle Arrest and Apoptosis of Bursa of Fabricius Induced by Low Selenium in Chickens

Peng

Cui

et al. 2010

Biol Trace Elem Res

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The purpose of this 42-day study was to investigate the effects of low selenium (Se) on immune function by determining cell cycle and apoptosis of bursa of Fabricius. One hundred twenty 1-day-old avian broilers were randomly assigned to 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 relative weight of bursa was significantly decreased in low Se group from 28 days of age in time-dependent manner when compared with that of control group. Cell cycle analysis by flow cytometry showed that low Se caused an increase in G₀G₁ phase cells that corresponded to a decrease in S phase cells in bursa of Fabricius. Ultrastructurally, mitochondria injury and increased apoptotic cells with condensed nuclei were observed. Low Se increased the percentage of Annexin V-positive cells, as measured by flow cytometry, in comparison with that of control group. These data suggested that low Se diet restrained the development of bursa of Fabricius by cell cycle arrest and apoptosis.

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“…Although dietary Se deficiency is known to induce degenerative muscle diseases in a variety of species (5,9) in addition to chicks (4,10), it still remains elusive as to its initial mechanism of biochemical pathogenesis prior to the onset of overt clinical symptoms. Although the Se deficiency-induced oxidative stress (11) and antioxidant protection of selenoproteins such as glutathione peroxidases (GPx) (12) are perceived to be involved in the pathogenesis of Se deficiency-related diseases (13,14), there has been little direct evidence for such a link in the case of chicks, in particular in the early phase of disease development.…”

Section: Introductionmentioning

confidence: 99%

Gene Expression of Endoplasmic Reticulum Resident Selenoproteins Correlates with Apoptosis in Various Muscles of Se-Deficient Chicks

Yao

Zhang

et al. 2013

The Journal of Nutrition

185

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Dietary selenium (Se) deficiency causes muscular dystrophy in various species, but the molecular mechanism remains unclear. Our objectives were to investigate: 1) if dietary Se deficiency induced different amounts of oxidative stress, lipid peroxidation, and cell apoptosis in 3 skeletal muscles; and 2) if the distribution and expression of 4 endoplasmic reticulum (ER) resident selenoprotein genes (Sepn1, Selk, Sels, and Selt) were related to oxidative damages in these muscles. Two groups of day-old layer chicks (n = 60/group) were fed a corn-soy basal diet (33 μg Se/kg; produced in the Se-deficient area of Heilongjiang, China) or the diet supplemented with Se (as sodium selenite) at 0.15 mg/kg for 55 d. Dietary Se deficiency resulted in accelerated (P < 0.05) cell apoptosis that was associated with decreased glutathione peroxidase activity and elevated lipid peroxidation in these muscles. All these responses were stronger in the pectoral muscle than in the thigh and wing muscles (P < 0.05). Relative distribution of the 4 ER resident selenoprotein gene mRNA amounts and their responses to dietary Se deficiency were consistent with the resultant oxidative stress and cell apoptosis in the 3 muscles. Expression of Sepn1, Sels, and Selt in these muscles was correlated with (r > 0.72; P < 0.05) that of Sepsecs encoding a key enzyme for biosynthesis of selenocysteine (selenocysteinyl-tRNA synthase). In conclusion, the pectoral muscle demonstrated unique expression patterns of the ER resident selenoprotein genes and GPx activity, along with elevated susceptibility to oxidative cell death, compared with the other skeletal muscles. These features might help explain why it is a primary target of Se deficiency diseases in chicks.

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Pathology of Selenium Deficiency in the Chick

Cited by 77 publications

References 13 publications

Differential Effects of Sodium Selenite and Nano-Se on Growth Performance, Tissue Se Distribution, and Glutathione Peroxidase Activity of Avian Broiler

Differential Effects of Sodium Selenite and Nano-Se on Growth Performance, Tissue Se Distribution, and Glutathione Peroxidase Activity of Avian Broiler

The Cell Cycle Arrest and Apoptosis of Bursa of Fabricius Induced by Low Selenium in Chickens

Gene Expression of Endoplasmic Reticulum Resident Selenoproteins Correlates with Apoptosis in Various Muscles of Se-Deficient Chicks

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