Histological Lesion of Spleen and Inhibition of Splenocyte Proliferation in Broilers Fed on Diets Excess in Selenium

Fang

et al. 2014

IJERPH

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Aflatoxin B1 (AFB1), which causes hepatocellular carcinoma and immune-suppression, is commonly found in feedstuffs. To evaluate the ability of selenium (Se) to counteract the deleterious effects of AFB1, two hundred 1-day-old male avian broilers, divided into five groups, were fed with basal diet (control group), 0.3 mg/kg AFB1 (AFB1 group), 0.3 mg/kg AFB1+0.2 mg/kg Se (+Se group I), 0.3 mg/kg AFB1+0.4 mg/kg Se (+Se group II) and 0.3 mg/kg AFB1+0.6 mg/kg Se (+Se group III), respectively. Compared with control group, the relative weight of spleen in the AFB1 group was decreased at 21 days of age. The relative weight of spleen in the three +Se groups was higher than that in the AFB1 group. By pathological observation, the major spleen lesions included congestion in red pulp and vacuoles appeared in the lymphatic nodules and periarterial lymphatic sheath in the AFB1 group. In +Se groups II and III, the incidence of major splenic lesions was decreased. The percentages of CD3+, CD3+CD4+ and CD3+CD8+ T cells in the AFB1 group were lower than those in control group from 7 to 21 days of age, while there was a marked increase in the three +Se groups compared to the AFB1 group. The results indicated that sodium selenite could improve the cellular immune function impaired by AFB1 through increasing the relative weight of spleen and percentages of splenic T cell subsets, and alleviating histopathological spleen damage.

Section: Discussionsupporting

confidence: 43%

Effects of Dietary Selenium on Histopathological Changes and T Cells of Spleen in Broilers Exposed to Aflatoxin B1

Chen

Fang

et al. 2014

IJERPH

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“…Application of the TUNEL staining assay furthermore showed that apoptotic cells with brown-stained nuclei distributed within the red pulp and white pulp of the spleens and had increased frequency of occurrence in 10 and 15 mg/kg Se groups in comparison with that of 0.2 mg/kg Se group. Characteristics of ultrastructural morphological features of apoptotic splenocytes include nuclear membrane breakdown, chromatin condensation and fragmentation, as we reported recently [14]. It has been demonstrated that sodium selenite-induced apoptosis is likely to be caused by DNA damage [11].…”

Section: Discussionsupporting

confidence: 59%

“…In our recent study [14][15][16], we found that excess dietary sodium selenite in the range of 5~15 mg/kg caused histological lesions of the thymus, bursa of Fabricius, and spleens in chickens. In the present study, apoptosis of splenocytes was determined by flow cytometer method, and glutathione peroxidase (GSH-Px), superoxide dismutase (SOD), and catalase (CAT) activities as well as malondialdehyde (MDA) contents in spleens were measured to assess the oxidative status of spleen.…”

Section: Introductionmentioning

confidence: 91%

Excess Dietary Sodium Selenite Alters Apoptotic Population and Oxidative Stress Markers of Spleens in Broilers

Cui

et al. 2011

Biol Trace Elem Res

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Three hundred 1-day-old avian broilers were fed on a basic diet (0.2 mg/kg selenium) or the same diet amended to contain 1, 5, 10, and 15 mg/kg selenium supplied as sodium selenite (n = 60/group). In comparison with those of 0.2 mg/kg selenium group, the percentages of annexin V-positive splenocytes were increased in 5, 10, and 15 mg/kg selenium groups. TUNEL assay revealed that apoptotic cells with brown-stained nuclei distributed within the red pulp and white pulp of the spleens with increased frequency of occurrence in 10 and 15 mg/kg selenium groups in comparison with that of 0.2 mg/kg Se group. Sodium selenite-induced oxidative stress in spleens of chickens was evidenced by decrease in glutathione peroxidase, superoxide dismutase, and catalase activities and increase in malondialdehyde contents. The results indicate that excess dietary selenium in the range of 5-15 mg/kg of feed causes oxidative stress, which may be mainly responsible for the increased apoptosis of splenocytes in chickens.

“…Se is an essential micronutrient to humans and animals and is required for anti-oxidant selenoenzymes [41], but high concentration of Se is toxic when it excesses the threshold [42]. According to previous study, Se could alleviate the destructive oxidative stress caused by various factors, like heroin, adriamycin, and cisplatin [43,44,45].…”

Section: Discussionmentioning

confidence: 99%

Protective Effects of Sodium Selenite against Aflatoxin B1-Induced Oxidative Stress and Apoptosis in Broiler Spleen

Wang

Shu

et al. 2013

IJERPH

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The aim of this study was to investigate the possible protective role of sodium selenite on aflatoxin B1-induced oxidative stress and apoptosis in spleen of broilers. Two hundred one-day-old male broilers, divided into five groups, were fed with basal diet (control group), 0.3 mg/kg AFB1 (AFB1 group), 0.3 mg/kg AFB1 + 0.2 mg/kg Se (+Se group I), 0.3 mg/kg AFB1 + 0.4 mg/kg Se (+Se group II) and 0.3 mg/kg AFB1 + 0.6 mg/kg Se (+Se group III), respectively. According to biochemical assays, AFB1 significantly decreased the activities of glutathione peroxidase, total superoxide dismutase, glutathione reductase, catalase and the level of glutathione hormone, while it increased the level of malondialdehyde. Moreover, AFB1 increased the percentage of apoptosis cells by flow cytometry and the occurrence of apoptotic cells by TUNEL assay. Simultaneous supplementation with sodium selenite restored these parameters to be close to those in control group. In conclusion, sodium selenite exhibited protective effects on AFB1-induced splenic toxicity in broilers by inhibiting oxidative stress and excessive apoptosis.