Protective Effect of Vitamin E on Cadmium-Induced Renal Oxidative Damage and Apoptosis in Rats.

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.

Selenium Rescues Aflatoxin B1-Inhibited T Cell Subsets and Cytokine Levels in Cecal Tonsil of Chickens.

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.

Effect of selenium supplementation on aflatoxin B1-induced histopathological lesions and apoptosis in bursa of Fabricius in broilers.

To investigate the effects of sodium selenite against aflatoxin B1 (AFB 1), 200 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 the control group, decreased relative weight of bursa of Fabricius and contents of serum immunoglobulin, more vacuoles and debris in the bursal lymphoid follicle, and increased percentage of apoptotic bursal cells were observed in the AFB1 group. Sodium selenite, however, could increase the relative weight of bursa of Fabricius and contents of serum immunoglobulin, and ameliorate histopathological lesions. The percentages of apoptotic bursal cells, through flow cytometry and terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling method, in the three +Se groups were lower than those in the AFB 1 group. Compared with the AFB 1 group, moreover, the mRNA expressions of Bax and Caspase-3 by qRT-PCR in the three +Se groups were decreased, while the expression of Bcl-2 was increased. The results indicate that sodium selenite in diet can protect chicken from AFB 1-induced impairment of humoral immune function by reducing bursal histopathological lesions and percentages of apoptotic bursal cells.

Effects of dietary selenium on histopathological changes and T cells of spleen in broilers exposed to aflatoxin B1.

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.

Protective effects of sodium selenite against aflatoxin B1-induced oxidative stress and apoptosis in broiler spleen.

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.

Protective role of sodium selenite on histopathological lesions, decreased T-cell subsets and increased apoptosis of thymus in broilers intoxicated with aflatoxin B1.

For evaluating the ability of selenium (Se) in counteracting the adverse effects of aflatoxin B1 (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), 0.3mg/kg AFB1+0.4 mg/kg Se (+Se group II) and 0.3mg/kg AFB1+0.6 mg/kg Se (+Se group III), respectively. Compared with control group, the decreased relative weight of thymus and percentages of mature thymocytes, congestion in medulla and much debris in cortex of thymus, and the increased apoptotic thymocytes were observed in AFB1 group. However, supplied dietary sodium selenite could increase the relative weight of thymus and percentages of mature thymocytes, and alleviate histopathological lesions. Compared with AFB1 group, the percentages of apoptotic thymocytes detected by terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling method and flow cytometry method in three +Se groups were decreased, the expression of Caspase-3 and Bax, through quantitative real-time PCR and immunohistochemical method, in three +Se groups were decreased, while the expression of Bcl-2 was increased. The results indicate that sodium selenite supplied in the diet, through a mechanism of apoptosis regulation, may ameliorated AFB1-induced lesions of thymus and accordingly improve the impaired cellular immune function.