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Effect Of Selenium On Oxidative Stress Injury Induced By Chromium(?) In The Chicken Brain

Posted on:2018-09-06Degree:MasterType:Thesis
Country:ChinaCandidate:P HaoFull Text:PDF
GTID:2323330515450640Subject:Clinical Veterinary Medicine
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The intake of hexavalent chromium can promote the body to produce cancer cells,mutations and other adverse effects.And lead to liver toxicity,lipid metabolism,mesenteric lymph nodes and other non-cancerous effects.As early as 2007 to 2011,the CDC of US has been listed chromium substances as a priority element.And because of human's wrong way,chromium???will still through by food,drinking water,daily necessities and other means into the body.Studies have shown that selenium?Se?can be combined with heavy metals through the complex interactions to reduce heavy metal toxicity.But selenium and chromium???have seldom been studied,our experiment aim was to evaluate the effect of Se supplementation at different doses in chicken brains,and determine the optimal dose for alleviating the toxic effects.In our study,acute poisoning experiments were carried out firstly,and determine the median lethal dose(LD50)and poisoning dose(6%LD50).A total of 105 Hyland brown male chickens were randomly divided into seven groups,including the control group,poisoned group [6%LD50 K2Cr2O7 body weight?B.W.?],and detoxification groups K2Cr2O7(6%LD50)+ Se?0.31,0.63,1.25,2.50,and 5.00 Na2SeO3 mg/kg B.W.?orally in water for 42 days.Each group of 15 chickens were weighed and sacrificed at 14?28 and 42 days according to the standard method.One part of organization was made into pathological sections,the others were made into homogenates.The chickens were detected by the activities of brain body ratio,superoxide dismutase?SOD?,malondialdehyde?MDA?,glutathione?GSH?,Ca2+-ATPase,and mitochondrial membrane potential?MMP?.The results showed that the brain body ratio and SOD level of 5.00 mg/kg Se supplement group were significantly higher than the other experimental groups,and declined with the prolonging time.The GSH level in the poisoned groups significantly decreased compared with the control group,Se increased the levels of GSH and peaked in the group of 1.25 mg/kg,but the GSH level also decreased significantly with the high concentration of Se.MDA levels were the highest in the poisoning group and lowest in the 0.63mg/kg Se supplementation group,while the level of GSH and MDA werenot significantly difference with the poisoning group.Ca2+-ATPase was mainly present in the mitochondrial lumen,sarcoplasmic reticulum and endoplasmic reticulum.In our study,Ca2+-ATPase activity of the poisoning group decreased significantly compared with the control group,Se treatment of 0.63 mg/kg B.W restored the levels of Ca2+-ATPase significantly compared with the poisoned groups.By contrast,Se supplementation of 2.50 and 5.00 mg/kg made these levels even lower than those of the poisoned groups.The result of MMP was agree with Ca2+-ATPase,MMP in K2Cr2O7 presented a significant decline compared with the control group.0.63 mg/kg Se significantly restored the MMP level to near normal values.However,Se supplementation of 5.00 mg/kg produced a significant inhibition to MMP.Histopathological examination showed that 0.63 mg/kg Se supplementation had significant recovery the vacuoles of neurons,capillaries and small vessel,and Se also inhibited the disorganization and reduction in Purkinje cells.In conclusion,Cr???exposure caused oxidative stress.Se exerted a remission effect on toxic responses in chicken brains.However,a high Se concentration was synergistic to the toxic effect of Cr???.
Keywords/Search Tags:Cr(?), Na2SeO3, Oxidative stress, Mitochondrial membrane potential, Ca2+-ATPase
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