Influences of Selenium on the Duckling Hepatic Mitochondrial Membrane Permeability Changes Induced by Aflatoxin B1

被引:0
|
作者
Shi, D. -Y. [1 ]
Liao, S. -Q. [2 ]
Guo, S. -N. [1 ]
Tang, Z. -X. [3 ]
机构
[1] South China Agr Univ, Coll Vet Med, Guangzhou, Guangdong, Peoples R China
[2] Guangdong Acad Agr Sci, Inst Vet Med, Guangzhou, Guangdong, Peoples R China
[3] South China Agr Univ, Coll Vet Med, Guangzhou, Guangdong, Peoples R China
关键词
Aflatoxin B-1; Hepatic mitochondrial; Membrane permeability; Duckling; Sodium selenite; OXIDATIVE STRESS; BREAST MUSCLE; TRANSITION; BROILERS; COMPLEX;
D O I
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中图分类号
T [工业技术];
学科分类号
08 ;
摘要
In order to observe the influences of aflatoxin B-1 (AFBI) on hepatic mitochondrial membrane permeability in ducklings and study the antagonistic effect of sodium selenite (Na2SeO3) on AFBI. Seven day-old ducklings were used as experimental animals. All animals were divided into three groups (30 animals each). The ducklings of group I was fed on the same volume of DMSO only with the other group as control. Group II, III were administered intragastrically AFB(1) at a dose 0.1mg/kg body weight respectively, and group HI was fed on sodium selenite at a dose 1mg/kg. All treatments were given once daily during 7-28 day-old. The duckling hepatic mitochondrial membrane permeability was detected on 7th, 14th, 21th day after treatment. The results showed that the ducklings hepatic mitochondrial membrane permeability in AFBI treated ducklings (Group II, III) was higher than group I (P < 0.05), and the hepatic mitochondrial membrane permeability of group II was higher than sodium selenite treated group (group III) (P < 0.05). These results revealed that sodium selenite could ameliorate the duckling hepatic mitochondrial membrane permeability changes induced by aflatoxin B-1.
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页码:171 / 174
页数:4
相关论文
共 12 条
  • [1] Mitochondrial free radical generation, oxidative stress, and aging
    Cadenas, E
    Davies, KJA
    [J]. FREE RADICAL BIOLOGY AND MEDICINE, 2000, 29 (3-4) : 222 - 230
  • [2] Feng Yao-sheng, 1997, J VET SCI TECHNOLOGY, V27, P28
  • [3] Mitochondria and apoptosis
    Green, DR
    Reed, JC
    [J]. SCIENCE, 1998, 281 (5381) : 1309 - 1312
  • [4] Regulated and unregulated mitochondrial permeability transition pores: a new paradigm of pore structure and function?
    He, LH
    Lemasters, JJ
    [J]. FEBS LETTERS, 2002, 512 (1-3) : 1 - 7
  • [5] Low feed efficient broilers within a single genetic line exhibit higher oxidative stress and protein expression in breast muscle with lower mitochondrial complex activity
    Iqbal, M
    Pumford, NR
    Tang, ZX
    Lassiter, K
    Wing, T
    Cooper, M
    Bottje, W
    [J]. POULTRY SCIENCE, 2004, 83 (03) : 474 - 484
  • [6] Johnson D., 1967, Methods Enzymol., V10, P94, DOI [10.1016/0076-6879(67)10018-9, DOI 10.1016/0076-6879(67)10018-9]
  • [7] Oxidative stress, mitochondrial permeability transition, and cell death in Cu-exposed trout hepatocytes
    Krumschnabel, G
    Manzl, C
    Berger, C
    Hofer, B
    [J]. TOXICOLOGY AND APPLIED PHARMACOLOGY, 2005, 209 (01) : 62 - 73
  • [8] The permeability transition pore complex:: A target for apoptosis regulation by caspases and Bcl-2-related proteins
    Marzo, I
    Brenner, C
    Zamzami, N
    Susin, SA
    Beutner, G
    Brdiczka, D
    Rémy, R
    Xie, ZH
    Reed, JC
    Kroemer, G
    [J]. JOURNAL OF EXPERIMENTAL MEDICINE, 1998, 187 (08): : 1261 - 1271
  • [9] Role of copper in mitochondrial biogenesis via interaction with ATP synthase and cytochrome c oxidase
    Medeiros, DM
    Jennings, D
    [J]. JOURNAL OF BIOENERGETICS AND BIOMEMBRANES, 2002, 34 (05) : 389 - 395
  • [10] Ruan Cui-cai, 1992, J GUANGXI MED U, V9, P8