title: [Changes in autophagy-related protein levels in nervous tissues of hens with tri-ortho-cresyl phosphate-induced delayed neuropathy].
abstract: OBJECTIVE
  To study the changes in the levels of autophagy-related proteins, Atg1, Atg5, and Beclin1, in organophosphate-induced delayed neuropathy (OPIDN) caused by tri-ortho-cresyl phosphate (TOCP), and to investigate the molecular pathogenic mechanism of OPIDN.
  
  
  METHODS
  Thirty adult Roman hens were randomly and equally divided into control group and 1, 5, 10, and 21 d intoxication groups. Each hen in the intoxication group was administered TOCP by gavage at a single dose of 750 mg/kg, while each hen in the control group was administered the same volume of corn oil. The hens were killed at the corresponding time points, and their tibial nerves and spinal cords were collected. The levels of Atg1, Atg5, and Beclin1 in the tibial nerves and spinal cords were measured by immunoblotting.
  
  
  RESULTS
  Compared with those in the control group, the levels of Atg1 in tibial nerves decreased by 29.8%, 64.4%, 43.5%, and 19.8% at 1, 5, 10, and 21 d, respectively, after intoxication ((P < 0.05); the levels of Atg5 in tibial nerves decreased by 36.8%, 49.6%, 51.2%, and 31.5% at 1, 5, 10, and 21 d, respectively, after intoxication (P < 0.05); the levels of Beclin1 in tibial nerves decreased by 68.5%, 66.3%, and 32.2% at 1, 5, and 10 d, respectively, after intoxication (P < 0.05). Compared with those in the control group, the levels of Atg1 in spinal cords decreased by 23.5%, 48.7%, and 20% at 1, 5, and 10 d, respectively, after intoxication (P < 0.05); the levels of Atg5 in spinal cords decreased by 32.7%, 51.5%, 47.3%, and 39.6% at 1, 5, 10, and 21 d, respectively, after intoxication (P < 0.05); the levels of Beclin1 in spinal cords decreased by 28.9%, 50.2%, 43.2%, and 28.3% at 1, 5, 10, and 21 d, respectively, after intoxication (P < 0.05).
  
  
  CONCLUSIONS
  The intoxication of TOCP is associated with the significant changes in the levels of autophagy-related proteins in the nervous tissues of hens, which might be involved in the pathogenesis of OPIDN.
authors.affiliation: Institute of Toxicology, Shandong University, Jinan 250012, China.
authors.forename: Chao-shuang
authors.initials: CS
authors.lastname: Zou
authors.forename: Rui-rui
authors.initials: RR
authors.lastname: Kou
authors.forename: Yuan
authors.initials: Y
authors.lastname: Gao
authors.forename: Ke-qin
authors.initials: KQ
authors.lastname: Xie
authors.forename: Fu-yong
authors.initials: FY
authors.lastname: Song
mesh_terms: D000818:Animals; D051017:Apoptosis Regulatory Proteins / Q000378:metabolism*; D001343:Autophagy / Q000187:drug effects*; D002645:Chickens; D005260:Female; D047908:Intracellular Signaling Peptides and Proteins / Q000378:metabolism; D008869:Microtubule-Associated Proteins / Q000378:metabolism; D009422:Nervous System Diseases / Q000139:chemically induced / Q000378:metabolism*; D016900:Neurofilament Proteins / Q000378:metabolism*; D013116:Spinal Cord / Q000378:metabolism; D013979:Tibial Nerve / Q000378:metabolism; D014317:Tritolyl Phosphates / Q000633:toxicity*
chemical_list: D051017:Apoptosis Regulatory Proteins; D047908:Intracellular Signaling Peptides and Proteins; D008869:Microtubule-Associated Proteins; D016900:Neurofilament Proteins; D014317:Tritolyl Phosphates