Spinal cord neuronal apoptosis induced by triorthocresyl phosphate poisoning in hens.
- Author:
Ying-peng WANG
1
;
Jun-feng SONG
;
Zhi-ren RAO
;
Dan-lei MOU
Author Information
- Publication Type:Journal Article
- MeSH: Animals; Apoptosis; drug effects; Chickens; Female; In Situ Nick-End Labeling; Insecticides; toxicity; Models, Animal; Neurons; drug effects; Spinal Cord; drug effects; Tritolyl Phosphates; toxicity
- From: Chinese Journal of Industrial Hygiene and Occupational Diseases 2004;22(1):19-21
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo investigate the role of neuronal apoptosis in organophosphorus poisoning-induced delayed neuropathy (OPIDN) and its dynamic pathological changes.
METHODSTo establish OPIDN animal model, triorthocresyl phosphate (TOCP)was given to hens with a single dose (1 000 mg/kg, im). Changes of neuropathology, number of neurons and apoptotic cells in the third lumbar spinal cord were observed by HE, Nissl and TUNEL methods 3, 5, 7, 10, 14, 18 days after injection.
RESULTSThe hens showed OPIDN typical signs (progressive ataxia and hypotonia) about 9 days after TOCP exposure. HE staining revealed dark red nucleus in neurons of anterior horn of lumbar spinal cord 5 days after exposure, but this phenomenon disappeared 18 days later. Nissl method showed that the number of neurons in anterior horn of spinal cord decreased [from (82 +/- 4) cell/mm(2) to (66 +/- 6) cell/mm(2)]. TUNEL positive cells began to appear [(22 +/- 2) cell/mm(2)] 5 days after TOCP exposure, and reached the peak [(27 +/- 3) cell/mm(2)] 7 days later, and disappeared 18 days later.
CONCLUSIONNeuronal apoptosis in anterior horn of spinal cord of hens appeared in OPIDN, suggesting that cellular apoptosis may play an important role in the pathogenesis of OPIDN.