Organophosphorus poisoning-induced delayed neuropathy hen model induced by triorthocresyl phosphate and phenylmethylsulfonyl fluoride intervention
10.3969/j.issn.2095-4344.2014.49.003
- VernacularTitle:磷酸三邻甲苯酯诱导鸡迟发神经毒性模型和苯甲基磺酰氟的预处理
- Author:
Enjun ZUO
;
Fengyuan PIAO
;
Ying JIANG
- Publication Type:Journal Article
- Keywords:
tissue engineering;
organophosphorus compound;
cytoskeleton;
mitochondrion;
endoplasmic reticulum
- From:
Chinese Journal of Tissue Engineering Research
2014;(49):7884-7890
- CountryChina
- Language:Chinese
-
Abstract:
BACKGROUND:Although incidents of organophosphorus poisoning-induced delayed neuropathy (OPIDN) have been documented for over a century, the molecular mechanisms underlying the axonopathy remain poorly understood. Therefore, OPIDN treatment has been increasingly concerned. OBJECTIVE:To construct the OPIDN hen model induced by triorthocresyl phosphate (TOCP) and to explore the effect of phenylmethylsulfonyl fluoride (PMSF) intervention. METHODS:Adult hens were randomly divided into four groups: two TOCP groups, a PMSF group and a control group. TOCP groups were treated with TOCP by gavage at a single dosage of 1 000 mg/kg and 750 mg/kg respectively; control group was given an equivalent volume of saline by gavage while hens in the PMSF group were subcutaneously injected with 40 mg/kg PMSF 24 hours after 1 000 mg/kg TOCP injection. OPIDN neurological signs were assessed by a six-point graded scale. The changes of the hen weight were recorded. The hens were kiled on day 5 and 21 post-dosing. The samples were cut into 50 nm thick sections and examined by transmission electron microscopy. RESULTS AND CONCLUSION:OPIDN neurological signs such as abnormal gaits progressed in severity with time (P < 0.05), and the hen weight was significantly decreased in TOCP groups (P < 0.05). However, no clinical signs of delayed neurotoxicity were observed in hens of the PMSF group and the control group during the experiment period. The mild mitochondrial sweling and the fragmentation of microfilament and microtubule arrangement in axons were observed on day 5 post-dosing, leaving the other organeles remained unchanged. On day 21, neuronal degeneration was apparent, including sweling of endoplasmic reticulum, abnormal change of mitochondria, and disordered arrangement of cytoskeleton. The optimal dose of TOCP was 1 000 mg/kg. Experimental findings indicate that, OPIDN hen model induced by TOCP and PMSF intervention hen model were successfuly constructed. PMSF intervention significantly improved the pathologic changes and clinical symptoms of OPIDN induced by TOCP in hens.
