A comparative study of delayed neurotoxicity in hens following repeated administration of organophosphorus compounds.
نویسندگان
چکیده
Hens treated with Mipafox (10 mg/kg, sc), sarin (50 micrograms/kg, sc) or parathion (1 mg/kg, sc) daily for 10 days exhibited severe, moderate and no ataxia respectively on 14th day after the start of exposure. The neurotoxic esterase (NTE) activity was significantly inhibited in the brain, spinal cord and platelets of hens treated with mipafox or sarin whereas no change was noticed with parathion treatment. All three compounds significantly inhibited acetylcholinesterase (AChE) activity in the platelets. Spinal cord of hens treated with mipafox, sarin or parathion showed axonal degeneration heavy, moderate and none respectively. It is concluded that repeated administration of equitoxic doses of mipafox, sarin and parathion to hens are marked, moderate and non-delayed neurotoxic respectively.
منابع مشابه
Organophosphorus and other inhibitors of brain 'neurotoxic esterase' and the development of delayed neurotoxicity in hens.
1. The delayed neurotoxic effects of some organophosphorus compounds are associated with phosphorylation of the active site of a nervous-tissue enzyme capable of hydrolysing phenyl phenylacetate. 2. Neurotoxic organophosphorus compounds and some carbamates and sulphonyl fluorides progressively inhibit the enzyme, attaching a substituent covalently at the active site. 3. Prolonged inhibition of ...
متن کاملThe delayed neurotoxic effect of some organophosphorus compounds. Identification of the phosphorylation site as an esterase.
1. Organophosphorus compounds that produce a delayed neurotoxic effect in hens phosphorylate a specific site in the brain soon after administration. 2. Phosphorylation of the specific site by di-isopropyl [(32)P]phosphorofluoridate in vitro is blocked by the prior addition of phenyl phenylacetate. 3. A small proportion of the total activity of hen brain hydrolysing phenyl phenylacetate in vitro...
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Delayed neurotoxicity experiments of an organophosphorus compound, TOCP, on hens and quails were carried out. The animals were orally exposed with TOCP in dose of 400 mg/kg, and maintained for 25 and 50 days under observation, respectively. They were sacrificed and dissected at different periods after the exposure, and the histopathological examinations were made on those animals. During the pe...
متن کاملDisturbed phospholipid homeostasis in endoplasmic reticulum initiates tri-o-cresyl phosphate-induced delayed neurotoxicity
Tri-o-cresyl phosphate (TOCP) is a widely used organophosphorus compound, which can cause a neurodegenerative disorder, i.e., organophosphate-induced delayed neurotoxicity (OPIDN). The biochemical events in the initiation of OPIDN were not fully understood except for the essential inhibition of neuropathy target esterase (NTE). NTE, located in endoplasmic reticulum (ER), catalyzes the deacylati...
متن کاملEffects of prednisolone and complex of vitamin B1, B2, B6 and B12 on organophosphorus compound-induced delayed neurotoxicity.
Protective effects of prednisolone as a synthetic adrenal cortical hormone and complex of vitamin B(1), B(2), B(6) and B (12) on organophosphorus compound-induced delayed neurotoxicity (OPIDN) caused by leptophos and tri-o-cresyl phosphate (TOCP) as organophosphates (OPs) were examined. Nine groups of hens (six for each) were used. Eight groups received intravenous injection of 30 mg/kg of lept...
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ورودعنوان ژورنال:
- Indian journal of physiology and pharmacology
دوره 39 1 شماره
صفحات -
تاریخ انتشار 1995