US EPA

2731520 

Journal Article 

Review 

The pathogenesis of organophosphate polyneuropathy 

Lotti, M 

1992 

Yes 

Critical Reviews in Toxicology
ISSN: 1040-8444
EISSN: 1547-6898 

Informa Healthcare 

BIOSIS/92/12441 

21 

6 

465-487 

English 

1666291 

10.3109/10408449209089884 

WOS:A1992HD20600004 

BIOSIS COPYRIGHT: BIOL ABS. This review discusses the facts regarding organophosphate-induced delayed polyneuropathy (OPIDP) as they as related to its pathogenesis rather than being a comprehensive review of all available data. Neuropathy target esterase (NTE) is considered to be the molecular target for OPIDP which is affected by several esterase inhibitors. Such inhibitors are ranked according to their toxicological efects as follows: 1. Phosphates, phosphoroamidates, and phosphonates cause OPIDP when high amounts of NTE are inhibited. In most cases 70 to 80% inhibition is enough, whereas in others much more is required. 2. Phosphinates, carbamates, and sulfonyl halides cause either protection from or promotion of OPIDP when given before or after a neuropathic OP, respectively. Both effects are related to doses that inhibit NTE. Neuropathy is also caused by the combined treatment with a carbamate and a sulfonyl fluoride. The potency of a given NTE inhibitor to cause OPIDP is related to the chemis 

Biomonitoring; Esterase inhibitors; Mechanism; Neuropathy target esterase; NTE; OPIDP; Organophosphate polyneuropathy; Promotion; Protection; Risk assessment; atropine; calcium antagonist; corticosteroid; ganglioside; methylprednisolone; neurotoxic esterase; organophosphate; organophosphate pesticide; biological monitoring; chicken; enzyme inhibition; histopathology; human; nonhuman; polyneuropathy; priority journal; review; risk assessment; Animal; Central Nervous System Diseases; Environmental Monitoring; Esterases; Human; Nervous System Diseases; Organophosphorus Compounds; Peripheral Nervous System Diseases; Risk Factors; Support, Non-U.S. Gov't