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Titolo:
Acute effects of an insect repellent, N,N-diethyl-m-toluamide, on cholinesterase inhibition induced by pyridostigmine bromide in rats
Autore:
Chaney, LA; Wineman, RW; Rockhold, RW; Hume, AS;
Indirizzi:
Univ Mississippi, Med Ctr, Dept Pharmacol & Toxicol, Jackson, MS 39216 USAUniv Mississippi Jackson MS USA 39216 ol & Toxicol, Jackson, MS 39216 USA
Titolo Testata:
TOXICOLOGY AND APPLIED PHARMACOLOGY
fascicolo: 2, volume: 165, anno: 2000,
pagine: 107 - 114
SICI:
0041-008X(20000601)165:2<107:AEOAIR>2.0.ZU;2-S
Fonte:
ISI
Lingua:
ENG
Soggetto:
BLOOD-BRAIN-BARRIER; TOXIC ENCEPHALOPATHY; PERCUTANEOUS-ABSORPTION; DERMAL APPLICATION; BRIEF EXPOSURE; HEAT-STRESS; DEET; PHARMACOKINETICS; DIETHYLTOLUAMIDE; NEUROPATHOLOGY;
Keywords:
cholinesterase inhibitors; cholinesterase; pyridostigmine bromide; DEET; N,N-diethyl-m-toluamide; insect repellent; organophosphates; toxicity; Gulf War illnesses;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
63
Recensione:
Indirizzi per estratti:
Indirizzo: Chaney, LA MCHB, TS, TTE, 5158 Blavkhawk Rd, Aberdeen Proving Ground, MD 21010 USA MCHB 5158 Blavkhawk Rd Aberdeen Proving Ground MD USA 21010 USA
Citazione:
L.A. Chaney et al., "Acute effects of an insect repellent, N,N-diethyl-m-toluamide, on cholinesterase inhibition induced by pyridostigmine bromide in rats", TOX APPL PH, 165(2), 2000, pp. 107-114

Abstract

Acute lethal interactions have been previously described between a cholinesterase (ChE) inhibitor, pyridostigmine bromide (PB), and the insect repellent, N,N-diethyl-m-tolumaide (DEET). The mechanism of toxic interaction between these agents is unknown. Alterations in membrane permeability caused by DEET could facilitate or enhance absorption, or alter the distribution ofperipherally restricted PB, causing increased inhibition of ChE at a givendose. Studies were conducted to investigate PB-induced ChE inhibition in the presence of DEET. Rats received ip injections of PB (1, 2, or 3 mg/kg), DEET (200 mg/kg), or PB + DEET at doses that potentiated acute lethality. ChE activity was measured in heart, diaphragm, blood, whole brain, or specific brain areas using a modified spectrophotometric assay. DEET did not alter PB-induced inhibition of ChE activity in rat diaphragm, heart, or blood. Administration of DEET alone had no effect on ChE activity. PB alone did not inhibit ChE in whole brain, but PB (3 mg/kg) + DEET (200 mg/kg) caused significant inhibition of whole brain ChE activity to approximately 60% of controls. In specific brain areas, (cortex, cerebellum, medulla, hypothalamus, hippocampus, midbrain, and striatum) PB alone did not inhibit ChE activity. PB (3 mg/kg) + DEET (200 mg/kg) reduced ChE activity to approximately 65-75% of controls in each brain area, but those results were not statistically significant. In conclusion, DEET did not alter PB-induced inhibition of ChE activity in the periphery. While DEET may have facilitated the access of PB into the CNS at high doses, it is doubtful that the resulting minor reduction in ChE activity would have resulted in death. It is unlikely that the lethal interaction between PB and DEET is mediated through a cholinergiceffect resulting from increased inhibition of ChE. (C) 2000 Academic Press.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 29/09/20 alle ore 13:19:27