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Titolo:
Glucose feeding exacerbates parathion-induced neurotoxicity
Autore:
Olivier, K; Liu, J; Karanth, S; Zhang, H; Roane, DS; Pope, CN;
Indirizzi:
Univ Louisana, Coll Pharm, Dept Toxicol, Monroe, LA USA Univ Louisana Monroe LA USA na, Coll Pharm, Dept Toxicol, Monroe, LA USA Univ Louisana, Coll Pharm, Dept Basic Pharmaceut Sci, Monroe, LA USA Univ Louisana Monroe LA USA m, Dept Basic Pharmaceut Sci, Monroe, LA USA
Titolo Testata:
JOURNAL OF TOXICOLOGY AND ENVIRONMENTAL HEALTH-PART A
fascicolo: 4, volume: 63, anno: 2001,
pagine: 253 - 271
SICI:
1528-7394(20010622)63:4<253:GFEPN>2.0.ZU;2-V
Fonte:
ISI
Lingua:
ENG
Soggetto:
BRAIN PROTEIN-SYNTHESIS; PHOSPHOROTHIONATE INSECTICIDES; CHOLINESTERASE INHIBITION; ACUTE TOXICITY; ADULT-RATS; PESTICIDES; ACETYLCHOLINESTERASE; CHLORPYRIFOS; PARAOXON; MOUSE;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Agriculture,Biology & Environmental Sciences
Life Sciences
Citazioni:
50
Recensione:
Indirizzi per estratti:
Indirizzo: Pope, CN Oklahoma State Univ, Coll Vet Med, Dept Physiol Sci, 264 Vet Med,Stillwater, OK 74078 USA Oklahoma State Univ 264 Vet Med Stillwater OK USA74078 74078 USA
Citazione:
K. Olivier et al., "Glucose feeding exacerbates parathion-induced neurotoxicity", J TOX E H A, 63(4), 2001, pp. 253-271

Abstract

Excessive dietary intake of sugars could alter various biotransformation processes and the pharmacological and toxicological properties of numerous xenobiotics. In the present study, the effects of glucose supplementation were examined on the neurotoxicity of the organophosphorus (OP) pesticide parathion (PS) and its active metabolite, paraoxon ( PO), a potent inhibitor of acetylcholinesterase (AChE). Rats ( n = 6-12/treatment group) were given free access to tap water or 15% glucose (w/v) in tap water beginning 7 d prior to OP toxicant exposure. Food, caloric intake, and body weight were measured daily. Animals were challenged with either PS (4.5, 9, or 18 mg/kg, sc) or PO (0.3, 0.5, or 0.7 mg/kg, sc) and clinical signs of neurotoxicity (i.e., autonomic dysfunction, involuntary movements) were recorded daily for the following 13 d. Glucose feeding was associated with a dramatic drop (similar to 50%) in feed intake and an increase (similar to 20%) in total caloric consumption over the 7 d prior to OP exposure. Functional toxicity associated with PS exposure was increased in glucose-fed (GF) rats, but the glucose diet had no apparent effect on clinical signs of toxicity following PO treatment. Glucose feeding increased the magnitude of AChE inhibition inthe frontal cortex and plasma at lower dosages (i.e., 4.5 and 9 mg/kg) 3 dfollowing PS treatment. Time-course studies (3, 7, and 11 d after PS exposure, 18 mg/kg, sc) indicated significantly greater brain and plasma AChE inhibition in glucose-fed animals at later time points. In contrast, glucose feeding had no effect on the degree of AChE inhibition following PO exposure. Neither liver microsomal oxidative desulfuration of PS, nor liver or plasma paraoxonase, nor liver or plasma carboxylesterase activities were measurably affected by glucose feeding. Downregulation of muscarinic receptors 7d after PS exposure (18 mg/kg, sc) was more extensive in GF rats. It is postulated that excessive glucose consumption decreases the intake of other dietary components, in particular amino acids, limiting the de novo synthesis of AChE and consequent recovery of synaptic transmission. Due to the shorter duration of inhibition following PO exposure, spontaneous reactivation of AChE may be more important than de novo protein synthesis in recovery offunction, and thus with the effects of glucose feeding on its toxicity. Individuals that derive a large proportion of their calories from sugars may be at higher risk of acute toxicity from organophosphorus pesticides such as PS.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 23/10/20 alle ore 14:23:29