title: Dietary modulation of parathion-induced neurotoxicity in adult and juvenile rats.
abstract: Previous studies indicated that dietary glucose (15% in drinking water) could markedly exacerbate the toxicity of parathion in adult rats. The present study evaluated the effect of consumption of the commonly used sweetener, high fructose corn syrup (HFCS), on parathion toxicity in adult and juvenile rats. Animals were given free access to either water or 15% HFCS in drinking water for a total of 10 days and challenged with parathion (6 or 18 mg/kg, s.c., for juveniles or adults, respectively) on the 4th day. Signs of cholinergic toxicity, body weight and chow/fluid intake were recorded daily. Acetylcholinesterase (AChE) activity and immunoreactivity (AChE-IR) in frontal cortex and diaphragm were measured at 2, 4, and 7 days after parathion. As HFCS was associated with significant reduction in chow intake, adult rats were also pair-fed to evaluate the effect of similar reduced chow intake alone on parathion toxicity. The results indicated that the cholinergic toxicity of parathion was significantly increased by HFCS feeding in both age groups. The excess sugar consumption, however, did not significantly affect parathion-induced AChE inhibition in either tissue or either age group. Enzyme immunoreactivity in frontal cortex was generally not affected in either age group while diaphragm AChE-IR was significantly reduced by parathion and HFCS alone in adult animals at 2 and 4 days timepoints, and more so by the combination of sugar feeding and parathion exposure in both age groups. Food restriction alone did not exacerbate parathion toxicity. While the mechanism(s) remains unclear, we conclude that voluntary consumption of the common sweetener HFCS can markedly amplify parathion acute toxicity in both juvenile and adult rats.
authors.affiliation: Department of Physiological Sciences, College of Veterinary Medicine, 264 McElroy Hall, Oklahoma State University, Stillwater, OK 74078, USA. popjl@okstate.edu
authors.forename: Jing
authors.initials: J
authors.lastname: Liu
authors.forename: Subramanya
authors.initials: S
authors.lastname: Karanth
authors.forename: Carey
authors.initials: C
authors.lastname: Pope
mesh_terms: D000110:Acetylcholinesterase / Q000378:metabolism; D000375:Aging / Q000187:drug effects / Q000378:metabolism*; D000818:Animals; D001835:Body Weight / Q000187:drug effects; D001921:Brain / Q000187:drug effects / Q000201:enzymology; D002800:Cholinesterase Inhibitors / Q000633:toxicity*; D004040:Dietary Carbohydrates / Q000008:administration & dosage*; D005260:Female; D005632:Fructose / Q000008:administration & dosage*; D008297:Male; D020258:Neurotoxicity Syndromes / Q000201:enzymology / Q000209:etiology*; D010278:Parathion / Q000633:toxicity*; D051381:Rats; D017207:Rats, Sprague-Dawley
chemical_list: D002800:Cholinesterase Inhibitors; D004040:Dietary Carbohydrates; D005632:Fructose; D010278:Parathion; D000110:Acetylcholinesterase