Literature DB >> 16249959

Repeated spike exposure to the insecticide chlorpyrifos interferes with the recovery of visual sensitivity in rats.

Andrew M Geller1, Laura D Sutton, Renée S Marshall, Deborah L Hunter, Victoria Madden, Robert L Peiffer.   

Abstract

Reports from Japan and India and data submissions to the US EPA indicate that exposure to cholinesterase (ChE)-inhibiting organophosphorous insecticides (OP) can produce ocular toxicity, in particular long-lasting changes in retinal physiology and anatomy. We have examined the effects of a 1 year dietary exposure to the OP chlorpyrifos (CPF) on retinal structure and function. Adult male Long-Evans rats were fed CPF in their diet at the rate of 0, 1 (low), or 5 (high) mg/kg body weight/day. In addition, half of each feeding group received an oral (spike) dose of CPF in corn oil (45 mg/kg) or corn oil (VEH) alone every 2 months, resulting in six exposure groups: Control-VEH, Control-CPF, Low-VEH, Low-CPF, High-VEH, and High-CPF. Dark-adapted electroretinograms (ERG) were measured 3-5 months (n= 15-18/group) after the completion of dosing. There were no significant differences between dose or spike groups in a-wave, b-wave, or oscillatory potential amplitudes or implicit times. In addition, the time course of dark adaptation were measured in a subset of these rats (6-8/group) eight months after the completion of dosing by determining the flash intensity needed to elicit a 40 microV b-wave at selected intervals after bleaching 90% of the photopigment. Rats receiving the episodic oral spike of CPF showed a slowed recovery of dark-adapted sensitivity compared to rats receiving the corn oil VEH across chronic dosing conditions. No effects were seen on retinal morphology. This result suggests that episodic high dose exposures to CPF may result in altered retinal function. This effect, akin to effects seen in aging humans and humans exposed to other ChE-inhibiting compounds, may reflect alterations in the photoreceptors and retinal pigment epithelium (RPE) complex necessary for regenerating photopigment.

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Year:  2005        PMID: 16249959     DOI: 10.1007/s10633-005-7347-8

Source DB:  PubMed          Journal:  Doc Ophthalmol        ISSN: 0012-4486            Impact factor:   2.379


  34 in total

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Authors:  G R Jackson; C Owsley; G McGwin
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Journal:  J Neurosci Methods       Date:  2000-10-30       Impact factor: 2.390

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5.  Developmental lead exposure selectively alters the scotopic ERG component of dark and light adaptation and increases rod calcium content.

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Journal:  Vision Res       Date:  1992-02       Impact factor: 1.886

6.  [Long termed follow up study of chronic organophosphate pesticide intoxication (Saku disease) with special reference to retinal pigmentary degeneration (author's transl)].

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Journal:  Nippon Ganka Gakkai Zasshi       Date:  1974-05-10

7.  Retinal degeneration in licensed pesticide applicators.

Authors:  F Kamel; W K Boyes; B C Gladen; A S Rowland; M C Alavanja; A Blair; D P Sandler
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8.  Age- and gender-related differences in the time course of behavioral and biochemical effects produced by oral chlorpyrifos in rats.

Authors:  V C Moser; S Padilla
Journal:  Toxicol Appl Pharmacol       Date:  1998-03       Impact factor: 4.219

9.  Fenthion produces a persistent decrease in muscarinic receptor function in the adult rat retina.

Authors:  P Tandon; S Padilla; S Barone; C N Pope; H A Tilson
Journal:  Toxicol Appl Pharmacol       Date:  1994-04       Impact factor: 4.219

10.  Validation of the use of 6,6'-dithiodinicotinic acid as a chromogen in the Ellman method for cholinesterase determinations.

Authors:  S Willig; D L Hunter; P D Dass; S Padilla
Journal:  Vet Hum Toxicol       Date:  1996-08
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Review 2.  Retinal Toxicity Induced by Chemical Agents.

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3.  Paraoxonase enzyme protects retinal pigment epithelium from chlorpyrifos insult.

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  3 in total

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