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Modulation of microvascular function following low-dose exposure to the organophosphorous compound malathion in human skin in vivo

Modulation of microvascular function following low-dose exposure to the organophosphorous compound malathion in human skin in vivo
Modulation of microvascular function following low-dose exposure to the organophosphorous compound malathion in human skin in vivo
This study investigates whether malathion, a widely used organophosphate insecticide, has its effects on cutaneous vasculature in healthy human volunteers through its anticholinergic activity or through the modulation of other, noncholinergic pathways. Acute, low-dose exposure to malathion (10 mg/ml for 5 h under occlusive dressing) caused a significant increase in cutaneous blood flux, monitored by using laser-Doppler flowmetry and imaging. It had little effect on tissue levels of ACh, nitric oxide, and histamine assayed in dermal dialysate collected from malathion-exposed and control-treated skin. The duration of the cutaneous vascular response to exogenous ACh (2%) delivered by iontophoresis was significantly enhanced by preexposure to malathion, both <1 h after its removal and 24 h later (P < 0.001). At <1 h, the time to 50% decay of the response was 24 ± 4 and 50 ± 8 min in control and malathion-treated skin, respectively.
Malathion also enhanced the size and duration of the axon reflex-mediated vasoresponse to ACh. The increase in blood flux to malathion and the endothelium-mediated response to exogenous ACh, both in the presence and absence of malathion, were attenuated by pretreatment of the skin with atropine and local anesthesia (P < 0.01). We conclude that short-term exposure to a single low dose of malathion causes prolonged modulation of the physiological function of the cutaneous vasculature and that this is, in part, through its action on acetylcholinesterase at both neuronal and nonneuronal sites.
endothelial cells, acetylcholine, vasodilatation
8750-7587
1091-1097
Boutsiouki, Paraskevi
7bcd1b5c-184a-4624-9419-0c2c78faa0df
Clough, Geraldine F.
9f19639e-a929-4976-ac35-259f9011c494
Boutsiouki, Paraskevi
7bcd1b5c-184a-4624-9419-0c2c78faa0df
Clough, Geraldine F.
9f19639e-a929-4976-ac35-259f9011c494

Boutsiouki, Paraskevi and Clough, Geraldine F. (2004) Modulation of microvascular function following low-dose exposure to the organophosphorous compound malathion in human skin in vivo. Journal of Applied Physiology, 97 (3), 1091-1097. (doi:10.1152/japplphysiol.00123.2004).

Record type: Article

Abstract

This study investigates whether malathion, a widely used organophosphate insecticide, has its effects on cutaneous vasculature in healthy human volunteers through its anticholinergic activity or through the modulation of other, noncholinergic pathways. Acute, low-dose exposure to malathion (10 mg/ml for 5 h under occlusive dressing) caused a significant increase in cutaneous blood flux, monitored by using laser-Doppler flowmetry and imaging. It had little effect on tissue levels of ACh, nitric oxide, and histamine assayed in dermal dialysate collected from malathion-exposed and control-treated skin. The duration of the cutaneous vascular response to exogenous ACh (2%) delivered by iontophoresis was significantly enhanced by preexposure to malathion, both <1 h after its removal and 24 h later (P < 0.001). At <1 h, the time to 50% decay of the response was 24 ± 4 and 50 ± 8 min in control and malathion-treated skin, respectively.
Malathion also enhanced the size and duration of the axon reflex-mediated vasoresponse to ACh. The increase in blood flux to malathion and the endothelium-mediated response to exogenous ACh, both in the presence and absence of malathion, were attenuated by pretreatment of the skin with atropine and local anesthesia (P < 0.01). We conclude that short-term exposure to a single low dose of malathion causes prolonged modulation of the physiological function of the cutaneous vasculature and that this is, in part, through its action on acetylcholinesterase at both neuronal and nonneuronal sites.

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More information

Published date: 2004
Keywords: endothelial cells, acetylcholine, vasodilatation

Identifiers

Local EPrints ID: 26953
URI: http://eprints.soton.ac.uk/id/eprint/26953
ISSN: 8750-7587
PURE UUID: 8becf631-8d97-4f2a-a391-6da2887ffdf2
ORCID for Geraldine F. Clough: ORCID iD orcid.org/0000-0002-6226-8964

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Date deposited: 25 Apr 2006
Last modified: 16 Mar 2024 02:54

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Author: Paraskevi Boutsiouki

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