Vapor Phase Exposure to Acetaldehyde Generated from Ethanol Inhibits Bovine Bronchial Epithelial Cell Ciliary Motility

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Abstract

Acetaldehyde is a toxic product of the oxidation of ethanol and is known to induce slowing of ciliary motility in airway epithelium. Alcohol ingestion results in high exhaled breath concentrations of ethanol where lung microsomes and upper airway bacterial flora are capable of metabolizing it to acetaldehyde. Because acetaldehyde is very volatile, we hypothesized that the production and release of acetaldehyde vapor into the airway may result in ciliary slowing or ciliastasis. To test this hypothesis, ciliated bovine bronchial airway epithelial cells were maintained on collagen‐coated dishes for 48 hr before coincubation with a separate dish containing control or test mixtures. In this arrangement, the ciliated cells were exposed only to the volatile components of the separate dish. The separate dish contained ethanol, acetaldehyde, or an acetaldehyde‐generating system (AGS) that consisted of ethanol + glucose + glucose oxidase + catalase. This mixture was placed next to the ciliated cells within in a transparent sealed chamber. Ciliary motility was recorded at room temperature by video microscopy, and ciliary beat frequency was determined using computerized frequency spectrum analysis. Exposure to the AGS resulted in time‐and concentration‐dependent ciliary slowing with complete ciliastasis, with as low as 20 mM ethanol in the AGS. Direct vapor phase exposure to acetaldehyde alone served as a positive control and also resulted in time‐dependent ciliary slowing with complete ciliastasis reached by 4 hr. The AGS‐induced ciliastasis was reached 2 hr later than with acetaldehyde alone. When cells were pretreated with cyanamide, which is known to block acetaldehyde dehydrogenase, the time to ciliastasis was decreased by 10–30 min compared with untreated cells. We conclude that acetaldehyde generated from ethanol is capable of inducing ciliastasis at concentrations of ethanol frequently encountered during drinking. In addition, our results suggest that ciliated airway epithelial cells have acetaldehyde dehydrogenase‐like activity that may be protective against aldehyde‐induced airway injury.

Original languageEnglish (US)
Pages (from-to)1252-1255
Number of pages4
JournalAlcoholism: Clinical and Experimental Research
Volume18
Issue number5
DOIs
StatePublished - Jan 1 1994

Fingerprint

Acetaldehyde
Cell Movement
Ethanol
Epithelial Cells
Vapors
Cyanamide
Video Microscopy
Glucose Oxidase
Poisons
Microsomes
Catalase
Spectrum analysis
Drinking
Spectrum Analysis
Microscopic examination
Epithelium
Eating
Alcohols
Glucose
Oxidation

Keywords

  • Ciliary Beat Frequency
  • Host Defense
  • Mucociliary Clearance

ASJC Scopus subject areas

  • Medicine (miscellaneous)
  • Toxicology
  • Psychiatry and Mental health

Cite this

@article{b29feaf0f2e048879fd7c6a0a423764d,
title = "Vapor Phase Exposure to Acetaldehyde Generated from Ethanol Inhibits Bovine Bronchial Epithelial Cell Ciliary Motility",
abstract = "Acetaldehyde is a toxic product of the oxidation of ethanol and is known to induce slowing of ciliary motility in airway epithelium. Alcohol ingestion results in high exhaled breath concentrations of ethanol where lung microsomes and upper airway bacterial flora are capable of metabolizing it to acetaldehyde. Because acetaldehyde is very volatile, we hypothesized that the production and release of acetaldehyde vapor into the airway may result in ciliary slowing or ciliastasis. To test this hypothesis, ciliated bovine bronchial airway epithelial cells were maintained on collagen‐coated dishes for 48 hr before coincubation with a separate dish containing control or test mixtures. In this arrangement, the ciliated cells were exposed only to the volatile components of the separate dish. The separate dish contained ethanol, acetaldehyde, or an acetaldehyde‐generating system (AGS) that consisted of ethanol + glucose + glucose oxidase + catalase. This mixture was placed next to the ciliated cells within in a transparent sealed chamber. Ciliary motility was recorded at room temperature by video microscopy, and ciliary beat frequency was determined using computerized frequency spectrum analysis. Exposure to the AGS resulted in time‐and concentration‐dependent ciliary slowing with complete ciliastasis, with as low as 20 mM ethanol in the AGS. Direct vapor phase exposure to acetaldehyde alone served as a positive control and also resulted in time‐dependent ciliary slowing with complete ciliastasis reached by 4 hr. The AGS‐induced ciliastasis was reached 2 hr later than with acetaldehyde alone. When cells were pretreated with cyanamide, which is known to block acetaldehyde dehydrogenase, the time to ciliastasis was decreased by 10–30 min compared with untreated cells. We conclude that acetaldehyde generated from ethanol is capable of inducing ciliastasis at concentrations of ethanol frequently encountered during drinking. In addition, our results suggest that ciliated airway epithelial cells have acetaldehyde dehydrogenase‐like activity that may be protective against aldehyde‐induced airway injury.",
keywords = "Ciliary Beat Frequency, Host Defense, Mucociliary Clearance",
author = "Sisson, {Joseph Harold} and Tuma, {D. J.}",
year = "1994",
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T1 - Vapor Phase Exposure to Acetaldehyde Generated from Ethanol Inhibits Bovine Bronchial Epithelial Cell Ciliary Motility

AU - Sisson, Joseph Harold

AU - Tuma, D. J.

PY - 1994/1/1

Y1 - 1994/1/1

N2 - Acetaldehyde is a toxic product of the oxidation of ethanol and is known to induce slowing of ciliary motility in airway epithelium. Alcohol ingestion results in high exhaled breath concentrations of ethanol where lung microsomes and upper airway bacterial flora are capable of metabolizing it to acetaldehyde. Because acetaldehyde is very volatile, we hypothesized that the production and release of acetaldehyde vapor into the airway may result in ciliary slowing or ciliastasis. To test this hypothesis, ciliated bovine bronchial airway epithelial cells were maintained on collagen‐coated dishes for 48 hr before coincubation with a separate dish containing control or test mixtures. In this arrangement, the ciliated cells were exposed only to the volatile components of the separate dish. The separate dish contained ethanol, acetaldehyde, or an acetaldehyde‐generating system (AGS) that consisted of ethanol + glucose + glucose oxidase + catalase. This mixture was placed next to the ciliated cells within in a transparent sealed chamber. Ciliary motility was recorded at room temperature by video microscopy, and ciliary beat frequency was determined using computerized frequency spectrum analysis. Exposure to the AGS resulted in time‐and concentration‐dependent ciliary slowing with complete ciliastasis, with as low as 20 mM ethanol in the AGS. Direct vapor phase exposure to acetaldehyde alone served as a positive control and also resulted in time‐dependent ciliary slowing with complete ciliastasis reached by 4 hr. The AGS‐induced ciliastasis was reached 2 hr later than with acetaldehyde alone. When cells were pretreated with cyanamide, which is known to block acetaldehyde dehydrogenase, the time to ciliastasis was decreased by 10–30 min compared with untreated cells. We conclude that acetaldehyde generated from ethanol is capable of inducing ciliastasis at concentrations of ethanol frequently encountered during drinking. In addition, our results suggest that ciliated airway epithelial cells have acetaldehyde dehydrogenase‐like activity that may be protective against aldehyde‐induced airway injury.

AB - Acetaldehyde is a toxic product of the oxidation of ethanol and is known to induce slowing of ciliary motility in airway epithelium. Alcohol ingestion results in high exhaled breath concentrations of ethanol where lung microsomes and upper airway bacterial flora are capable of metabolizing it to acetaldehyde. Because acetaldehyde is very volatile, we hypothesized that the production and release of acetaldehyde vapor into the airway may result in ciliary slowing or ciliastasis. To test this hypothesis, ciliated bovine bronchial airway epithelial cells were maintained on collagen‐coated dishes for 48 hr before coincubation with a separate dish containing control or test mixtures. In this arrangement, the ciliated cells were exposed only to the volatile components of the separate dish. The separate dish contained ethanol, acetaldehyde, or an acetaldehyde‐generating system (AGS) that consisted of ethanol + glucose + glucose oxidase + catalase. This mixture was placed next to the ciliated cells within in a transparent sealed chamber. Ciliary motility was recorded at room temperature by video microscopy, and ciliary beat frequency was determined using computerized frequency spectrum analysis. Exposure to the AGS resulted in time‐and concentration‐dependent ciliary slowing with complete ciliastasis, with as low as 20 mM ethanol in the AGS. Direct vapor phase exposure to acetaldehyde alone served as a positive control and also resulted in time‐dependent ciliary slowing with complete ciliastasis reached by 4 hr. The AGS‐induced ciliastasis was reached 2 hr later than with acetaldehyde alone. When cells were pretreated with cyanamide, which is known to block acetaldehyde dehydrogenase, the time to ciliastasis was decreased by 10–30 min compared with untreated cells. We conclude that acetaldehyde generated from ethanol is capable of inducing ciliastasis at concentrations of ethanol frequently encountered during drinking. In addition, our results suggest that ciliated airway epithelial cells have acetaldehyde dehydrogenase‐like activity that may be protective against aldehyde‐induced airway injury.

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