Simultaneous Quantitation of Allyl Alcohol, Ethanol, and Their Metabolites in the Blood by Head-Space Gas Chromatography

Lee, Jooyoung; Chung, Sun-Hwa; Kim, Mee-Jeong; Chung, Jin‐Ho

doi:10.3109/15376519509049117

Cited by 5 publications

(1 citation statement)

References 11 publications

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“…Blood concentrations of ethanol, acetaldehyde, and allyl alcohol were determined by headspace gas chromatography as described by Lee et al (1995). Briefly, 0.1 ml of blood was collected from the orbital sinus and then hemolyzed with 0.4 ml distilled water containing n-propanol as an internal standard in a 5-ml vial.…”

Section: Determination Of Ethanol Acetaldehyde and Allyl Alcohol Inmentioning

confidence: 99%

Ethanol Co-Exposure Increases Lethality of Allyl Alcohol in Male Sprague-Dawley Rats

Lee¹

1999

Journal of Toxicology and Environmental Health, Part A

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Since allyl alcohol and ethanol are both metabolized by alcohol dehydrogenase (ADH) and aldehyde dehydrogenase (ALDH), ethanol could affect allyl-alcohol induced toxicity under in vivo coexposure conditions. Male Sprague-Dawley rats were treated with ethanol (2 g/kg, i.p.) simultaneously or 2 h before with allyl alcohol (40 mg/kg, i.p.). Coexposure to allyl alcohol and ethanol resulted in neither enhancement nor protection in allyl alcohol-induced hepatotoxicity at 24 h. However, markedly increased lethality was observed under our coexposure conditions. Pretreatment with 4-methylpyrazole (4-MP) to inhibit ADH did not result in increased lethality to allyl alcohol or ethanol alone, but significantly reduced the lethality of the combined treatment. In contrast, ALDH inhibition increased the lethality of allyl alcohol alone as well as that of the combined allyl alcohol and ethanol treatment. Kinetic studies revealed that combined treatment with allyl alcohol and ethanol resulted in higher blood allyl alcohol levels compared to allyl alcohol alone, and these were accompanied by greater lethality. ADH inhibition increased allyl alcohol blood levels significantly when rats were treated with allyl alcohol alone or allyl alcohol plus ethanol, leading to protection against lethality. In contrast, ALDH inhibition did not affect blood allyl alcohol levels, but resulted in increased lethality. These data suggest a possible role for a metabolite of allyl alcohol, acrolein, in the increased lethality of allyl alcohol and ethanol coexposure in rats.

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Section: Determination Of Ethanol Acetaldehyde and Allyl Alcohol Inmentioning

confidence: 99%

Ethanol Co-Exposure Increases Lethality of Allyl Alcohol in Male Sprague-Dawley Rats

Lee¹

1999

Journal of Toxicology and Environmental Health, Part A

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Dose-dependent liver regeneration in chloroform, trichloroethylene and allyl alcohol ternary mixture hepatotoxicity in rats

2005

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The present study was designed to examine the hypothesis that liver tissue repair induced after exposure to chloroform (CF) + trichloroethylene (TCE) + allyl alcohol (AA) ternary mixture (TM) is dose-dependent similar to that elicited by exposure to these compounds individually. Male Sprague Dawley (S-D) rats (250-300 g) were administered with fivefold dose range of CF (74-370 mg/kg, ip), and TCE (250-1250 mg/kg, ip) in corn oil and sevenfold dose range of AA (5-35 mg/kg, ip) in distilled water. Liver injury was assessed by plasma alanine amino transferase (ALT) activity and liver tissue repair was measured by (3) H-thymidine incorporation into hepatonuclear DNA. Blood and liver levels of parent compounds and two major metabolites of TCE [trichloroacetic acid (TCA) and trichloroethanol (TCOH)] were quantified by gas chromatography. Blood and liver CF and AA levels after TM were similar to CF alone or AA alone, respectively. However, the TCE levels in blood and liver were substantially decreased after TM in a dose-dependent fashion compared to TCE alone. Decreased plasma and liver TCE levels were consistent with decreased production of metabolites and elevated urinary excretion of TCE. The antagonistic interaction resulted in lower liver injury than the summation of injury caused by the individual components at all three-dose levels. On the other hand, tissue repair showed a dose-response leading to regression of injury. Although the liver injury was lower and progression was contained by timely tissue repair, 50% mortality occurred only with the high dose combination, which is several fold higher than environmental levels. The mortality could be due to the central nervous system toxicity. These findings suggest that exposure to TM results in lower initial liver injury owing to higher elimination of TCE, and the compensatory liver tissue repair stimulated in a dose-dependent manner mitigates progression of injury after exposure to TM.

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Gas chromatographic determination of primary alcohols as their formylbenzoic esters by gas-phase luminescence detection

Lin

Aue

1999

Journal of Chromatography A

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Simultaneous Quantitation of Allyl Alcohol, Ethanol, and Their Metabolites in the Blood by Head-Space Gas Chromatography

Cited by 5 publications

References 11 publications

Ethanol Co-Exposure Increases Lethality of Allyl Alcohol in Male Sprague-Dawley Rats

Ethanol Co-Exposure Increases Lethality of Allyl Alcohol in Male Sprague-Dawley Rats

Dose-dependent liver regeneration in chloroform, trichloroethylene and allyl alcohol ternary mixture hepatotoxicity in rats

Gas chromatographic determination of primary alcohols as their formylbenzoic esters by gas-phase luminescence detection

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