Development of a gas chromatographic test for the quantification of the biomarker 3-bromopropionic acid in human urine

B’Hymer, Clayton; Cheever, Kenneth L.

doi:10.1016/j.jchromb.2003.12.004

Cited by 20 publications

(13 citation statements)

References 20 publications

(23 reference statements)

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“…In this regard, cytochrome P-450 (CYP)-dependent oxidation and GSH-dependent conjugation may be the primary metabolic routes of 1-BP activation in rats ( Figure 1) (Jones & Walsh, 1979;Barnsley et al, 1966). Two major routes of 1-BP metabolism include oxidation at C2 or C3 via the CYP-associated monooxygenase system and formation of GSH conjugates via GSH S-transferase (B'Hymer & Cheever, 2004). CYP 2E1 was implicated to activate a variety of small hydrophobic chemicals, including a number of epoxideforming and environmentally important toxicants similar to 1-BP (Ghanayem & Hoffler, 2007).…”

Section: Role Of Metabolism In 1-bromopropane-induced Hepatotoxicity mentioning

confidence: 99%

“…When the study of in vitro metabolism of 1-BP in hepatic microsome from phenobarbital-induced rats was performed in the presence of exogenous GSH, the following metabolites were also detected: propene, 1,2-epoxypropane, 1,2-propanediol, propionic acid, S-(1-propyl) GSH, and S-(2-hydroxyl-1-propyl) GSH (Tachizawa et al, 1982). Moreover, two major routes of 1-BP metabolism included the oxidation on C2 or C3 via the CYP monooxygenase system and the formation of GSH conjugates via GSH S-alkyltransferase (B'Hymer & Cheever, 2004). All of these results indicated the possible interaction of 1-BP with CYP and GSH.…”

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confidence: 99%

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Role of Metabolism In 1-Bromopropane-Induced Hepatotoxicity in Mice

Lee

Kang

Jeon

et al. 2010

Journal of Toxicology and Environmental Health, Part A

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A possible role of metabolism in 1-bromopropane (1-BP)-induced hepatotoxicity was investigated in male ICR mice. The depletion of glutathione (GSH) by formation of GSH conjugates was associated with increased hepatotoxicity in 1-BP-treated mice. The formation of S-propyl and 2-hydroxypropyl GSH conjugates were identified in the liver following 1-BP treatment. In addition, the formation of reactive metabolites of 1-BP by certain cytochrome P-450 (CYP) may be involved in 1-BP-induced hepatotoxicity. The decreased content of hepatic GSH produced by 1-BP was associated not only with increased activities of alanine aminotransferase (ALT) and aspartate aminotransferase (AST) but also with elevated levels of hepatic thiobarbituric acid-reactive substance (TBARS) in mice where metabolic enzymes were induced by pretreatment with phenobarbital. In addition, the hepatotoxicity induced by 1-BP was prevented by pretreatment with SKF-525A. Taken together, the formation of reactive metabolites by CYP and depletion of GSH may play important roles in hepatotoxicity induced by 1-BP.

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Section: Role Of Metabolism In 1-bromopropane-induced Hepatotoxicity mentioning

confidence: 99%

mentioning

confidence: 99%

Role of Metabolism In 1-Bromopropane-Induced Hepatotoxicity in Mice

Lee

Kang

Jeon

et al. 2010

Journal of Toxicology and Environmental Health, Part A

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“…The extraction procedure was an adaptation of one described previously (B'Hymer et al 2003;B'Hymer and Cheever 2004).…”

Section: Extraction and Esterification Of Meaa From Mouse Urinementioning

confidence: 99%

A Test Procedure for the Determination of (2-Methoxyethoxy)acetic Acid in Urine from Jet Fuel-Exposed Mice

B’Hymer

Keil

Cheever

2005

Toxicology Mechanisms and Methods

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A test procedure for the determination of (2-methoxyethoxy)acetic acid (MEAA) was adapted and applied to urine samples from jet fuel (JP-8)-exposed mice using capillary gas chromatography with a mass selective detector (MSD). MEAA is a metabolite and proposed biomarker for exposure to 2-(2-methoxyethoxy)ethanol, a glycol ether component in the formulation of JP-8. The collected urine samples were spiked with deuterated butoxyacetic acid internal standard, and extracted with ethyl acetate, and esterified with ethanol and sulfuric acid, and the esters of the glycol ethers were extracted with methylene chloride. The chromatographic conditions used easily separate the MEAA ethyl ester from interferences within mouse urine. The application of this procedure to urine samples collected from mice demonstrated that MEAA was detectable after oral (2000 mg/kg) or dermal (50 mu L) exposure for 7 days to JP-8 at levels as high as 8.5 or 6.5 mu g/mL, respectively. This pilot demonstration indicated that total urinary MEAA was a viable biomarker for the two routes of JP-8 exposure in laboratory mice.

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“…The current study involves development of a procedure for an exposure biomarker for 1-BP. The general utility of analytical techniques for measuring urinary markers to evaluate 1-BP exposure has led to the development of tests which include the analysis of urinary bromine [27,28], 3-bromopropionic acid [29], 1-BP [30], or mercapturic acids as stable biomarkers [31][32][33][34]. The purpose of the work described here was to design a sensitive and specific method for the quantification of AcPrCys using HPLC ESI-MS Specific Ion Monitoring (SIM).…”

Section: Introductionmentioning

confidence: 99%