Core-flood experiment for transport of reactive fluids in rocks.

Investigation of the transport of reactive fluids in porous rocks is an intriguing but challenging task and relevant in several areas of science and engineering such as geology, hydrogeology, and petroleum engineering. We designed and constructed an experimental setup to investigate physical and chemical processes caused by the flow of reactive and volatile fluids such as supercritical CO(2) and/or H(2)S in geological formations. Potential applications are geological sequestration of CO(2) in the frame of carbon capture and storage and acid-gas injection for sulfur disposal and/or enhanced oil recovery.

DNA adducts in rats and mice following exposure to [4-14C]-1,2-epoxy-3-butene and to [2,3-14C]-1,3-butadiene.

1,3-Butadiene (BD) is a major industrial chemical and a rodent carcinogen, with mice being much more susceptible than rats. Oxidative metabolism of BD, leading to the DNA-reactive epoxides 1,2-epoxy-3-butene (BMO), 1,2-epoxy-3,4-butanediol (EBD) and 1,2:3,4-diepoxybutane (DEB), is greater in mice than rats. In the present study the DNA adduct profiles in liver and lungs of rats and mice were determined following exposure to BMO and to BD since these profiles may provide qualitative and quantitative information on the DNA-reactive metabolites in target tissues.

A novel DNA adduct, originating from 1,2-epoxy-3,4-butanediol, is the major DNA adduct after exposure to [2,3-(14)C]-1,3-butadiene,[4-(14)C]-1,2-epoxy-3-butane.

1,3-Butadiene is a rodent carcinogen and its epoxide metabolites, 1,2-epoxy-3-butene (EB), 1,2-epoxy-3,4-butanediol (EBD), and 1,2:3,4-diepoxybutane (DEB) have been suggested as ultimate carcinogens. This study aimed at identification and quantification of DNA adducts in rats and mice following exposure to BD and its major metabolite EB to identify the reactive epoxide(s) in target tissues. Reaction of [4-(14)C]-EB with 2'-deoxyguanosine (dG) or DNA gave equal amounts of N7-(2-hydroxy-3-butenyl)guanine (G1) and N7-(1-(hydroxymethyl)-2-propenyl)guanine (G2).

Disposition of [Ring-U-(14)C]styrene in rats and mice exposed by recirculating nose-only inhalation.

The disposition of styrene was studied in a group of 12 Sprague Dawley rats and two groups of 30 CD1 mice exposed separately to 160 ppm [ring-U-(14)C]styrene of high specific radioactivity of 1.92 TBq x mol(-1) (52 Ci x mol(-1)) for 6 h. A nose-only exposure system was successfully adapted to (1) recirculate a portion of the flow to limit the amount of (14)C-styrene required, and (2) avoid any polymerization of the compound.

Quantification of DNA adducts formed in liver, lungs, and isolated lung cells of rats and mice exposed to (14)C-styrene by nose-only inhalation.

Bronchiolo-alveolar tumors were observed in mice exposed chronically to 160 ppm styrene, whereas no tumors were seen in rats up to concentrations of 1000 ppm. Clara cells, which are predominant in the bronchiolo-alveolar region in mouse lungs but less numerous in rat and human lung, contain various cytochrome P450s, which may oxidize styrene to the rodent carcinogen styrene-7,8-oxide (SO) and other reactive metabolites. Reactive metabolites may form specific DNA adducts and induce the tumors observed in mice.

Metabolic inactivation of five glycidyl ethers in lung and liver of humans, rats and mice in vitro.

1. Some glycidyl ethers (GE) have been shown to be direct mutagens in short-term in vitro tests and consequently GE are considered to be potentially mutagenic in vivo. However, GE may be metabolically inactivated in the body by two different enzymatic routes: conjugation of the epoxide moiety with the endogenous tripeptide glutathione (GSH) catalysed by glutathione S-transferase (GST) or hydrolysis of the epoxide moiety catalysed by epoxide hydrolase (EH).

Metabolic inactivation of 2-oxiranylmethyl 2-ethyl-2,5-dimethylhexanoate (C10GE) in skin, lung and liver of human, rat and mouse.

The inactivation of 2-oxiranylmethyl 2-ethyl-2,5-dimethylhexanoate (C10GE), one of the most abundant isomers of the epoxy-resin Carduras E-10 glycidyl ester, was studied in subcellular fractions of human, C3H mouse and F344 rat liver, lung and skin. C10GE is chemically very stable and resistant to aqueous hydrolysis, but it was rapidly metabolized in both cytosolic and microsomal fractions of all organs by epoxide hydrolase (EH)-catalysed hydrolysis of the epoxide moiety as well as carboxylesterase (CE)-catalysed hydrolysis of the ester bond. In cytosol the epoxide group was also efficiently conjugated with glutathione, catalysed by glutathione S-transferase (GST), but this conjugation was much less important than hydrolysis in human as well as rodent samples.