In vivo endotoxin enhances biliary ethanol-dependent free radical generation.

Endotoxemia is associated with alcoholic liver diseases; however, the effect of endotoxin on the oxidation of ethanol is not known. We tested the hypothesis that endotoxin treatment enhances hepatic ethanol radical production. The generation of free radicals by the liver was studied with spin-trapping technique utilizing the primary trap ethanol (0.8 g/kg) and the secondary trap alpha-(4-pyridyl-1-oxide)-N-t-butylnitrone (4-POBN; 500 mg/kg). Electron paramagnetic resonance (EPR) spectra of bile showed six-line signals, which were dependent on ethanol, indicating the trapping of ethanol-dependent radicals. Intravenous injections of Escherichia coli lipopolysaccharide (0.5 mg/kg) 0.5 h before 4-POBN plus ethanol treatment caused threefold increases of biliary radical adducts. EPR analyses of bile from [1-13C]ethanol-treated endotoxic rats showed the presence of species attributable to alpha-hydroxyethyl adduct, carbon-centered adducts, and ascorbate radical. The generation of endotoxin-induced increases of ethanol-dependent radicals was suppressed by 50% on GdCl3 (20 mg/kg i.v.) or desferrioxamine mesylate (1 g/kg i.p.) treatment. Our data show that in vivo endotoxin increases biliary ethanol-dependent free radical formation and that these processes are modulated by Kupffer cell activation and catalytic metals.

The effect of abscisic acid on the uptake of potassium and chloride into Avena coleoptile sections.

The effect of abscisic acid (ABA) on uptake of potassium ((86)Bb(+) or (42)K(+)) by Avena sativa L. coleoptile sections was investigated. ABA lowered the potassium uptake rate within 30 min after its application and inhibition reached a maximum (ca. 75%) after 2 h. The inhibition of K(+) uptake increased with ABA concentration over a range of 0.03 to 10 µg/ml ABA. At a higher K(+) concentration (20 mM) the percentage inhibition decreased. The percentage inhibition of K(+) uptake by ABA remained constant with external K(+) varied from 0.04 to 1.0 mM. After a loading period in 20 mM K(+) ((86)Rb(+)), apparent efflux of potassium was only slightly increased by ABA. Experiments in which growth was greatly reduced by mannitol or by omission of indole-3-acetic acid from the medium indicated there was no simple quantitative correspondence between ABA inhibition of coleoptile elongation and ABA inhibition of K(+) uptake. Chloride uptake was also inhibited by ABA but to a smaller degree than was K(+) uptake. No specificity for counterions was observed for K(+) uptake. Uptake of 3,0-methylglucose and proline were inhibited by ABA to a much smaller extent (14 and 11%) than that of K(+), a result which suggests that ABA acts on specific ion uptake mechanisms.