Heparin inhibits the "quasi-lipoxygenase" activity of hemoglobin toward linoleic acid by oxidant scavenging.

Previous studies have shown heparin to have antiinflammatory properties. We have attempted to determine if the mechanism involves the inhibition of lipid oxidation by utilizing a model system where linoleic acid is oxidized in the presence of oxygen and methemoglobin. Heparin inhibits this "quasi-lipoxygenase" activity prolonging the lag phase and slowing the rate of lipid peroxidation. An oxidant scavenging mechanism is also inferred from the fact that heparin is capable of inhibiting luminol-dependent chemiluminescence resulting from the reduction of 15-HPETE by methemoglobin. It is concluded that heparin, in at least this model system, is capable of inhibiting lipoxygenation by an oxidant scavenging mechanism.

Preliminary studies on the metabolism of 3,2'-dimethyl-4-aminobiphenyl in the rat.

Distribution of 3,2-dimethyl-4-aminobiphenyl (DMAB) and its metabolites in vivo and the metabolism of DMAB by liver in vitro have been studied in the Wistar rat. DMAB-HCI purified by recrystallization and dissolved in ethanol was injected subcutaneously and extractions made from liver, feces, and urine. Similar technical procedures were used to study in vitro metabolism in rat liver homogenates. Two components were isolated from urine and liver having Rf values (thin-layer chromatography) of 0.13 and 0.59, respectively. Three additional metabolites were found in the hydrolyzed fecal fraction. Rechromatography of the major fecal component yielded 6 fluorescent compounds. Gas-liquid chromatography of the most highly fluorescent of these indicated at least 3 additional metabolites. The evidence presented indicates that the liver transforms DMAB to several metabolites which are rapidly transferred in conjugated form to the intestine via the bile. The urine does not appear to be the major excretory route. We have examined the purity of commercially available DMAB free base and DMAB-HCL and found an impurity that comprises approximately 10-24% of the total samle upon GLC analysis, depending upon the supplier. This contaminant was completely removed by recrystallization of the hydrochloride and the chemical identity of purified compound as DMAB confirmed. Recommendations are presented for the use of this purified compound in a biological system.