ABSTRACT
Bilirubin, biliverdin and their serum albumin complexes were tested as oxyradical scavengers (superoxide generated by the xanthine/xanthine oxidase system and peroxyl radical-trapping antioxidant ability). As superoxide scavengers the free bile pigments showed activities near to that of serum albumin, higher than the water soluble vitamin E analog Trolox and lower than ascorbic acid. The peroxyl radical-trapping antioxidant abilities of the tested bile pigments were much higher than those of the serum albumin and of the same order as their serum albumin complexes. This interaction with peroxyl radicals showed different stoichiometric factors for bilirubin (approximately 2) and biliverdin (approximately 4).
Subject(s)
Antioxidants/pharmacology , Bile Pigments/pharmacology , Animals , Antioxidants/chemistry , Bile Pigments/chemistry , Bilirubin/chemistry , Bilirubin/pharmacology , Biliverdine/chemistry , Biliverdine/pharmacology , Cattle , Free Radical Scavengers , Humans , In Vitro Techniques , Oxidation-Reduction , Serum Albumin/chemistry , Superoxides/chemistryABSTRACT
Free radical species have been implicated as important agents in ischemia-reperfusion injury associated to transplantation procedures. This study was carried out to investigate the possible relationship between phospholipase A2 activity (PLA2), lipoperoxidation, and the changes in arachidonic acid metabolism during ischemia reperfusion injury in pancreas transplantation, as well as the effect of a free radical scavenger such as superoxide dismutase on these changes. For this purpose male Lewis rat groups (n = 7) were classified as follows: group I--control; group II--syngenic pancreas transplantation after 15 min preservation in Collins solution at 4 degrees C; group III--syngenic pancreas transplantation after 18 hr preservation in the same conditions; group IV--same as III but with administration of SOD (i.v.) immediately before revascularization in the recipient rat. The results indicate that significant increases in PLA2 activity and lipoperoxide levels occur concomitantly with an increase of thromboxane B2 (TXB2) and 6-keto prostaglandin F1 alpha (6-keto PGF1 alpha) in pancreatic tissue after pancreas transplantation. The counteracting effect of a free radical scavenger such as SOD supports the role of oxygen free radicals (OFR) mediating activation of PLA2 and subsequent formation of eicosanoids in pancreas transplantation.
Subject(s)
Arachidonic Acids/metabolism , Lipid Peroxidation , Pancreas Transplantation , Pancreas/metabolism , Phospholipases A/analysis , Animals , Arachidonic Acid , Free Radicals , Male , Malondialdehyde/analysis , Phospholipases A2 , Rats , Rats, Inbred Lew , Superoxide Dismutase/pharmacologyABSTRACT
PGE2 and TXA2 levels and their modulation by nicardipine, a calcium blocking agent, have been studied in patients suffering from migraine. The levels of both metabolites were determined in saliva obtained during the migraine attacks, during the intervals between attacks, and after 2 months of treatment with nicardipine (20 mg every 8 h.) or placebo. The therapeutic response was evaluated on the basis of the number of migraine attacks. The results show a significant increase in the levels of both eicosanoids during the migraine attacks. In contrast to the placebo group, the number of migraine attacks and the levels of both arachidonic acid metabolites are markedly lower in the nicardipine group. Our results suggest calcium entry into the cytosol as an explanation for the increase in PGE2 and TXA2. Nicardipine interferes with calcium mobilization, thereby inhibiting arachidonic acid metabolite synthesis.
Subject(s)
Calcium Channel Blockers/pharmacology , Dinoprostone/analysis , Migraine Disorders/drug therapy , Nicardipine/therapeutic use , Saliva/analysis , Thromboxane A2/analysis , Adolescent , Adult , Female , Humans , Male , Middle Aged , Migraine Disorders/etiologyABSTRACT
BW775C, an inhibitor of the lipoxygenase and cyclo-oxygenase pathways, inhibits the respiratory distress induced by arachidonic acid in rats. The degree of respiratory distress was measured in terms of respiratory rate using electrodes implanted at each side of the thorax. Indomethacin, an inhibitor of the cyclooxygenase pathway, failed to influence the respiratory distress induced by arachidonic acid. The results implicate the lipoxygenase pathway, i.e. the leukotrienes synthesis inhibition, in the respiratory distress induced by arachidonic acid.