ABSTRACT
The antioxidant effect of 5-Aminosalicylic acid (5-ASA) on copper-mediated LDL oxidation was followed either by the emitted chemiluminiscence (CL) or by UV-vis spectroscopy. 5-ASA addition extends the lag phase in a concentration-dependent manner without changes in the rate of the process in the autoaccelerated phase. The antioxidant behavior of 5-ASA was very similar to that of Trolox, a very efficient water soluble antioxidant. The copper-binding capacity of 5-ASA was evaluated by UV-visible spectroscopy. The addition of copper to a 5-ASA solution increases the absorbance at 332 nm and generates a new band at 298 nm. These changes in the UV-vis spectra indicate formation of a complex between 5-ASA and copper. However, LDL protection by 5-ASA is unrelated to its copper chelating capacity.
Subject(s)
Aminosalicylic Acids/pharmacology , Antioxidants/pharmacology , Copper/chemistry , Lipoproteins, LDL/metabolism , Aminosalicylic Acids/chemistry , Aminosalicylic Acids/metabolism , Antioxidants/chemistry , Antioxidants/metabolism , Copper/toxicity , Luminescent Measurements , Oxidation-Reduction/drug effects , Spectrophotometry, Ultraviolet , Time FactorsABSTRACT
En 1942 la reumatóloga sueca Dra. Nana Svartz comunicó los favorables resultados obtenidos con la administración de asulfidina a pacientes portadores de artritis y diarrea
Subject(s)
Sulfasalazine/therapeutic use , Aminosalicylic Acids/pharmacology , Sulfapyridine/pharmacology , Sulfasalazine , Sulfasalazine/chemistry , Sulfasalazine/pharmacologySubject(s)
Humans , Cholinergic Agents , Anti-Ulcer Agents , Antidiarrheals , Cathartics/classification , Gastric Acid , Aminosalicylic Acids/pharmacology , Cimetidine/chemistry , Colitis, Ulcerative/drug therapy , Crohn Disease/drug therapy , Dopamine Antagonists/pharmacology , Gastrointestinal Motility/drug effects , Immunosuppressive Agents/pharmacology , Inflammatory Bowel Diseases/drug therapy , Nizatidine/adverse effects , Ranitidine/chemistryABSTRACT
1. Evidence is presented for the occurrence of type 1 prostaglandin 15-hidroxydehydrogenase in human rectal mucosa. No evidence of the presence of type 2 dnzyme was found. 2. A 15-keto-prostaglandin reductase, responsible for the breakdown of 13, 14-dihydro 15-keto prostaglandins to 13, 14-dihydro prostaglandins, was also present in human rectal mucosa. 3. Ulcerative colitis patients catabolized prostaglandins to the same extent as the control group. PGE was catabolized significantly better than PGF2 alfa. 4. 5-Aminosalicylic acid and sulphapyridine did not affect prostaglandin catabolism. Sulphasalazine, methilsulphasalazine, indomethacin, flurbiprofen, disodium cromoglycate, sodium salicylate and carbenoxolone sodium inhibited prostaglandin catabolism to the same extent in both groups.Salicylazosulphadimidine was a more potent inhibitor of PGE1 catabolism than of PGF2alfa. 5. The increased prostaglandin synthesis reported for ulcerative colitis patients was not paralleled by increased catabolism, a fact possibly contributing to the accumulation of such compounds in the diseased state