Detail of "55127-92-9"

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Effects of administration of antioxidants in acute intermittent porphyria

Effects of administration of antioxidants in acute intermittent porphyria. Thunell, Stig; Andersson, Dan; Harper, Pauline; Henrichson, Ann; Floderus, Ylva; Lindh, Ulf (Porphyria Center Sweden, St. Goran's Hospital, Stockholm S-11281, Swed.). European Journal of Clinical Chemistry and Clinical Biochemistry, 35(6), 427-433 (English) 1997 de Gruyter. CODEN: EJCBEO. ISSN: 0939-4974. DOCUMENT TYPE: Journal CA Section: 1 (Pharmacology) The involvement of free radical in acute porphyric crisis was studied by antioxidants administration to 2 acute intermittent porphyria patients with long-standing recurrent attacks. Clin. condition and urinary excretion of porphyrins and porphyrin precursors were monitored before, during, and after an 8 wk therapy with daily doses of vitamin E, b-carotene, ascorbic acid, selenium, vitamin Q, acetylcysteine, mannitol and carnitine. Blood cell trace element profiles were followed. The administration of the compd. antioxidant formula did not further impair the clin. or biochem. conditions of the patients but the incidence of the recurrent crises or the severity of the symptoms were not pos. affected. Aberrant blood cell trace element profiles with increased granulocyte Mn were normalized during treatment, on cessation of the therapy again resuming the abnormal pretreatment patterns, which may suggest an origin in oxidative stress. No correlation was obsd. between the concn. 55127-92-9 which is the cas registry number of one of substances is just one of reagents here. of granulocyte Mn and the excretion of 5-aminolaevulinic acid. Indications for participation of this porphyrin precursor in a radical generating process leading to generalized mitochondrial superoxide dismutase induction, as conceivably signaled by increased intracellular Mn, were thus not obtained. The failure to note a clin. response to antioxidant therapy may be due to factors dependent upon dosage of, or interaction between, the antioxidant compds. given, or on restricted bioavailability of the antioxidants at crit. anatomical sites, and does not per se invalidate the model of acute porphyria as a hyperoxidative condition. .