Fatty-acid peroxidation in relation to trace elements in serum of patients with homozygous sickle-cell anemia and beta-thalassemia: a gas-chromatographic study.
Due mainly to a deeply disturbed iron metabolism, intense production of oxygen-derived free radicals occurs in genetic hemoglobinopathies such as homozygous sickle-cell anemia and beta-thalassemia. Together with impairments in the natural factors involved in oxy-radical detoxication, this results in intense oxidative stress leading to lipid peroxidation in the blood components. In search of peroxidation effects, we undertook a gas chromatographic study of both the total and phospholipid-bound fatty acids in the serum from sickle-cell disease and beta-thalassemia patients. Specific alterations of pathologic origin have been evidenced in the profiles of total and phospholipidic fatty acids, as well as in the elongation-desaturation ratios of the total fatty acids. Results are consistent with lipid peroxidations and fatty-acid biosynthesis disturbances in both diseases, but more severe in thalassemia than in sickle-cell anemia. Increased serum selenium in the latter disease might exert a protective action against lipid peroxidation.
Preoteasa
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EA
Institute of Atomic Physics, IFIN Laboratory, Bucharest, Romania.
Ionescu
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D000328:Adult; D000755:Anemia, Sickle Cell / Q000097:blood*; D002849:Chromatography, Gas; D005227:Fatty Acids / Q000097:blood* / Q000378:metabolism*; D005260:Female; D006801:Humans; D015227:Lipid Peroxidation; D008297:Male; D010743:Phospholipids / Q000097:blood; D012643:Selenium / Q000097:blood; D014131:Trace Elements / Q000097:blood*; D017086:beta-Thalassemia / Q000097:blood*
D005227:Fatty Acids; D010743:Phospholipids; D014131:Trace Elements; D012643:Selenium