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Oxidative hemolysis of erythrocytes and its inhibition by free radical scavengers.

Abstract
The oxidative hemolysis of rabbit erythrocytes induced by free radicals and its inhibition by chain-breaking antioxidants have been studied. The free radicals were generated from either a water-soluble or a lipid-soluble azo compound which, upon its thermal decomposition, gave carbon radicals that reacted with oxygen immediately to give peroxyl radicals. The radicals generated in the aqueous phase from a water-soluble azo compound induced hemolysis in air, but little hemolysis was observed in the absence of oxygen. Water-soluble chain-breaking antioxidants, such as ascorbic acid, uric acid, and water-soluble chromanol, suppressed the hemolysis dose dependently. Vitamin E in the erythrocyte membranes was also effective in suppressing the hemolysis. 2,2,5,7,8-Pentamethyl-6-chromanol, a vitamin E analogue without phytyl side chain, incorporated into dimyristoylphosphatidylcholine liposomes, suppressed the above hemolysis, but alpha-tocopherol did not suppress the hemolysis. Soybean phosphatidylcholine liposomes also induced hemolysis, and a lipid-soluble azo initiator incorporated into the soybean phosphatidylcholine liposomes accelerated the hemolysis. The chain-breaking antioxidants incorporated into the liposomes were also effective in suppressing this hemolysis.
AuthorsE Niki, E Komuro, M Takahashi, S Urano, E Ito, K Terao
JournalThe Journal of biological chemistry (J Biol Chem) Vol. 263 Issue 36 Pg. 19809-14 (Dec 25 1988) ISSN: 0021-9258 [Print] United States
PMID3198651 (Publication Type: Journal Article)
Chemical References
  • Antioxidants
  • Free Radicals
  • Liposomes
  • Phosphatidylcholines
  • Ascorbic Acid
Topics
  • Animals
  • Antioxidants (pharmacology)
  • Ascorbic Acid (pharmacology)
  • Erythrocytes (drug effects, ultrastructure)
  • Free Radicals
  • Hemolysis (drug effects)
  • In Vitro Techniques
  • Liposomes
  • Oxidation-Reduction
  • Phosphatidylcholines
  • Rabbits
  • Reference Values
  • Vitamin E Deficiency (blood)

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