Journal of Okayama Medical Association
Published by Okayama Medical Association

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Full-text articles are available 3 years after publication.

腹水肝癌細胞(AH-130)の脂質過酸化反応欠損とその機構

後藤 信行 岡山大学医学部癌源研究施設生化学部
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抄録
Various tissue homogenates can produce lipid peroxide during incubation with Fe(++) or Co(++) in the presence of oxygen. But the homogenate of actively growing cells diminishes or fails to elicit the lipid peroxide formation. In the present report the author studied the mechanism of the failure of lipid peroxidation reaction of ascites hepatoma cells (AH-130) and the following results were obtained. 1. One of the facts of failure of lipid peroxidation reaction was the reduced arachidonic acid content in phospholipid fraction of ascites hepatoma cells. 2. The other facter was the presence of an inhibitor of lipid peroxidation in acetone soluble fraction of the ascites hepatoma cell membrane fractions. Therefore, the phospholipid fraction of the ascites hepatoma cells shows the lipid peroxidation reaction by the treatment with Fe(++). 3. The inhibitor was also found in the acetone soluble fraction of normal rat liver cells but the content was quite low. 4. The chemical nature of the inhibitor was different from the well known, antioxidant such as α-tocopherol, Coenzyme Q and Vitamin K. The chemical structure has not been identified yet, On the basis of these data the author discussed about the mechanism of the regulation of lipid peroxidation reaction in the cells with respect to the regulation of cell growth and cancer cell specificity and to the aging.
ISSN
0030-1558
NCID
AN00032489