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Fatty acid metabolism and cell proliferation. VII. Antioxidant effects of tocopherols and their quinones
Author(s) -
Lindsey Jenifer A.,
Zhang Hanfang,
Kaseki Hisayuki,
Morisaki Nobuhiro,
Sato Takasi,
Cornwell David G.
Publication year - 1985
Publication title -
lipids
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.601
H-Index - 120
eISSN - 1558-9307
pISSN - 0024-4201
DOI - 10.1007/bf02534247
Subject(s) - antioxidant , chemistry , biochemistry , lipid peroxidation , cumene hydroperoxide , metabolism , malondialdehyde , alpha (finance) , catalysis , medicine , construct validity , nursing , patient satisfaction
The antioxidant capacities of α‐ and γ‐tocopherols (α‐E and γ‐E) and their quinones (α‐EQ and γ‐EQ) were determined in non‐biological and biological systems. The non‐biological system consisted of arachidonic acid [20∶4 (n−6)], the oxidant cumene hydroperoxide, and a Fe 3+ catalyst to facilitate malondialdehyde (MDA) formation from lipid peroxides. α‐E and γ‐E had similar antioxidant capacities in this system. α‐EQ also functioned as an antioxidant, while γ‐EQ exhibited a crossover effect by functioning as an antioxidant at low concentrations and a prooxidant at high concentrations. Biological lipid peroxidation in smooth muscle cells challenged with 20∶4 (n−6) was measured both by MDA formation in confluent cultures and by cell growth in proliferating cultures. α‐E, γ‐E and α‐EQ had similar antioxidant capacities, but γ‐EQ was highly cytotoxic for cells in both confluent and proliferating cultures. Cellular retention of antioxidants was estimated indirectly from MDA formation when cells were loaded with an antioxidant (preincubation) and then incubated for varying periods of time in fresh media containing 20∶4 (n−6). Cellular retention also was measured directly with tritiated α‐E and tritiated αEQ. These studies showed that cellular retention decreased in the sequence γ‐E>α‐E>α‐EQ. Thus, cellular retention does not explain the enhanced antioxidant capacity of α‐E compared to γ‐E that has been reported for animal systems. The antioxidant capacity of αE evidently is enhanced by its metabolism to a quinone which, unlike the quinone from γ‐E, functions as a biological antioxidant.