Palozza P, Krinsky N I
Institute of General Pathology, Catholic University, Rome, Italy.
Free Radic Biol Med. 1991;11(4):407-14. doi: 10.1016/0891-5849(91)90158-y.
Rat liver microsomal lipids in hexane solution were exposed to the lipid-soluble radical initiator, azobis-isobutyronitrile (AIBN), and the antioxidant activities of alpha-tocopherol and beta-carotene have been compared. Lipid peroxidation was monitored both by conjugated diene formation at 233 nm, and by malondialdehyde (MDA) formation in the thiobarbituric acid assay at 535 nm. Diene formation was continuous for at least 120 min in the presence of 85 micrograms/ml lipid and 4 mM AIBN. Both alpha-tocopherol and beta-carotene acted as chain-breaking antioxidants, suppressing lipid peroxidation and producing an induction period at concentrations as low as 0.5 and 8 microM, respectively. When both of these lipid-soluble antioxidants were present together, the oxidation was strongly suppressed and the induction period was the sum of the individual antioxidants, alpha-Tocopherol and beta-carotene also inhibited MDA generation. In the presence of 170 micrograms/ml lipid and 8 mM AIBN, beta-carotene exhibited an IC50 of 1.1 microM and inhibited completely at 15 microM. Using beta-carotene, an induction period was observed, although much less pronounced than with alpha-tocopherol. Furthermore, beta-carotene inhibited MDA production in a concentration-dependent manner and exhibited an IC50 of 50 microM. In addition, added beta-carotene delayed the radical-initiated destruction of the endogenous alpha-tocopherol and gamma-tocopherol in this system.
将己烷溶液中的大鼠肝脏微粒体脂质暴露于脂溶性自由基引发剂偶氮二异丁腈(AIBN),并比较了α-生育酚和β-胡萝卜素的抗氧化活性。通过在233nm处共轭二烯的形成以及在535nm处硫代巴比妥酸测定中丙二醛(MDA)的形成来监测脂质过氧化。在存在85微克/毫升脂质和4毫摩尔AIBN的情况下,二烯的形成持续至少120分钟。α-生育酚和β-胡萝卜素均作为链断裂抗氧化剂,分别在低至0.5和8微摩尔的浓度下抑制脂质过氧化并产生诱导期。当这两种脂溶性抗氧化剂同时存在时,氧化受到强烈抑制,诱导期是各个抗氧化剂诱导期的总和。α-生育酚和β-胡萝卜素也抑制MDA的生成。在存在170微克/毫升脂质和8毫摩尔AIBN的情况下,β-胡萝卜素的IC50为1.1微摩尔,并在15微摩尔时完全抑制。使用β-胡萝卜素时,观察到诱导期,尽管不如α-生育酚明显。此外,β-胡萝卜素以浓度依赖的方式抑制MDA的产生,IC50为50微摩尔。此外,添加的β-胡萝卜素延迟了该系统中自由基引发的内源性α-生育酚和γ-生育酚的破坏。