Södergren E, Cederberg J, Vessby B, Basu S
Section for Geriatrics/Clinical Nutrition Research, PO Box 609, 75125 Uppsala, Sweden.
Eur J Nutr. 2001 Feb;40(1):10-6. doi: 10.1007/pl00007381.
Lipid peroxidation is believed to be involved in the pathophysiology of a number of diseases and in the process of aging. This study investigates the effects of dietary supplementation with vitamin E (20 g/kg diet of all-rac-alpha-tocopheryl succinate for 3 weeks) on both non-enzymatic and enzymatic lipid peroxidation in experimental rats with carbon tetrachloride (CCl4)-induced hepatotoxicity (2.5 mL/kg body).
Plasma, urine and liver samples from control rats (n = 6), CCl4-treated rats (n = 6), and rats supplemented with vitamin E prior to CCl4 treatment (n = 8) were collected. Non-enzymatic lipid peroxidation induced by free radicals was investigated by measurement of a major F2-iso-prostane, 8-iso-prostaglandin F2 alpha (8-iso-PGF2 alpha). Cyclooxygenase-catalyzed enzymatic lipid peroxidation was measured with a major PGF2 alpha metabolite, 15-keto-13,14-dihydro-prostaglandin F2 alpha (15-K-DH-PGF2 alpha). Malondialdehyde and antioxidants in plasma were also quantified.
CCl4 treatment alone resulted in significantly higher levels of plasma, urinary and liver 8-iso-PGF2 alpha, and of plasma and urinary 15-K-DH-PGF2 alpha compared to controls. Rats supplemented with vitamin E prior to CCl4 treatment had significantly lower levels of urinary and liver 8-iso-PGF2 alpha, urinary 15-K-DH-PGF2 alpha, and plasma malondialdehyde than rats treated with CCl4 alone. However, plasma 8-iso-PGF2 alpha and plasma 15-K-DH-PGF2 alpha were not affected by vitamin E supplementation.
Thus, both non-enzymatic and enzymatic lipid peroxidation during experimental hepatic oxidative injury were suppressed by dietary vitamin E supplementation in rats.
脂质过氧化被认为与多种疾病的病理生理学以及衰老过程有关。本研究调查了膳食补充维生素E（以20 g/kg饲料的全消旋α-生育酚琥珀酸酯持续3周）对四氯化碳（CCl4）诱导肝毒性（2.5 mL/kg体重）的实验大鼠非酶促和酶促脂质过氧化的影响。
收集来自对照大鼠（n = 6）、CCl4处理大鼠（n = 6）以及在CCl4处理前补充维生素E的大鼠（n = 8）的血浆、尿液和肝脏样本。通过测量主要的F2-异前列腺素8-异前列腺素F2α（8-iso-PGF2α）来研究自由基诱导的非酶促脂质过氧化。用主要的PGF2α代谢物15-酮-13,14-二氢-前列腺素F2α（15-K-DH-PGF2α）来测量环氧化酶催化的酶促脂质过氧化。还对血浆中的丙二醛和抗氧化剂进行了定量分析。
与对照组相比，单独CCl4处理导致血浆、尿液和肝脏中8-iso-PGF2α水平显著升高，以及血浆和尿液中15-K-DH-PGF2α水平显著升高。在CCl4处理前补充维生素E的大鼠，其尿液和肝脏中8-iso-PGF2α、尿液中15-K-DH-PGF2α以及血浆丙二醛水平显著低于单独接受CCl4处理的大鼠。然而，血浆8-iso-PGF2α和血浆15-K-DH-PGF2α不受维生素E补充的影响。
因此，膳食补充维生素E可抑制大鼠实验性肝脏氧化损伤过程中的非酶促和酶促脂质过氧化。
