Rojas C, Cadenas S, Herrero A, Méndez J, Barja G
Department of Animal Biology-II (Animal Physiology), Faculty of Biology Complutense University, Madrid, Spain.
Life Sci. 1996;59(8):649-57. doi: 10.1016/0024-3205(96)00346-3.
The effect of acute endotoxin-induced septic shock on myocardium oxidative stress after low or high vitamin C and/or E dietary supplementation was studied in guinea pigs, laboratory animals which, like human, do not have capacity for ascorbate synthesis. Neither the antioxidant enzymes or GSH were modified by endotoxin and vitamin treatments. Vitamin E showed a strong capacity to protect the myocardium against both enzymatic and non-enzymatic lipid peroxidation even in the presence of endotoxin. Vitamin C supplementation increased heart ascorbate whereas endotoxic shock totally depleted the heart ascorbate of vitamin C supplemented animals without changing vitamin E. Endotoxin significantly increased myocardium uric acid, a marker of ischemia induced oxidative stress, in animals fed with low vitamin C levels. This increase was totally prevented in vitamin C supplemented, but not in vitamin E supplemented animals. Strongly depressed levels of plasma vitamin C have been recently described in sepsis in human patients. The results suggest that ascorbate is a primary antioxidant target in the heart of endotoxin treated mammals lacking the capacity to synthesize ascorbate and that ascorbate can have a protective value against endotoxin-induced free radical damage in the myocardium. Implications of these results for the possible preventive role of vitamin C in humans during sepsis are discussed.
在豚鼠（一种像人类一样没有合成抗坏血酸能力的实验动物）中，研究了低或高剂量维生素C和/或E饮食补充后，急性内毒素诱导的脓毒症休克对心肌氧化应激的影响。内毒素和维生素处理均未改变抗氧化酶或谷胱甘肽（GSH）。即使存在内毒素，维生素E也显示出强大的保护心肌免受酶促和非酶促脂质过氧化的能力。补充维生素C可增加心脏中的抗坏血酸含量，而内毒素休克会使补充维生素C的动物心脏中的抗坏血酸完全耗尽，而维生素E含量不变。在维生素C水平低的动物中，内毒素显著增加了心肌尿酸，这是缺血诱导氧化应激的标志物。在补充维生素C的动物中，这种增加被完全阻止，但在补充维生素E的动物中则没有。最近在人类脓毒症患者中描述了血浆维生素C水平严重降低的情况。结果表明，抗坏血酸是缺乏合成抗坏血酸能力的内毒素处理哺乳动物心脏中的主要抗氧化靶点，并且抗坏血酸可以对心肌中内毒素诱导的自由基损伤具有保护作用。讨论了这些结果对维生素C在人类脓毒症期间可能的预防作用的影响。
