Slyshenkov V S, Rakowska M, Moiseenok A G, Wojtczak L
Nencki Institute of Experimental Biology, Warsaw, Poland.
Free Radic Biol Med. 1995 Dec;19(6):767-72. doi: 10.1016/0891-5849(95)00084-b.
Preincubation of Ehrlich ascites tumor cells at 22 or 32 degrees C, but not at 0 degree C, with pantothenic acid, 4'-phosphopantothenic acid, pantothenol, or pantethine reduced lipid peroxidation (measured by production of thiobarbituric acid-reactive compounds) induced by the Fenton reaction (Fe2+ + H2O2) and partly protected the plasma membrane against the leakiness to cytoplasmic proteins produced by the same reagent. Pantothenic acid and its derivatives did not inhibit (Fe2+ + H2O2)-induced peroxidation of phospholipid multilamellar vesicles, thus indicating that their effect on the cells was not due to the scavenging mechanism. Homopantothenic acid and its 4'-phosphate ester (which are not precursors of CoA) neither protected Ehrlich ascites tumor cells against lipid peroxidation nor prevented plasma membrane leakiness under the same conditions. Incubation of the cells with pantothenic acid, 4'-phosphopantothenic acid, pantothenol, or pantethine significantly increased the amount of cellular CoA and potentiated incorporation of added palmitate into phospholipids and cholesterol esters. It is concluded that pantothenic acid and its related compounds protect the plasma membrane of Ehrlich ascites tumor cells against the damage by oxygen free radicals due to increasing cellular level of CoA. The latter compound may act by diminishing propagation of lipid peroxidation and promoting repair mechanisms, mainly the synthesis of phospholipids.
将艾氏腹水瘤细胞在22或32摄氏度（而非0摄氏度）下与泛酸、4'-磷酸泛酸、泛醇或泛硫乙胺预孵育，可降低由芬顿反应（Fe2+ + H2O2）诱导的脂质过氧化（通过硫代巴比妥酸反应性化合物的产生来衡量），并部分保护质膜免受同一试剂导致的细胞质蛋白渗漏。泛酸及其衍生物不抑制（Fe2+ + H2O2）诱导的磷脂多层囊泡的过氧化，因此表明它们对细胞的作用并非由于清除机制。同型泛酸及其4'-磷酸酯（它们不是辅酶A的前体）在相同条件下既不能保护艾氏腹水瘤细胞免受脂质过氧化，也不能防止质膜渗漏。用泛酸、4'-磷酸泛酸、泛醇或泛硫乙胺孵育细胞显著增加了细胞内辅酶A的量，并增强了添加的棕榈酸掺入磷脂和胆固醇酯的能力。得出的结论是，泛酸及其相关化合物通过提高细胞内辅酶A水平来保护艾氏腹水瘤细胞的质膜免受氧自由基的损伤。后一种化合物可能通过减少脂质过氧化的传播和促进修复机制（主要是磷脂的合成）来发挥作用。
