肿瘤坏死因子可致机体脂质过氧化损伤

Tumor necrosis factor can ca use peroxidative injury

采用ＳＤ大鼠持续泵入人工重组肿瘤坏死因子。型（ｒｈ－ＴＮＦ－ａ），以６×１０￣５Ｕ·ｋｇ￣－１／ｄ速度作用７２ｈ，观察血浆及组织丙二醛（ＭＤＡ）含量，全血和组织超氧化物歧化酶（ＳＯＤ）活性，组织超弱发光和白细胞吞噬发光的变化。结果：血浆及组织ＭＤＡ含量明显增加，全血ＳＯＤ活性显著下降，组织ＳＯＤ活性所受影响较小，肾、肠组织超弱发光明显增强，白细胞吞噬发光无明显变化。实验表明：持续７２ｈ泵入ＴＮＦ作用于大鼠，可使机体自由基产生增加，自由基清除系统部分受损，而导致脂质过氧化损伤，但对分叶核粒细胞的呼吸爆发作用无明显影响。

We investigated the relasionship between tumornecrosis factor and free radicals in 21 SD rats,rh-TNF was administered intravenouslyto 14 rats at a speed of 2.5 ml·kg￣-1 /h, and 7 rats ascontrols receiving the same volume of caline. The ani-mals were decapitated at 24 h or 72 h. The levels ofTNF and MDA and activities of superoxide dismutase(SOD)in blood and tissues were determined, The ultra-weak chemiluminescence of tissues and luminol-dependent chemiluminescence of polymorphonuclears(PMN)were measured.The level of TNF in plasma of the 24 h group wasslgnificantly higlier than that of the controls and the 72h group, and TNF in most tissues were undetectable.The contents of MDA in both plasma and tissues wereincreased markedly in the 24 h and the 72 h groups. Theactivities of SOD in whole bled were significantly decreased both in the 24 h and the 72 h groups.The ultra-weak chemiluminescence of renal and ileum tissues ofthe 72 h group increasd significantly than that of thecontrol group. There was no difference in the luminol-dependent chemiluminescence of PMN between the 72 hand the control groups.It is suggested t hat the comtinuous intravenous ad-ministration of rh-TNF-a(6× 10￣ 5U·kg￣-1/d)to ratsfor 72 hours may induce oxygen free radicals in plasmaand tissues and then lead to lipid peroxideformation andmembrane damage.