Chugh S N, Kolley T, Kakkar R, Chugh K, Sharma A
Department of Medicine and Biochemistry, Postgraduate Institute of Medical Sciences, Rohtak, Haryana, India.
Magnes Res. 1997 Sep;10(3):225-30.
The anti-peroxidant effect of intravenous magnesium was evaluated in 50 patients with acute aluminium phosphide poisoning. The patients were divided into two groups, one who received magnesium sulphate therapy (Group I) and the other who did not (Group II). The clinical and biochemical parameters in both groups were comparable. Finding of increased mean malonyl-di-aldehyde (MDA) levels in group I (3.18 +/- 0.93 micromol/L) and group II (3.15 +/- 0.78 mmol/L) combined with low blood levels of reduced glutathione (18.5 +/- 1.6 mg/dl in group I) and (17.8 +/- 1.4 mg/dl in group II) indicated oxidative stress leading to accelerated lipid peroxidation in the early phase (0-6 h) of AlP poisoning. A significant fall in MDA levels was observed after 2 h in the magnesium treated group (group I) compared to the non-treated group (group II) and levels became normal between 48-72 h. Similarly reduced glutathione started recovering between 12-24 h which became significant after 24 h and full recovery took place between 48-72 h in the magnesium treated group (group I). Both these parameters suggested an anti-peroxidant effect of magnesium. There was also a slight fall in MDA levels and a rise in reduced glutathione in the non-treated group II patients. This could be due to elimination of phosphine (PH3). We hypothesize that oxidative stress in AlP poisoning buffered the magnesium leading to a transient fall in magnesium and magnesium dependent GSH, resulting in increased susceptibility of oxygen free radical injury and accelerated lipid peroxidation. The fall in MDA and slower rise in GSH in group I than in group II suggested magnesium combated free radical stress slowly and independent of elimination of phosphine. This hypothesis was further strengthened by similar observations when both these parameters were compared in survivors in both groups. Mortality was higher in group II than in group I (44 per cent vs 20 per cent) and was probably related directly to oxidative stress.
对50例急性磷化铝中毒患者评估了静脉注射镁的抗氧化作用。患者被分为两组,一组接受硫酸镁治疗(第一组),另一组未接受治疗(第二组)。两组的临床和生化参数具有可比性。第一组(3.18±0.93微摩尔/升)和第二组(3.15±0.78毫摩尔/升)丙二醛(MDA)平均水平升高,同时两组血中还原型谷胱甘肽水平较低(第一组为18.5±1.6毫克/分升,第二组为17.8±1.4毫克/分升),这表明在急性磷化铝中毒的早期阶段(0 - 6小时)存在氧化应激,导致脂质过氧化加速。与未治疗组(第二组)相比,镁治疗组(第一组)在2小时后MDA水平显著下降,在48 - 72小时之间恢复正常。同样,还原型谷胱甘肽在12 - 24小时开始恢复,在24小时后变得显著,在镁治疗组(第一组)中48 - 72小时完全恢复。这两个参数均提示镁具有抗氧化作用。未治疗的第二组患者MDA水平也略有下降,还原型谷胱甘肽水平有所上升。这可能是由于膦(PH3)的清除。我们推测,急性磷化铝中毒中的氧化应激缓冲了镁,导致镁和镁依赖性谷胱甘肽短暂下降,从而增加了氧自由基损伤的易感性并加速了脂质过氧化。第一组MDA的下降和谷胱甘肽的上升比第二组慢,表明镁对抗自由基应激的作用缓慢,且与膦的清除无关。当在两组幸存者中比较这两个参数时,类似的观察结果进一步支持了这一假说。第二组的死亡率高于第一组(44%对20%),这可能与氧化应激直接相关。