Effects of vitamin E, ascorbic acid and mannitol on alloxan-induced lipid peroxidation in rats.
Effects of vitamin E, ascorbic acid and mannitol on alloxan-induced lipid peroxidation in rats.
复制标题
维生素 E、抗坏血酸和甘露醇对四氧嘧啶诱导的大鼠脂质过氧化的影响。
DOI：
10.1016/0003-9861(82)90205-3
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发表时间：
1982
影响因子：
3.9
通讯作者：
Tappel,AL
中科院分区：
文献类型：
--
作者：
Dillard,CJ;Kunert,KJ;Tappel,AL
ω6-和ω3-不饱和脂质氢过氧化物分解分别产生戊烷和乙烷。在大鼠腹腔注射20 mg四氧嘧啶/100 g体重诱导脂质过氧化过程中，研究了四氧嘧啶毒性与戊烷和乙烷的关系。注射15分钟后，维生素E缺乏的大鼠呼出的戊烷和乙烷分别是注射前的102倍和11.2倍。在四氧嘧啶处理前30 min注射75 mg/100 g体重的抗坏血酸可延长过氧化反应发生的时间，所有维生素E缺乏大鼠在4 h内死亡。在四氧嘧啶治疗前30分钟注射100 mg自由基清除剂甘露醇/ 100 g体重的维生素E缺乏大鼠完全免受脂质过氧化作用的影响，4 h内无大鼠死亡。喂食40 iudl-α-生育酚乙酸酯/kg饲料或注射100 mgdl-α-生育酚/100 g体重的大鼠可完全免受四氧嘧啶和四氧嘧啶-抗坏血酸诱导的过氧化作用，或仅受到轻微影响，如极低水平的戊烷和乙烷产生所示。四氧嘧啶治疗后4 h血浆、肝脏和胰腺中的硫代巴比妥酸反应物反映了抗坏血酸和四氧嘧啶的促氧化性质、大鼠的维生素E状况和甘露醇的保护作用。四氧嘧啶注射后4小时的血浆葡萄糖水平在维生素E注射大鼠中最低，在维生素E缺乏大鼠中最高。只有在维生素E缺乏的大鼠脂质过氧化和显着升高的血浆葡萄糖水平观察后4小时四氧嘧啶治疗。
ω6- and ω3-unsaturated lipid hydroperoxides decompose to yield pentane and ethane, respectively. Alloxan toxicity was studied in rats in relation to pentane and ethane produced during lipid peroxidation induced by intraperitoneal injection of 20 mg of alloxan/100 g body wt. Fifteen minutes after injection, vitamin E-deficient rats exhaled 102- and 11.2-fold more pentane and ethane, respectively, than prior to injection. Injection of 75 mg ascorbic acid/100 g body wt 30 min prior to alloxan treatment prolonged the time over which peroxidation occurred and all vitamin E-deficient rats died before 4 h. Vitamin E-deficient rats injected with 100 mg of the radical scavenger mannitol/ 100 g body wt 30 min prior to alloxan treatment were completely protected against lipid peroxidation, and none of the rats died by 4 h. Rats fed 40 iudl-α-tocopherol acetate/kg diet or injected with 100 mgdl-α-tocopherol/100 g body wt were either totally protected against alloxan and alloxan-ascorbic acid-induced peroxidation or were only slightly affected as shown by very low-level pentane and ethane production. Thiobarbituric acid reactants in plasma, liver and pancreas 4 h after alloxan treatment reflected the prooxidant nature of ascorbic acid and alloxan, the vitamin E status of the rats and the protective effect of mannitol. Plasma glucose levels 4 h after alloxan injection were lowest in vitamin E-injected rats and highest in vitamin E-deficient rats. Only in vitamin E-deficient rats were both lipid peroxidation and significantly elevated plasma glucose levels observed by 4 h post-alloxan treatment.