Dietary docosahexaenoic acid-induced generation of liver lipid peroxides is not suppressed further by elevated levels of glutathione in ODS rats.
Dietary docosahexaenoic acid-induced generation of liver lipid peroxides is not suppressed further by elevated levels of glutathione in ODS rats.
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DOI：
10.1016/j.nut.2005.09.005
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发表时间：
2006-04
期刊：
影响因子：
4.4
通讯作者：
S. Sekine;K. Kubo;T. Tadokoro;M. Saito
中科院分区：
文献类型：
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作者：
S. Sekine;K. Kubo;T. Tadokoro;M. Saito
抗坏血酸（阿萨）和谷胱甘肽（GSH）对细胞凋亡的影响（GSH;实验1）和GSH在对乙酰氨基酚喂养大鼠（实验2）对膳食二十二碳六烯酸（DHA）诱导的组织脂质过氧化的影响。AsA需要型成骨障碍Shionogi/Shi-od/od（ODS）大鼠饲喂含DHA的大豆蛋白饲料（10.0%总能量）和阿萨（50（低）或300（正常）mg/kg，不含（低）或含（正常）蛋氨酸2 g/kg，持续32 d。实验2中，ODS大鼠饲喂含DHA（总能量的7.8%）和对乙酰氨基酚（4 g/kg）的饲料，并添加不同水平的蛋氨酸（分别为0、3、6和9 g/kg的低、中、高和过量）。实验1中，低AsA组肝脏脂质过氧化物水平低于正常AsA组，但低AsA组肾脏和睾丸脂质过氧化物水平高于正常AsA组。膳食蛋氨酸倾向于降低组织过氧化脂质水平，但没有减少维生素E（VE）的消耗。在实验2中，高水平的蛋氨酸（6 g/kg）降低肝脏脂质过氧化物水平和VE消耗。然而，产生的组织脂质过氧化物和VE消费量没有进一步降低了更高剂量的蛋氨酸（9 g/kg）。CONCLUSIONSShigher比正常水平的饮食蛋氨酸不一定与减少饮食DHA诱导的产生的组织脂质过氧化物和VE消费量，除了GSH的需求增加，如对乙酰氨基酚喂养的条件。
OBJECTIVESWe examined the effects of ascorbic acid (AsA) and glutathione (GSH; experiment 1) and of GSH in acetaminophen-fed rats (experiment 2) on dietary docosahexaenoic acid (DHA)–induced tissue lipid peroxidation.METHODSIn experiment 1, AsA-requiring Osteogenic Disorder Shionogi/Shi-od/od (ODS) rats were fed soybean protein diets containing DHA (10.0% total energy) and AsA at 50 (low) or 300 (normal) mg/kg without (low) or with (normal) methionine at 2 g/kg for 32 d. In experiment 2, ODS rats were fed diets containing DHA (7.8% total energy) and acetaminophen (4 g/kg) with different levels of dietary methionine (low, moderate, high, and excessive at 0, 3, 6, and 9 g/kg, respectively) for 30 d. Tissue lipid peroxides and antioxidant levels were determined.RESULTSIn experiment 1, liver lipid peroxide levels in the low-AsA group were lower than those in the normal-AsA group, but kidney and testis lipid peroxide levels in the low-AsA group were higher than those in the normal-AsA group. Dietary methionine tended to decrease tissue lipid peroxide levels but did not decrease vitamin E (VE) consumption. In experiment 2, a high level of methionine (6 g/kg) decreased liver lipid peroxide levels and VE consumption. However, generation of tissue lipid peroxides and VE consumption were not decreased further by a higher dose of methionine (9 g/kg).CONCLUSIONSHigher than normal levels of dietary methionine are not necessarily associated with decreased dietary DHA-induced generation of tissue lipid peroxides and VE consumption except that the GSH requirement is increased in a condition such as acetaminophen feeding.