Koul A, Bhatia V, Bansal M P
Department of Biophysics, Panjab University, Chandigarh-160014, India.
BMC Biochem. 2001;2:14. doi: 10.1186/1471-2091-2-14. Epub 2001 Nov 16.
Free radicals generated in biological systems by cigarette smoke (CS) inhalation can cause oxidative stress in tissues, resulting in lipid peroxidation (LPO). In view of the antioxidant properties of alpha-tocopherol (AT), in the present study, effects of AT on antioxidant defence system and LPO were investigated in mice inhaling CS for different time intervals.
Male Balb/c mice were fed orally with AT (5 I.U./Kg.b.wt.) and /or exposed to CS for 2, 4, 6 or 8 weeks. No effect was observed on body growth, diet consumption, water intake and lung weight due to AT and /or CS treatment in any of the groups as compared to their control counterparts. After two weeks of treatment, no change in LPO, reduced glutathione (GSH) levels and antioxidant enzymes were observed except for glutathione reductase (GR) which increased in all the treated groups. A significant increase in pulmonary LPO levels was observed in mice exposed to CS inhalation for 4, 6 or 8 weeks. There was a gradual increase in the LPO levels as the extent of CS inhalation increased from 4 to 8 weeks. However, the extent of increase in LPO levels due to CS exposure for 4, 6 or 8 weeks in the mice treated with AT was comparatively less. A significant decrease in the GSH levels was also observed in all the animals exposed to CS for 4, 6 or 8 weeks. There was a significant increase in the activities of catalase, glutathione peroxidase (GSH-Px) and GR observed in all the groups exposed to CS for 4,6 or 8 weeks. The increase in above antioxidant enzymes seems to be insufficient to combat the oxidative stress posed by CS inhalation. There was a marked decrease observed in the LPO levels in the animals treated with AT alone for 4, 6, or 8 weeks, when compared to their control counterparts. However, the supplementation of AT for 4, 6 or 8 weeks demonstrated a significant increase in GSH levels.
It appears from our studies that AT exhibits its antioxidant role either directly by scavenging the oxidative species or indirectly by modulating the GSH levels.
吸入香烟烟雾（CS）在生物系统中产生的自由基可导致组织氧化应激，进而引发脂质过氧化（LPO）。鉴于α-生育酚（AT）的抗氧化特性，在本研究中，研究了AT对不同时间间隔吸入CS的小鼠抗氧化防御系统和LPO的影响。
雄性Balb/c小鼠口服AT（5国际单位/千克体重）和/或暴露于CS中2、4、6或8周。与对照小鼠相比，在任何组中，AT和/或CS处理对体重增长、饮食消耗、水摄入量和肺重量均无影响。处理两周后，除谷胱甘肽还原酶（GR）在所有处理组中均增加外，未观察到LPO、还原型谷胱甘肽（GSH）水平和抗氧化酶的变化。在吸入CS 4、6或8周的小鼠中，观察到肺LPO水平显著升高。随着CS吸入时间从4周增加到8周，LPO水平逐渐升高。然而，在用AT处理的小鼠中，由于CS暴露4、6或8周导致的LPO水平升高程度相对较小。在所有暴露于CS 4、6或8周的动物中，也观察到GSH水平显著降低。在所有暴露于CS 4、6或8周的组中，过氧化氢酶、谷胱甘肽过氧化物酶（GSH-Px）和GR的活性显著增加。上述抗氧化酶的增加似乎不足以对抗吸入CS引起的氧化应激。与对照小鼠相比，单独用AT处理4、6或8周的动物中LPO水平显著降低。然而，补充AT 4、6或8周显示GSH水平显著增加。
从我们的研究来看，AT似乎通过清除氧化物质直接发挥其抗氧化作用，或通过调节GSH水平间接发挥作用。
