Choi Jeong-Hwa, Chang Hyeun-Wook, Rhee Soon-Jae
Department of Food Science and Nutrition, Catholic University of Daegu, Kyongsan-si, Korea.
Asia Pac J Clin Nutr. 2002;11(4):292-7. doi: 10.1046/j.1440-6047.2002.00305.x.
The purpose of this study was to investigate the effect of green tea catechin on the cyclooxygenase and lipoxygenase pathways in chronic cadmium-poisoned rats. Sprague-Dawley male rats weighing 100 +/- 10 g were randomly assigned to one normal and three cadmium-poisoned groups. The cadmium groups were classified as catechin-free diet group (Cd-0C), 0.25% catechin diet group (Cd-0.25C) and 0.5% catechin diet group (Cd-0.5C), in accordance with the level of catechin supplement. The phospholipase A2 activity was remarkably increased 117% in the Cd-0C group and 60% in the Cd-0.25C group compared with the normal group, and the level in the Cd-0.5C group was the same as the normal group. Activity of platelet cyclooxygenase increased 284% in the Cd-0C group, 147% in the Cd-0.25C group and 193% in the Cd-0.5C group. The synthesis of platelet thromboxane A2 (TXA2) increased 157% in the Cd-0C group and 105% in the Cd-0.25C group, compared with the normal group. The Cd-0.5C group showed the same level as the normal group. Prostacyclin (PGI2) formation in the aorta decreased 24% in the Cd-0C group and 18% in the Cd-0.25C group. The ratio of PGI2/TXA2, the thrombocyte synthesis index, decreased 70% in the Cd-0C group and 59% in the Cd-0.25C group. The activity of 5'-lipoxygenase in the polymorphonuclear leukocyte was increased 40% in the Cd-0C group as compared with the normal group. Catechin-supplemented Cd-0.25C and Cd-0.5C groups showed the level of the normal group. In this study, the observed content of leukotriene B4, which induces the inflammatory process, increased 54% in the Cd-0C group, and in catechin-supplemented groups, showed the same level as in the normal group. The serum peroxide value increased 60% in the Cd-0C group compared with the normal group; but in the Cd-0.5C group, it showed the level of the normal group. These results indicate that chronic cadmium poisoning in rats accelerates arachidonic acid metabolism. Inhibition of arachidonic acid metabolism due to catechin supplementation, however, decreases platelet aggregation and inflammatory action. In conclusion, it would appear that green tea catechin supplementation in chronic cadmium-poisoned rats inhibits the arachidonic acid cascade by regulating the activity of phospholipase A2.
本研究的目的是探讨绿茶儿茶素对慢性镉中毒大鼠环氧化酶和脂氧合酶途径的影响。将体重100±10 g的Sprague-Dawley雄性大鼠随机分为一个正常组和三个镉中毒组。根据儿茶素补充水平，镉中毒组分为无儿茶素饮食组（Cd-0C）、0.25%儿茶素饮食组（Cd-0.25C）和0.5%儿茶素饮食组（Cd-0.5C）。与正常组相比，Cd-0C组磷脂酶A2活性显著升高117%，Cd-0.25C组升高60%，Cd-0.5C组水平与正常组相同。血小板环氧化酶活性在Cd-0C组升高284%，Cd-0.25C组升高147%，Cd-0.5C组升高193%。与正常组相比，Cd-0C组血小板血栓素A2（TXA2）合成增加157%，Cd-0.25C组增加105%。Cd-0.5C组水平与正常组相同。主动脉中前列环素（PGI2）生成在Cd-0C组降低24%，Cd-0.25C组降低18%。血小板合成指数PGI2/TXA2比值在Cd-0C组降低70%，Cd-0.25C组降低59%。与正常组相比，Cd-0C组多形核白细胞中5'-脂氧合酶活性升高40%。补充儿茶素的Cd-0.25C组和Cd-0.5C组水平与正常组相同。在本研究中，诱导炎症过程白三烯B4的观察含量在Cd-0C组升高54%，在补充儿茶素组中与正常组水平相同。与正常组相比，Cd-0C组血清过氧化物值升高60%；但在Cd-0.5C组，其水平与正常组相同。这些结果表明，大鼠慢性镉中毒加速了花生四烯酸代谢。然而，补充儿茶素对花生四烯酸代谢的抑制作用降低了血小板聚集和炎症作用。总之，慢性镉中毒大鼠补充绿茶儿茶素似乎通过调节磷脂酶A2的活性来抑制花生四烯酸级联反应。
