Advanced glycation endproducts (AGEs) induce oxidant stress in the gingiva: A potential mechanism underlying accelerated periodontal disease associated with diabetes
Advanced glycation endproducts (AGEs) induce oxidant stress in the gingiva: A potential mechanism underlying accelerated periodontal disease associated with diabetes
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DOI：
10.1111/j.1600-0765.1996.tb01417.x
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发表时间：
1996-10-01
影响因子：
3.5
通讯作者：
Lamster, IB
中科院分区：
文献类型：
--
作者：
Schmidt, AM;Weidman, E;Lamster, IB
我们假设糖尿病晚期牙周病的一个潜在机制可能涉及牙龈中的氧化应激，由晚期糖基化终产物（AGE 5）的作用诱导，晚期糖基化终产物是非酶糖化的不可逆产物，蛋白质和脂质的氧化在糖尿病血浆和组织中积累：输注AGE白蛋白，一种原型配体，与在牙龈中输注非糖化白蛋白相比，以及在肺、肾和脑中。用抗氧化剂普罗布考或N-乙酰半胱氨酸（NAC）对动物进行预处理可以防止牙龈中产生泪液。与非糖尿病对照组相比，亲和纯化的AGEs抗体显示链脲佐菌素诱导的糖尿病小鼠牙龈血管和结缔组织中AGEs的免疫反应性增加。通过免疫组化和ELISA，糖尿病患者牙龈中AGEs的免疫反应性也比非糖尿病患者增加。与这些数据一致，血红素加氧酶-1的免疫组织化学，增强氧化应激的掩蔽物，增加了糖尿病小鼠和人类的牙龈血管与非糖尿病对照组相比。这些数据表明，AGEs存在于。糖尿病牙龈可能与氧化应激增强的状态有关，这是加速组织损伤的潜在机制。
We hypothesizes that one mechanism underlying advanced periodontal disease in diabetes may involve oxidant stress in the gingiva, induced by the effects of Advanced Glycation Endproducts (AGE5), the irreversible products of non-enzymatic glycation and oxidation of proteins and lipids which accumulate in diabetic plasma and tissue: Infusion of AGE albumin, a prototypic ligand, into mice resulted in increased generation of thiobarbituric acid reactive substances (TEARS) compared with infusion of non-glycated albumin in the gingiva: as well as in the lung, kidney and brain. Pretreatment of the animals with the antioxidants probucol or N-acetylcysteine (NAC) prevented the generation of TEARS in the gingiva. Affinity-purified antibody to AGEs demonstrated increased immunoreactivity for AGEs in the vasculature and connective tissues of the gingiva in streptozotocin-induced diabetic mice compared to non-diabetic controls. Increased immunoreactivity for AGEs was also demonstrated in the gingiva of diabetic humans compared with non-diabetic individuals via immunohistochemistry and ELISA. Consistent with these,data, immunohistochemistry for heme oxygenase-1, a masker of enhanced oxidant stress, was increased in the gingival vasculature of diabetic mice and humans compared with non-diabetic controls. These data suggest that AGEs present in. diabetic gingiva may be associated with a state of enhanced oxidant stress, a potential mechanism for accelerated tissue injury.