Kandaz Mustafa, Ertekin Mustafa Vecdi, Erdemci Burak, Kızıltunç Ahmet, Koçer İbrahim, Özmen Hilal Kızıltunç, Aktan Meryem Işık, Beşe Ayşe Vildan
Atatürk University, Faculty of Medicine, Department of Radiation Oncology, Erzurum, Turkey.
Atatürk University, Faculty of Medicine, Department of Biochemistry, Erzurum, Turkey.
Eurasian J Med. 2009 Aug;41(2):110-5.
There is currently substantial clinical interest in zinc (Zn) as an antioxidant and a protective agent against radiation-related normal tissue injury. To further assess the potential antioxidative effects, the effects of Zn were studied in rat lenses, a model of radiation-induced oxidative stress.
Sprague-Dawley rats were divided into three equal groups. Group 1 received neither Zn nor irradiation (control group). Group 2 (RT group) and 3 (RT+Zn group) were exposed to total cranium irradiation of 5 Gy in a single dose by using a cobalt-60 teletherapy unit. In addition to irradiation, group 3 was administered 10 mg/kg/day Zn. At the end of 10 days, the rats were killed. Their eyes were enucleated to measure the activities of antioxidant enzymes and the levels of iron, calcium, sodium and potassium.
Irradiation significantly increased malondialdehyde levels as an end product of lipid peroxidation, glutathione peroxidase activity, and iron and calcium concentrations. Irradiation decreased super-oxide dismutase activities and zinc concentrations in the rat lens, indicating an increased oxidative stress generated by the decomposition of water and/or Fenton reaction. Malondialdehyde levels and iron and calcium concentrations were significantly decreased, and superoxide dismutase and glutathione peroxidase activities and zinc concentrations were increased, in the rat lenses of the RT+Zn group. No differences were detected in any final measurement of sodium and potassium in the direct comparison among all groups.
Zinc, acting as an antioxidant agent, may protect the lens from radiation-induced injury by improving oxidative stress generated by the decomposition of water and/or Fenton reaction.
目前，锌作为一种抗氧化剂以及预防辐射相关正常组织损伤的保护剂，在临床上备受关注。为进一步评估其潜在的抗氧化作用，我们在大鼠晶状体（一种辐射诱导氧化应激的模型）中研究了锌的作用。
将斯普拉格 - 道利大鼠分为三组，每组数量相等。第1组既未接受锌处理也未接受辐射（对照组）。第2组（放疗组）和第3组（放疗 + 锌组）使用钴 - 60远距离治疗装置单次接受5 Gy的全颅照射。除照射外，第3组给予10 mg/kg/天的锌。10天后，处死大鼠。摘除其眼球以测量抗氧化酶活性以及铁、钙、钠和钾的水平。
辐射显著增加了脂质过氧化终产物丙二醛水平、谷胱甘肽过氧化物酶活性以及铁和钙的浓度。辐射降低了大鼠晶状体中超氧化物歧化酶活性和锌浓度，表明水分解和/或芬顿反应产生的氧化应激增加。在放疗 + 锌组的大鼠晶状体中，丙二醛水平以及铁和钙的浓度显著降低，超氧化物歧化酶和谷胱甘肽过氧化物酶活性以及锌浓度升高。在所有组的直接比较中，钠和钾的任何最终测量值均未检测到差异。
锌作为一种抗氧化剂，可能通过改善水分解和/或芬顿反应产生的氧化应激，保护晶状体免受辐射诱导的损伤。
