Chandra Jagetia Ganesh, Rajanikant G K, Rao Shaival K, Shrinath Baliga M
Department of Radiobiology, Kasturba Medical College, Manipal-576 119, India.
Clin Chim Acta. 2003 Jun;332(1-2):111-21. doi: 10.1016/s0009-8981(03)00132-3.
In spite of the immense therapeutic gains produced by the fractionated irradiation (IR) regimen, radiation burden on the skin increases significantly. Protection of skin might enable use of higher radiation doses for better therapeutic gains. Ascorbic acid (AA), an essential ingredient of the human diet, is known to be a free radical scavenger and radioprotective agent. This study was undertaken to evaluate the effect of ascorbic acid on the radiation-induced changes in the status of glutathione (GSH), glutathione peroxidase (GPx), superoxide dismutase (SOD) and lipid peroxidation (LPx) in the skin of mice exposed to 10, 16 and 20 Gy of fractionated gamma radiation.
One group of the animals was administered daily with double distilled water (DDW), while the other group received 250 mg/kg b. wt. of ascorbic acid once daily, consecutively for 5, 8 or 10 days, before hemibody (below rib cage) exposure to 2 Gy/day of gamma-rays. Skin biopsies from both the groups were collected for the biochemical estimations.
The irradiation of animals resulted in a dose-dependent decline in the activities of superoxide dismutase, glutathione peroxidase and glutathione contents. Ascorbic acid pretreatment resulted in a significant increase in the activities of both the enzymes and glutathione in the irradiated mouse skin. Normal concentrations of glutathione could not be restored even by day 6 post-irradiation. Conversely, lipid peroxidation increased in a dose-dependent manner in both the groups reaching a peak concentration by 3 h post-irradiation, while the ascorbic acid pretreatment inhibited the radiation-induced increase in lipid peroxidation.
The ascorbic acid treatment arrested the decline in the activities of superoxide dismutase and glutathione peroxidase, glutathione contents and inhibited the radiation-induced lipid peroxidation in the skin of mice exposed to different doses of fractionated gamma radiation.
尽管分次照射方案带来了巨大的治疗效果，但皮肤所承受的辐射负担显著增加。保护皮肤或许能使人们使用更高的辐射剂量以获得更好的治疗效果。抗坏血酸（AA）是人类饮食中的一种必需成分，已知它是一种自由基清除剂和辐射防护剂。本研究旨在评估抗坏血酸对接受10、16和20 Gy分次γ射线照射的小鼠皮肤中谷胱甘肽（GSH）、谷胱甘肽过氧化物酶（GPx）、超氧化物歧化酶（SOD）状态以及脂质过氧化（LPx）的辐射诱导变化的影响。
一组动物每日给予双蒸水（DDW），另一组在半侧身体（肋骨以下）每天接受2 Gyγ射线照射前，连续5、8或10天每天给予250 mg/kg体重的抗坏血酸。收集两组动物的皮肤活检样本进行生化测定。
动物照射导致超氧化物歧化酶、谷胱甘肽过氧化物酶活性及谷胱甘肽含量呈剂量依赖性下降。抗坏血酸预处理使照射小鼠皮肤中两种酶的活性及谷胱甘肽显著增加。即使在照射后第6天，谷胱甘肽的正常浓度也未能恢复。相反，两组脂质过氧化均呈剂量依赖性增加，在照射后3小时达到峰值浓度，而抗坏血酸预处理抑制了辐射诱导的脂质过氧化增加。
抗坏血酸处理阻止了接受不同剂量分次γ射线照射的小鼠皮肤中超氧化物歧化酶和谷胱甘肽过氧化物酶活性、谷胱甘肽含量的下降，并抑制了辐射诱导的脂质过氧化。
