辐射所致脂类过氧化及WR-2721防护作用的研究

以4～10Gy与5～20Gy分别照射大鼠与小鼠。照后第三天,动物的肝、脑、肾、心和骨髓细胞等组织脂类过氧化物(LPO)较未照射动物显著增高,而且随照射剂量增加而增加,但腹腔注射WR-2721可使5～20Gy照射后小鼠各组织LPO明显降低。8Gy与8.5Gy分别照射大鼠与小鼠,可使照后10天内,动物的肝、脑、肾、心、脾、睾丸、骨髓细胞等组织与肝的亚细胞器脂类过氧化率均有不同程度的增高,而且其时相性变各有差异。给予WR-2721可使照射小鼠的组织与细胞器中LPO水平显著降低。     

茜甙对辐射所致脂类过氧化的影响 Ⅱ.小鼠组织

全身一次照射8.5Gy后,LACA小鼠的肝、脑与睾丸发生不同程度的脂类过氧化,但照射前腹腔注射茜甙,可使其脂类过氧化程度显著减轻。茜甙对辐射所致脂类过氧化的影响可能是在强氧化剂的作用下,茜甙的分子结构中(?)OH可氧化为(?)O,起到抗氧化剂的类似效应。     

茜甙对辐射所致脂类过氧化的影响 Ⅰ.卵磷脂脂质体

本文将卵磷脂脂质体作为人工膜,以观察茜甙对离体照射条件下脂类过氧化的影响。其主要结果为:(1) 辐射确可引发卵磷脂脂质体的脂类过氧化,如300～800Gy照射使脂质体的脂类过氧化值较照射前增高;900～1000 Gy照射尚可使脂类过氧化值增高6～7倍。(2) 茜甙可减轻辐射所致脂质体脂类过氧化,但照射前加入茜甙的效果显著高于照射后加入。     

ADP-FeCl_3-黄嘌呤-黄嘌呤氧化酶体系产生的活性氧对脂质体的过氧化影响

ADP-FeCl_3-黄嘌呤-黄嘌呤氧化酶体系能引发卵磷脂脂质体的过氧化,但加入超氧化物歧化酶或过氧化氢酶能显著抑制该反应,而且两种酶的合并效应高于单独酶.根据这些结果,提出了ADP-FeCl_3-黄嘌呤-黄嘌呤氧化酶体系产生的活性氧对脂质体过氧化影响的机理.     

失血和输血后照射小鼠造血干细胞从屏蔽骨髓的迁移

许多工作都证明了,给动物过多地输入红细胞,可导致红细胞生成的抑制,而失血则能刺激红细胞生成。众所周知,用致死剂量照射动物时,由于注入红细胞生成素或由于出血刺激了红细胞的生成,都能增加屏蔽骨髓的防护作用,表现出动物的活存率增加。同样也证明了,失血可使受致死量照射     

民航飞行人员的血清过氧化脂质水平

目的　观察职业性受高空宇宙射线照射的民航飞行人员血清过氧化脂质水平及抗氧化能力。方法　以化学比色法测定血清过氧化脂质、超氧化物歧化酶及总抗氧化活性 ;以宇宙辐射航线有效剂量计算软件CARI 6估算有效剂量。结果　飞行人员血清过氧化脂质、超氧化物歧化酶、总抗氧化活性均显著高于地面人员 (P <0 0 5 )。随着年均飞行小时、年均有效剂量的增加血清过氧化脂质水平有增加的趋势 ,但和累积飞行小时累积有效剂量及飞行人员的年龄没有平行关系。近期内飞行连续性变化 ,过氧化脂质水平也呈现相应的动态变化。结论　飞行人员体内脂质受到宇宙射线的氧化损伤 ,同时机体的抗氧化能力代偿性增强 ;近期飞行负荷、受照射频率明显影响血清过氧化脂质水平 ;过氧化脂质或可作为飞行人员辐射防护的监测指标。     

天葡圣航片对小鼠辐射损伤的保护作用

目的 观察天葡圣航片对小鼠γ射线辐射损伤的保护作用. 方法 将200只雌性昆明种小鼠随机分为Ⅰ(外周血白细胞计数)、Ⅱ(骨髓有核细胞计数)、Ⅲ(小鼠骨髓细胞微核检测),Ⅳ(血中超氧化物歧化酶活性测定)、Ⅴ(血清溶血素测定)5大组(每组n=40),每大组又随机分为低、中、高剂量药物组和辐射对照组(每小组n=10).低、中、高剂量按0.12 g/kg、0.24 g/kg、0.72 g/kg灌胃给药,1次/d,连续21 d;辐射对照组给等量蒸馏水.各组根据不同指标选择不同的照射剂量,各实验项目剂量组与相应的对照组均以同一剂量γ射线全身照射1次,照射后继续灌胃给药至实验结束.分别对每大组中各药物剂量组间进行相应检测指标的比较. 结果 以3 Gy剂量照射实验后第3天,中、高剂量药物组及第14天中剂量药物组的外周血白细胞计数明显高于辐射对照组(P<0.01或P<0.05);照射后第3天,中、高剂量药物组的骨髓有核细胞数明显高于辐射对照组(P<0.05或P<0.01),高剂量药物组的骨髓细胞微核率明显低于辐射对照组(χ~2=6.301,P<0.05);以6 Gy剂量照射后第7天,高剂量组的血清超氧化物歧化酶活性明显高于辐射对照组(P<0.05),以上差异有统计学意义.以2 Gy剂量照射后第14天,各剂量药物组的血清溶血素水平与辐射对照组比较差异无统计学意义. 结论 天葡圣航片对小鼠γ射线辐射损伤具有明显的保护作用.     

海生多糖肽对亚急性辐射损伤小鼠的防护作用

目的 研究海生多糖肽对小鼠亚急性辐射损伤的防护作用。方法 给小鼠饲以海生多糖肽制剂，用^60Coγ射线进行全身性亚急性照射，检测外周血白细胞、脾淋巴细胞转化率、红细胞超氧化物歧化酶、丙二醛和过氧化酶含量、精子畸形率、睾丸精母细胞染色体畸变率和肝细胞半胱氨酸蛋白酶-3等指标。结果 海生多糖肽高、低剂量组小鼠的血白细胞数量、脾淋巴细胞转化率、红细胞超氧化物歧化酶值和过氧化酶值均高于照射对照组，红细胞丙二醛值、精子畸形率、睾丸精母细胞染色体畸变率和肝细胞半胱氨酸蛋白酶-3阳性表达率则低于照射对照组，差异有显著性。结论 海生多糖肽对亚急性辐射损伤有良好的防护作用。     

rhCu/ZnSOD对γ-线照射小鼠抗氧化酶活性的影响

γ线照射可导致小鼠细胞内外超氧化物歧化酶、谷胱甘肽过氧化物酶以及过氧化氢酶活力明显降低。分别于照射前后，单纯照射前及单纯照射后给小鼠腹腔注射基因工程重组人铜锌超氧化物歧化酶，给药组小鼠细胞内外各抗氧化酶活力的降低程度明显减轻；平均活存时间和死亡率亦与对照组有显著差异。     

60Co γ射线诱发小鼠外周血网织红细胞微核率的研究

目的 通过观察不同剂量⁶⁰Co γ射线照射后小鼠外周血网织红细胞微核率的变化,为使外周血网织红细胞微核成为探索快速高通量的生物剂量计提供科学依据。方法 ⁶⁰Co γ射线照射ICR小鼠,按不同照射剂量分为0、0.5、1、2、4和8 Gy组,眼球取血,流式细胞术(FCM)检测和显微镜观察小鼠外周血网织红细胞微核率的变化。结果 流式细胞术检测网织红细胞微核率随剂量增加逐渐增加,2 Gy达峰值,之后随剂量的增加而减少;显微镜观察的网织红细胞微核率变化趋势与流式细胞术检测结果基本一致。照射剂量在0~2 Gy剂量范围内,小鼠的外周血网织红细胞微核率的剂量-效应关系满足直线模型(R²=0.9063),并且2 Gy照射组与0 Gy组相比差异有统计学意义(t=-2.856,P<0.05)。结论 流式细胞术检测外周血网织红细胞微核率,在一定剂量范围内可成为早期快速、高通量的辐射损伤生物剂量计。     

电离辐射对小鼠血和肝细胞生物氧化酶活性的影响

报道了经不同剂量（３，６，９和１２Ｇｖ）照射后小鼠血液和肝细胞浆内生物氧化酶活力的变化。结果显示：随着受照剂量的增加，血液和肝细胞浆内总ＳＯＤ、铜锌ＳＯＤ、谷胱甘肽过氧化物酶和过氧化氢酶活力明显降低，而锰ＳＯＤ含量没有明显变化。血液和肝细胞浆内脂质过氧化物在受照大剂量组明显增加。上述结果提示：电离辐射对生物氧化酶活力有明显影响。其影响程度与受照剂量有关。受照后生物氧化酶活力降低是脂质过氧化物升高的主要原因。     

红芪胶囊对辐射损伤大鼠的药效作用研究

目的观察中药红芪胶囊对^60Co-γ辐射损伤大鼠的防护效果。方法将大鼠进行2Gy^60Co-γ全身性照射,照后不同剂量红芪胶囊连续灌胃给药21d,观察其不同时间点（0、4、7、10、14、21d）外周血白细胞和红细胞数,以及脑、肺、血清中超氧化物歧化酶和丙二醛含量的变化。结果辐照后大鼠白细胞、红细胞含量较正常对照组明显降低,脑、肺和血清中丙二醛的含量均较正常对照组明显降低,超氧化物歧化酶活性有升高趋势;辐照给药后,大鼠外周血白细胞数升高,红细胞数降低缓慢,脑和肺组织超氧化物歧化酶活性明显升高,丙二醛含量有降低的趋势。结论红芪胶囊可提高机体氧化和还原反应的比值,清除体内过剩的自由基反应,显著减轻辐射对机体的损伤。     

Status of the lipid peroxidation system in the tissues of rats following a 7-day flight on the Kosmos-1667 biosatellite

Rats flown for 7 days on Cosmos-1667 were for the first time used to measure antioxidative enzymes (superoxide dismutase, glutathione peroxidase, glutathione reductase, catalase), lipid peroxidation products (diene conjugates, malonic dialdehyde, Schiff bases) and tocopherol. Enhanced lipid peroxidation in the heart was completely compensated by activation of antioxidative enzymes. The content of all lipid peroxidation products measured in the liver increased; this was accompanied by a decrease of glutathione peroxidase and an increase of superoxide dismutase activities. It is suggested that lipid peroxidation was activated in response to altered gravity.     

Contribution of antioxidant enzymes to the adaptive response to ionizing radiation of human lymphoblasts.

PURPOSE: To investigate whether the adaptive response to ionizing radiation triggered by a low-dose pre-exposure could be due to the activation of the antioxidant defence system. MATERIALS AND METHODS: Human lymphoblastoid AHH-1 cells were irradiated with a 0.02 Gy gamma-radiation and 6 h later were exposed to a 3 Gy challenge dose according to a protocol allowing mutagenic adaptation. Controls included cells left unirradiated or exposed to a single dose (0.02 Gy or 3 Gy). The activities of the main cellular antioxidant enzymes (AOE) - copper-zinc superoxide dismutase (SOD1), manganese superoxide dismutase (SOD2), catalase (CAT), glutathione peroxidase (GPX), glutathione-S-transferase (GST), glutathione reductase (GSR) and glucose 6-phosphate dehydrogenase (G6PD) - were evaluated at different times after treatment. The levels of SOD2 and CAT proteins were also analysed using the immuno Western blot method. RESULTS: Compared with non-irradiated controls, the effect of 3 Gy alone was shown to increase GPX and CAT activities at 20 h after irradiation. Pre-exposure of cells did not change these late alterations. Soon after irradiation the activities of SOD2, GST, GPX and CAT were slightly higher in adapted than in non-adapted cells. CONCLUSION: The data suggest that the increased activities of some AOE observed soon after the challenge dose would result in a rapid scavenging of radicals and consequently less damage in adapted cells. Due to the moderate alterations of these AOE, the activation of antioxidant defences would only partly contribute to the protective mechanism underlying the radioadaptation of AHH-1 lymphoblasts.     

Differential modification by caffeine of oxygen-dependent and independent effects of gamma-irradiation on rat liver mitochondria

PURPOSE: Following the demonstration that caffeine effectively competes with oxygen for electrons and also scavenges hydroxyl radicals and singlet oxygen, the differential modification of oxygen-dependent and independent effects of gamma-radiation by caffeine in membranes was examined, using rat liver mitochondria as a model system. MATERIALS AND METHODS: Mitochondria were isolated from the livers of Wistar rats and exposed to gamma-radiation in the dose range of 45-600 Gy (dose rate 15 Gy/min) in the presence or absence of caffeine. To examine the 'oxygen effect', post-irradiation incubation was carried out in the presence of oxygen or nitrogen in buffers saturated with the respective gases. Membrane damage was examined as lipid peroxidation (assessed as formation of thiobarbituric acid-reactive substances (TBARS), lipid hydroperoxides (LOOH) and conjugated dienes (CD), protein oxidation, depletion of protein thiols, superoxide dismutase or glutathione. RESULTS: Lipid peroxidation increased as a function of radiation dose, from 45 to 600 Gv. Post-irradiation incubation of mitochondria under nitrogen decreased the response, while incubation under oxygen saturation enhanced it significantly. The presence of caffeine during radiation exposure inhibited lipid peroxidation significantly as a function of concentration, in the range of 5 microM to 4 mM. The inhibition was highest with 4 mM of caffeine. Under oxic conditions, inhibition at 1 mM was significantly more than under anoxia. Anoxia was either ineffective or marginally increased peroxidation in the presence of caffeine. A similar observation was obtained when membrane damage was assessed as protein oxidation. Radiation-induced depletion of protein thiols was greatly enhanced by oxygen saturation and this was completely prevented by caffeine. This compound also protected against the radiation-induced loss of the antioxidant glutathione and the enzyme superoxide dismutase. CONCLUSIONS: The results suggest that caffeine effectively protected membranes against the oxic component of damage but may not do so for the anoxic component.     

Differential modification by caffeine of oxygen-dependent and independent effects of γ-irradiation on rat liver mitochondria

Purpose : Following the demonstration that caffeine effectively competes with oxygen for electrons and also scavenges hydroxyl radicals and singlet oxygen, the differential modification of oxygen-dependent and independent effects of gamma-radiation by caffeine in membranes was examined, using rat liver mitochondria as a model system. Materials and methods : Mitochondria were isolated from the livers of Wistar rats and exposed to γ-radiation in the dose range of 45-600Gy (dose rate 15 Gy/min) in the presence or absence of caffeine. To examine the 'oxygen effect', post-irradiation incubation was carried out in the presence of oxygen or nitrogen in buffers saturated with the respective gases. Membrane damage was examined as lipid peroxidation (assessed as formation of thiobarbituric acid-reactive substances (TBARS), lipid hydroperoxides (LOOH) and conjugated dienes (CD), protein oxidation, depletion of protein thiols, superoxide dismutase or glutathione. Results : Lipid peroxidation increased as a function of radiation dose, from 45 to 600Gy. Post-irradiation incubation of mitochondria under nitrogen decreased the response, while incubation under oxygen saturation enhanced it significantly. The presence of caffeine during radiation exposure inhibited lipid peroxidation significantly as a function of concentration, in the range of 5 μ m to 4 mm. The inhibition was highest with 4 mm of caffeine. Under oxic conditions, inhibition at 1 mm was significantly more than under anoxia. Anoxia was either ineffective or marginally increased peroxidation in the presence of caffeine. A similar observation was obtained when membrane damage was assessed as protein oxidation. Radiation-induced depletion of protein thiols was greatly enhanced by oxygen saturation and this was completely prevented by caffeine. This compound also protected against the radiation-induced loss of the antioxidant glutathione and the enzyme superoxide dismutase. Conclusions : The results suggest that caffeine effectively protected membranes against the oxic component of damage but may not do so for the anoxic component.     

褪黑素对重离子辐射损伤小鼠肺的防护作用研究

目的探讨褪黑素(melatonin,MLT)对重离子辐射损伤小鼠肺的防护作用。方法预先给小鼠腹腔注射10mg/kg的MLT,1h后给予0、0.5、1.0、2.0及4.0Gy的全身12C6+束均匀照射,剂量率约1.4Gy/min,辐射后8h,检测辐射损伤小鼠肺组织的SOD活性和MDA、GSH含量,并通过单细胞凝胶电泳技术检测辐射损伤小鼠肺细胞的拖尾长度和尾距。结果和单纯辐射组相比,10mg/kg的MLT腹腔注射能有效抑制重离子辐射引起的小鼠肺组织SOD活性降低、GSH含量下降和MDA含量提高;同时,MLT还能使受损小鼠肺细胞的拖尾长度和尾距显著降低,且都存在剂量效应关系。结论MIT对重离子全身辐射所致小鼠的抗氧化系统有一定的激活效应,对辐射损伤有一定的防护作用,这可能与对抗膜脂质过氧化、清除自由基及其减轻DNA损伤有一定的关系。     

Endogenous Superoxide Dismutase and Catalase Activities and Radiation Resistance in Mouse Cell Lines

Summary

The relationship between the endogenous cytoplasmic levels of the enzymes superoxide dismutase and catalase and the inhibition of cell proliferation by radiation has been studied in 11 mouse cell lines. The resistance of these mouse cell lines to radiation was found to vary by over 25-fold. No correlation was found between the cytoplasmic level of CuZn-superoxide dismutase or catalase and the resistance to radiation as measured by extrapolation number (EN), quasi-threshold dose (D_q), or D₀. None of the cell lines had detectable cytoplasmic Mn-superoxide dismutase. The apparent K_i of potassium cyanide for mouse CuZn-superoxide dismutase was determined (K_i = 6·5 µmol dm^?3).     

Effects of gamma radiation (γ) on biochemical and antioxidant properties in black gram (Vigna mungo L. Hepper)

Abstract

Purpose: The present study focused on the role of primary metabolites, antioxidant activities in black gram (Vigna mungo L. Hepper) variety Vamban-4 under the impact of gamma irradiation.

Materials and methods: The black gram seeds were irradiated at a different dose of gamma rays viz., 200, 400, 600, 800, 1000 and 1200 Gray (Gy), and analyzed the changes of biochemical and antioxidant contents.

Results: Biochemical contents increased with increasing doses up to 800?Gy and reduced at higher dose viz.,1000 and 1200?Gy of gamma-ray treatment, while malondialdehyde content increased at higher dose 1200?Gy compared to control, this indicates that the formation of more lipid peroxidation at higher radiation level. Gamma irradiation enhanced the activity of antioxidant enzymes such as catalase, peroxidase and superoxide dismutase with increasing doses rather than control plants. These studies depict that the effect of gamma irradiation on seeds increased the free radicals compared to control, which emphasize by the Electron spin resonance spectroscopy (ESR). Gamma irradiated seed samples contain more fractions of protein, lipids, amino acid and polysaccharides compared to control plants observed from the Fourier infrared transform spectroscopy (FTIR).

Conclusion: The present result concludes that cellular metabolites and the antioxidant enzymes increased and these alterations of metabolism due to the effect of gamma rays which induced free radical production in seeds and plants grown under irradiation stress. These results confirm that the exposure of gamma irradiation produced free radicals as well as counteract by antioxidant enzymes and in addition to that accumulation and alteration of primary metabolites.     

Structural and functional damages of whole body ionizing radiation on rat brain homogenate membranes and protective effect of amifostine

Purpose: To investigate the effects of whole body ionizing radiation at a sublethal dose on rat brain homogenate membranes and the protective effects of amifostine on these systems at molecular level.

Materials and methods: Sprague-Dawley rats, in the absence and presence of amifostine, were whole-body irradiated at a single dose of 8?Gy and decapitated after 24?h. The brain homogenate membranes of these rats were analyzed using Fourier Transform Infrared (FTIR) spectroscopy.

Results: Ionizing radiation caused a significant increase in the lipid to protein ratio and significant decreases in the ratios of olefinic?=?CH/lipid, CH₂/lipid, carbonyl ester/lipid and CH₃/lipid suggesting, respectively, a more excessive decrease in the protein content and the degradation of lipids as a result of lipid peroxidation. In addition, radiation changed the secondary structure of proteins and the status of packing of membrane lipid head groups. Furthermore, it caused a decrease in lipid order and an increase in membrane fluidity. The administration of amifostine before ionizing radiation inhibited all the radiation-induced alterations in brain homogenate membranes.

Conclusions: The results revealed that whole body ionizing radiation at a sublethal dose causes significant alterations in the structure, composition and dynamics of brain homogenate membranes and amifostine has a protective effect on these membranes.