60Coγ射线重过滤低剂量率照射剂量学研究

Luckey1980年发现低剂量辐射能诱导机体适应性反应，近年来刘树铮教授等亦通过流行病学和实验室研究，证实了低剂量辐射能提高机体免疫。     

低剂量X射线全身照射对小鼠IL-12和CD2、CD48表达的影响

目的　检测低剂量辐射 (LDR)对小鼠腹腔巨噬细胞IL 12的影响 ,同时观察胸腺细胞CD2及腹腔巨噬细胞表面分子CD48的变化并分析其与IL 12变化的关系。方法　分别采用Northernblot和ELISA检测了 0 0 75GyX射线全身照射后IL 12转录水平、蛋白水平的变化 ;采用荧光免疫流式细胞术检测CD2、CD48蛋白表达的变化。结果　 (1)IL 12的改变 :0 0 75GyX射线全身照射后 1h巨噬细胞中IL 12、p3 5及p40亚基mRNA水平均迅速升高 ,分别达到假照组的 13 1%和 192 %(P <0 0 5) ,而后开始回降直至照后 16～ 48h恢复正常 ;巨噬细胞分泌IL 12在照后 4～ 8h明显增高(P <0 0 5)。 (2 )CD2、CD48表达变化 :0 0 75GyX射线照射后 4h胸腺细胞CD2表达即开始升高 ,至8h达峰值 (P <0 0 5～ 0 0 1) ;巨噬细胞CD48表达在照射后 2h开始升高 ,至 48h仍明显高于假照水平 (P <0 0 5～ 0 0 1) ;4h量效结果显示 ,50 ,75,10 0和 2 0 0mGy均使CD2、CD48表达上调 (P <0 0 5)。结论　LDR可引起IL 12表达上调 ,CD2、CD48分子与IL 12的变化具有一致性 ,提示两者可能参与IL 12的免疫调控     

^60Co-γ辐射对大鼠巨噬细胞一氧化氮产生的影响

目的 本主要研究8Gy的^60Co-γ辐射对大鼠体内及体外MФ西中NO的产生、iNOS表达、iNOS mRNA转录等的影响。方法 用电子自旋共振(ESR)技术观察对8Gy的^60Co-γ辐射MФ西中NO产生变化，免疫组化法研究MФ中一氧化氮合酶(iNOS)表达．原位杂交(ISH)检测研究MФ中iNOS mRNA的转录。结果 ^60Co-γ辐射大鼠不仅可使体内MФ的诱导产生大量减少，而且，诱导MФ中NO的产生也相对有所减弱。体外诱导MФ受辐射后产生的NO有所减少，MФ中iNOS表达减弱，iNOS mRNA转录降低，但LPS和IFN可在一定程度上扭转辐射的这种效应。结论 8Gy的^60 Co-γ辐射可引起大鼠体外MФ中NO的产生、iNOS表达、iNOS mRNA转录等的变化。     

不同低剂量率慢性γ射线照射对大鼠精子发生的影响

本研究用日剂量18.2,47.6和91.8mGy⁶⁰Co γ射线连续照射Wistar大鼠,共90天。观察剂量率和累积剂量对生精能力的损伤和恢复。结果表明: 受日剂量47.6mGy照射的大鼠,生精上皮可受到明显损伤,停照后3个月,恢复生精过程。在日剂量91.8mGy照射过程中,睾丸不断萎缩,精原细胞消失,精子也逐渐消失。停照后,生精过程未见恢复。结果提示,生精上皮对γ辐射是非常敏感的。     

复方红景天胶囊对小鼠60Coγ射线的影响

笔者观察了复方红景天胶囊对小鼠6 0 Ｃｏγ射线照射的影响。一、材料和方法 :①动物 :昆明种小白鼠 ,体重 18～ 2 2ｇ ,雄性 ,上海医科大学实验动物部提供。②样品 :复方红景天胶囊 (ＴＰＹＳ)由红景天、冬虫夏草组成。上海中医药大学科技发展公司研制。③实验方法 :小白鼠 5 0只 ,随机分成 5组。正常对照 (灌胃蒸馏水 10ｍｌ·ｋｇ- 1 ·ｄ- 1 ,不照射 ) ,单纯照射(照射加 10ｍｌ·ｋｇ- 1 ·ｄ- 1 蒸馏水 ) ,低剂量 (照射加样品 0 15ｇ·ｋｇ- 1 ·ｄ- 1 ) ,中剂量 (照射加样品 0 3ｇ·ｋｇ- 1 ·ｄ- 1 )和高剂量(照射加 0 9ｇ·ｋｇ-…     

125I粒子持续低剂量率照射和60Co γ射线高剂量率照射对H1299细胞生物学效应的比较研究

目的：探讨125I粒子持续低剂量率（CLDR）内照射和60Co γ射线高剂量率（HDR）外照射对非小细胞肺癌（NSCLC）细胞株H1299的细胞生物学效应。方法 H1299细胞处于指数生长期时分别行125I粒子CLDR照射和60Coγ射线HDR照射;克隆形成实验检测细胞存活分数,流式细胞术检测细胞周期和细胞凋亡率,Western blot检测Bax、Bcl-2蛋白表达水平。结果随着照射剂量增大,125I粒子CLDR照射比60Coγ射线HDR照射抑制H1299细胞增殖效应更明显。照射剂量为4 Gy时125I粒子组H1299细胞G2/M期百分比、细胞凋亡率分别为21．77±0．31%、13．79±0．50%;同样照射剂量下,60Co照射组H1299细胞G2/M期百分比仅为18．85±0．99%,细胞凋亡率仅为8．79±0．22%（P<0．05）。125I粒子CLDR照射明显上调Bax蛋白表达,同时下调Bcl-2蛋白表达。结论125I粒子CLDR内照射比60Coγ射线HDR外照射抑制H1299细胞增殖效应更明显。 Bcl-2/Bax蛋白比失衡在125I粒子CLDR照射抗肿瘤效应中可能发挥重要作用。     

重离子12C对60Coγ射线诱发人染色体畸变效应的比较研究

目的 重离子和高剂量率^60Coγ射线照射离体人血建立染色体畸变的剂量-效应曲线；比较重离子^12C照射与^60Coγ射线照射诱发染色体畸变的相对生物效能。方法 重离子^12和^60Coγ射线照射离体人血，吸收剂量率为3Gy/min，吸收剂量为1．0～8．0Gy。主要记录染色体型畸变的非稳定性畸变，对双着丝粒体和着丝粒环做曲线拟合，并检验回归系数的显著性和曲线的拟合度。结果 重离子^12C和^60Coγ射线照射离体血诱发的染色体畸变(双 环)，在0—8Gy范围内，呈良好的剂量一效应关系。^12C离子诱发染色体畸变的RBE值是不恒定的，它随吸收剂量增加而减少，在0．3—8．0Gy范围内，RBE值(Dr/Dc)从2．62到1．00，平均1．58。结论 ^12C离子对^60Coγ射线照射诱发染色体畸变，在照射剂量较低时，有较高的生物效应。     

E803药物对^60Co—γ射线照射小鼠造血系统的防护作用

目的 观察E803对^60Co-γ射线照射小鼠造血系统的辐射防护作用。方法 C57小鼠一次全身照射前灌胃给药E803和523，测定脾指数、CFU—S(7．5Gy)、外周血象(5．5Gy)、造血祖细胞集落形成(3．5Gy)。结果 7．5Gy照后第7d测定各给药组的脾指数、CFU—S明显较照射组增多。5．5Gy照射引起的小鼠的外周血细胞数量的降低以白细胞发生最早，照后24h给药组的WBC数量均比照射对照组有不同程度的升高，以E803各给药组最为明显，药物未能使照射引起的外周血细胞最低值升高，而有降低的趋势。但给药对照射后期外周血象的总体恢复有较好的促进作用。3．5Gy照后第7d观察给药组的造血祖细胞集落的形成能力强于照射对照组，并且E803组明显优于523组。结论 E803对^60Co-γ射线引起的小鼠造血系统损伤有保护作用。     

60Coγ射线照射诱导人卵巢癌细胞凋亡及细胞周期的改变

目的：探讨^60Coγ射线照射对人卵巢癌细胞株A2780及其顺铂耐药株A2780－CP体外生长、凋亡及细胞周期的影响。方法：采用四甲基偶唑蓝（MTT）比色法分析不同辐照剂量（1－10Gy)对A2780及A2780－CP两种细胞株体外生长的影响,用流式细胞术（FCM）比较两者辐照后凋亡及细胞周期的变化。结果：（1）1－10^60Coγ射线照射引起A2780细胞株明显的生长抑制和凋亡,而A2780－CP细胞则表现出明显的辐照抗性。（2）6Gy ^60Coγ射线照射后6－48hA1780细胞呈现G1期细胞阻滞和S期细胞比较下降,A2780－CP细胞则呈G1期细胞比例减少和S期细胞比例增加。结论卵癌耐药细胞具有辐射抗性和物征性的细胞周期变化,流式细胞术测定辐照诱导肿瘤细胞凋讯及细胞周期的变化可预测恶性肿瘤细胞的辐射敏性。     

60Coγ射线对成年小鼠脑内海马区组织形态上的影响

目的：探讨电离辐射对成年动物海马组织损伤的特点,方法选用昆明品系雄性小白鼠,用＾６０Ｃｏγ射线对照射组织进行全身均匀分次照射,隔日１次,每交２．０Ｇｙ,从存活小鼠及对照组各随机取８只小鼠,分别取脑,石蜡包埋,连续地平切片,Ｎｉｓｓｌ和Ｗｅｌ染色及图像分析测量。结果照射组海马的锥体层中的神经元数量较正常组减少,神经元的主要病理改变是细胞体积变小,核固缩,核溶解,照射组海马辐射层的神经纤维的面密度明显     

Effect of subsequent acute-dose irradiation on cell survival in vitro following low dose-rate exposures

Purpose : Following acute irradiation, excess radiosensitivity is generally seen at doses <1 Gy, a phenomenon termed 'low-dose hyper-radiosensitivity' (HRS). A very strong, HRS-like inverse dose-rate effect has also been described following continuous low dose-rate (LDR) irradiation at <30 cGy h -1. We report on the sequential irradiation of a cell line by such LDR exposures followed by low acute doses, where either treatment individually would elicit a hypersensitive response. The aim was to determine if a prior LDR exposure would remove the HRS normally seen in response to very small acute radiation doses. Materials and methods : T98G human glioma cells were given single continuous LDR exposures of 5-60 cGy h -1 using a 60 Co γ-source. At intervals of 0 or 4 h following LDR irradiation, cells were further irradiated with a range of acute doses using 240-kVp X-rays. The response to the combined treatment was assessed using high-precision clonogenic cell survival assays, and the amount of HRS at acute doses <1 Gy was determined. Results : LDR at ≥60 cGy h -1 to total doses up to 5 Gy in asynchronously growing cells did not remove HRS in the subsequent acute-dose survival curve. In confluent cultures, subsequent acute-dose HRS was not present after an LDR dose of 5 Gy at either 60 or 30 cGy h -1, but returned if a 4-h interval was left between LDR and acute-dose irradiation. In confluent cultures, acute-dose HRS remained for LDR treatments at 5 or 10 cGy h -1 or if the total dose was 2 Gy. Taking all cultures and dose-rates together, the 'degree' of acute-dose HRS, as measured by α s, was significantly greater in cells irradiated at LDR to a total dose of 2 than of 5Gy. Conclusions : Initial LDR exposure can affect a subsequent HRS response. HRS is reduced after LDR exposures at greater dose intensity, but can recover again within 4 h of completion of LDR exposure. This suggests that processes determining increased resistance to small acute doses (removal of HRS) might be governed by the level of repairable DNA lesions.     

Effect of subsequent acute-dose irradiation on cell survival in vitro following low dose-rate exposures

PURPOSE: Following acute irradiation, excess radiosensitivity is generally seen at doses <1 Gy, a phenomenon termed "low-dose hyper-radiosensitivity" (HRS). A very strong, HRS-like inverse dose-rate effect has also been described following continuous low dose-rate (LDR) irradiation at <30 cGy h(-1). We report on the sequential irradiation of a cell line by such LDR exposures followed by low acute doses, where either treatment individually would elicit a hypersensitive response. The aim was to determine if a prior LDR exposure would remove the HRS normally seen in response to very small acute radiation doses. MATERIALS AND METHODS: T98G human glioma cells were given single continuous LDR exposures of 5-60 cGy h(-1) using a (60)Co gamma-source. At intervals of 0 or 4 h following LDR irradiation, cells were further irradiated with a range of acute doses using 240-kVp X-rays. The response to the combined treatment was assessed using high-precision clonogenic cell survival assays, and the amount of HRS at acute doses <1 Gy was determined. RESULTS: LDR at > or = 60 cGy h(-1) to total doses up to 5 Gy in asynchronously growing cells did not remove HRS in the subsequent acute-dose survival curve. In confluent cultures, subsequent acute-dose HRS was not present after an LDR dose of 5 Gy at either 60 or 30 cGy h(-1), but returned if a 4-h interval was left between LDR and acute-dose irradiation. In confluent cultures, acute-dose HRS remained for LDR treatments at 5 or 10 cGy h(-1) or if the total dose was 2 Gy. Taking all cultures and dose-rates together, the "degree" of acute-dose HRS, as measured by alpha(s), was significantly greater in cells irradiated at LDR to a total dose of 2 than of 5Gy. CONCLUSIONS: Initial LDR exposure can affect a subsequent HRS response. HRS is reduced after LDR exposures at greater dose intensity, but can recover again within 4 h of completion of LDR exposure. This suggests that processes determining increased resistance to small acute doses (removal of HRS) might be governed by the level of repairable DNA lesions.     

Radiation-induced apoptosis in the scid mouse spleen after low dose-rate irradiation

PURPOSE: To elucidate the process of radioadaptation, the role of DNA-PK activity was examined using the scid mouse defective in DNA-PKcs. MATERIALS AND METHODS: The induction of apoptosis in the spleens of the C.B-17 Icr scid mouse and the parental mouse was studied after chronic irradiation with gamma-rays at 1.5 Gy (0.001 Gy min(-1) for 25 h) followed by challenge irradiation with X-rays at 3.0 Gy (1.0 Gy min(-1) for 3 min). RESULTS: When the wild-type mouse was previously exposed to chronic irradiation (1.5 Gy) at a low dose-rate (0.001 Gy min(-1)), apoptosis induced by acute irradiation (3.0 Gy, 1.0 Gy min(-1)) was significantly suppressed, especially in the splenic white pulp. There was no change by acute irradiation after chronic irradiation in the scid mouse, although an effect was detected in the spleen after acute irradiation alone. CONCLUSIONS: These data suggest that DNA-PK activity might play a major role in the radioadaptive response following pre-irradiation at a low dose-rate.     

Radiation-induced apoptosis in the scid mouse spleen after low dose-rate irradiation

Purpose : To elucidate the process of radioadaptation, the role of DNA-PK activity was examined using the scid mouse defective in DNA-PKcs. Materials and methods : The induction of apoptosis in the spleens of the C.B-17 Icr scid mouse and the parental mouse was studied after chronic irradiation with γ-rays at 1.5 Gy (0.001Gy min -1 for 25 h) followed by challenge irradiation with X-rays at 3.0 Gy (1.0 Gy min -1 for 3 min). Results : When the wild-type mouse was previously exposed to chronic irradiation (1.5Gy) at a low dose-rate (0.001 Gy min -1) , apoptosis induced by acute irradiation (3.0 Gy, 1.0Gy min -1) was significantly suppressed, especially in the splenic white pulp. There was no change by acute irradiation after chronic irradiation in the scid mouse, although an effect was detected in the spleen after acute irradiation alone. Conclusions : These data suggest that DNA-PK activity might play a major role in the radioadaptive response following pre-irradiation at a low dose-rate.     

Absence of genomic instability in mice following prenatal low dose-rate gamma-irradiation

PURPOSE: To determine whether mice exposed to an extended low dose of gamma-irradiation during most of their prenatal period express increased frequencies of micronucleated polychromatic erythrocytes (fMPCE) and/or micronucleated normochromatic erythrocytes (fMNCE) several weeks after the end of irradiation. METHODS: Female CBA/Ca mice were gamma-irradiated for an average of 16 days during their pregnancy. The mice were exposed to dose rates of 0, 44, 99 and 265 mGy/day. At 1-2 days prior to parturition the mice were removed from exposure. Then, 36 days after birth, peripheral blood was drawn from all offspring (74 mice). Using flow-cytometer-based analysis, the frequencies of MPCE and MNCE were determined. From each animal about 170,000 PCE were analysed. RESULTS: No delayed effects in terms of higher fMPCE or fMNCE were observed among the in utero exposed mice of either gender. On the contrary, a significant (p<0.001) reduction of fMPCE was found among the male offspring exposed at the highest dose rate. CONCLUSION: Gamma-irradiation of mice during their prenatal stage did not induce damage in erythroid stem cells that can be detected as persistent or delayed chromosome aberrations (i.e. micronucleated erythrocytes) at 35 days after the end of exposure.     

鼻咽癌中白细胞介素-10、白细胞介素-12检测及其意义

目的检测鼻咽癌患者白细胞介素-10（interleukin-10,IL-10）及白细胞介素-12（interleukin-12,IL-12）浓度。方法用酶联免疫法（Enzyme Linked Immunosorbent Assay,ELISA）检测43例鼻咽癌患者血清IL-10及IL—12浓度,并用22例健康成年人血清作为对照。结果鼻咽癌组IL—10浓度明显高于对照组,鼻咽癌组IL—12浓度明显低于对照组,IL-10浓度在晚期T分期组（T3／T4）明显高于早期T分期组（Ⅰ／Ⅱ）W〈0．01）、晚期临床分期组（Ⅲ/Ⅳ）明显高于早期临床分期组（Ⅰ／Ⅱ）,但在不同性别、年龄组及有无淋巴结转移组浓度差异无统计学意义（P〉0．05）。而IL-12在晚期T分期组（T3／T4）N显低于早期T分期组（Ⅰ／Ⅱ）（P〈0．01）、晚期临床分期组（Ⅲ/Ⅳ）明显低于早期临床分期组（Ⅰ/Ⅱ）,但在不同性别、年龄组及有无淋巴结转移组浓度差异无统计学意义（P〉0．05）。且IL-10及IL-12浓度呈负相关关系。结论鼻咽癌中高浓度的IL-10可能抑制IL-12的产生,帮助肿瘤细胞免疫逃避,损害机体肿瘤免疫,从而促进肿瘤发展。