The role of repair in radiobiology

Summary Apart from cancer and mutation induction, radiobiological effects on mammals are mostly attributable to cell death, defined as loss of proliferative capacity. Survival curves relate retention of that capacity to radiation dose, and often manifest a quasi-threshold (shoulder). The shoulder is attributable to an initial mechanism of repair (Q-repair) which is gradually depleted as dose increases. Another form of repair, which is not depleted (P-repair), increases the dose required to deliver an average of one lethal event per cell (dose D₀). Neither form of repair can unambiguously be linked with repair of defects in isolated DNA. An important initial lesion may well be disruption of the complex structural relationship between the DNA, nuclear membrane and associated proteins. One form of P-repair may be restoration of that structural relationship.     

Bacterial suicide through stress

Outside of the laboratory, bacterial cells are constantly exposed to stressful conditions, and an ability to resist those stresses is essential to their survival. However, the degree of stress required to bring about cell death varies with growth phase, amongst other parameters. Exponential phase cells are significantly more sensitive to stress than stationary phase ones, and a novel hypothesis has recently been advanced to explain this difference in sensitivity, the suicide response. Essentially, the suicide response predicts that rapidly growing and respiring bacterial cells will suffer growth arrest when subjected to relatively mild stresses, but their metabolism will continue: a burst of free-radical production results from this uncoupling of growth from metabolism, and it is this free-radical burst that is lethal to the cells, rather than the stress per se. The suicide response hypothesis unifies a variety of previously unrelated empirical observations, for instance induction of superoxide dismutase by heat shock, alkyl-hydroperoxide reductase by osmotic shock and catalase by ethanol shock. The suicide response also has major implications for current [food] processing methods. Received 29 March 1999; received after revision 14 May 1999; accepted 17 May 1999     

亚致死温度热休克对凡纳滨对虾的保护作用

以亚致死温度(35 ℃)热休克凡纳滨对虾Litopenaeus vannamei 2 h,再进行致死温度(40 ℃)热刺激,凡纳滨对虾的存活率为54.2%.以亚致死温度对凡纳滨对虾热休克2 h,正常水温(25±0.5)℃下分别恢复2、6、12和24 h,再对其进行白斑综合症病毒(white spot syndrome virus, WSSV)注射感染,得到凡纳滨对虾的平均存活时间分别为101.43、98.07、76.92和63.28 h,与未经35 ℃热休克的对照组的平均存活时间(46.89 h)相比,均存在极显著差异性(P<0.01).证明了适当的热休克应激,不仅能提高凡纳滨对虾对高温的热耐受性,还显著地增强了凡纳滨对虾对WSSV感染的抵抗性.     

氯化汞对中华绒螯蟹幼蟹蜕皮、生长和存活的影响

通过向水体添加不同浓度的汞(Hg2+),观察其对中华绒螯蟹幼蟹(2.01士0.16)g的毒性影响.结果表明,Hg2+对其24,48,72,96 h的半致死浓度(LC50)分别为0.542 8,0.471 6,0.433 2和0.342 3 mg/L.中华绒螯蟹幼蟹在0,0.01,0.05,0.10,0.20,0.30 mg/L的Hg2+条件下饲养40 d后,各浓度组幼蟹存活率分别为96.67%,86.67%,73.33%,63.33%,56.67%,43.33%;增重率和蜕皮率随着Hg2+浓度的升高而降低.可见水体中的Hg2+能够抑制中华绒螯蟹的生长和蜕皮,高浓度的Hg2+甚至会造成幼蟹的死亡.根据Hg2+对中华绒螯蟹的毒性作用确定水体中汞的最大允许量为0.034 2 mg/L.     

紫外线对番茄青枯菌致病性变化的影响

紫外线的亚致死剂量、致死剂量对青枯雷尔氏菌作用的实验表明:亚致死剂量照射不同时间对青枯雷尔氏菌强致病力菌株有不同程度地促进作用,而无杀灭作用及任何抑制和致弱现象;致死剂量照射对强致病力菌株和无致病力菌株影响不同,结果差异极显著,无致病力菌株对紫外线的耐受力要高于强致病力菌株.致死剂量紫外线对强致病力菌株处理2min,抑制率即达100%,致弱率为0;无致病力菌株照射2min与4min的处理,抑制率分别为70.3%和96.3%,处理8min以上,抑制率达100%.     

Cell kinetics and radiation pathology

Conclusion Radiation pathology is a general term describing the damage that occurs in tissues after irradiation. After the very low doses, received by the normal working population, no major pathology is seen. There is a hazard of cancer induction if DNA damage that has been inflicted in an individual cell is repaired in such a way that the DNA remains intact but rearranged. This radiation carcinogenesis is however a low risk compared with many chemical carcinogens in the environment and in cancer chemotherapy.The treatment of cancer by radiation is now commonly accepted as one of the most effective forms of treatment. It can kill tumour cells effectively, but the dose that can be given is limited by the normal tissues that are inevitably included in the beam. Cell function is maintained for some time even after very large doses. However normal tissues show a loss of function and structure because the proliferating subcompartment of each tissue is depleted as the radiation injured cells fail to divide and die. The time at which the cell deficit is detected varies from hours in some tissues to months or years in others. It depends upon the normal rate of cell turnover. The apparent sensitivity of each tissue therefore depends upon the time at which the assessment is made. Lung and kidney would appear very resistant at 1–3 months post irradiation, but would seem very radiosensitive at 6–12 months as their latent damage is expressed.The ultimate expression of radiation pathology is the death of the whole animal as the essential organ function fails. The time of this death is only comprehensible if the time sequence and the proliferation kinetics of the target cells are taken into account. It must be recognised that it is initial damage to the clonogenic cells, not to the differentiated cells per se that is important.     

亚致死剂量百草枯对七星瓢虫捕食及限域搜索行为的影响

 采用室内生物测定方法对七星瓢虫在亚致死剂量百草枯作用下的捕食和限域搜索行为进行了测定.毒力实验研究结果表明,田间常用百草枯体积比(20 mL/L)低于七星瓢虫成虫的LC₅₀,对七星瓢虫幼虫的杀伤作用死亡率为95.7%.捕食速率测定结果显示,LC20剂量的百草枯会对七星瓢虫尤其是其幼虫的捕食速率产生显著影响,24 h七星瓢虫幼虫、雌成虫、雄成虫的捕食速率分别下降了31.32%,23.47%和25.60%.此外,百草枯对七星瓢虫的限域搜索行为也产生了显著影响,百草枯处理后七星瓢虫搜索速率降低,搜索范围缩小.