Effect of microwave electromagnetic field on skeletal muscle fibre activity

The aim of the present study was to investigate the influence of microwave irradiation on fatiguing activity of isolated frog skeletal muscle fibres. The changes in the electrical and mechanical activity were used as criteria for the exposure effects. Repetitive suprathreshold stimulation with interstimulus interval of 200 ms for 3 min was applied. Intracellular (ICAP) and extracellular (ECAP) action potentials and twitch contractions (Tw) of muscle fibres after 1 hour microwave exposure (2.45 GHz, 20 mW/cm( 2) power density) were compared with those recorded after one hour sham exposure (control). The duration of uninterrupted activity in the trial (endurance time; ET) was not significantly affected by microwave field exposure. After microwave irradiation, the ICAP amplitude was higher, the rising time was shorter, and the resting membrane potential was more negative compared to controls. There was a slower rate of parameters changes during ET in potentials obtained from irradiated fibres. Microwave exposure increased the propagation velocity of excitation, the ECAP and Tw amplitudes, as well as shortened their time parameters. We concluded that a 2.45 GHz microwave field possesses a stimulating effect on muscle fibre activity, which is in part due to its specific, non-thermal properties. The microwave induced-changes in muscle fibre activity may reduce development of skeletal muscle fatigue.     

Effects of cadmium on carbohydrate and protein metabolisms in the freshwater crab Sinopotamon yangtsekiense

The physiological impact of Cd(2+) on Sinopotamon yangtsekiense was evaluated through changes of selected parameters considered as key elements of carbohydrate and protein metabolisms. Crab were exposed to 0.725, 1.45, 2.9mg·L(-1) Cd(2+) for 7, 14 and 21 days. A time- and/or concentration- dependent decrease in muscle glycogen and increase in LDH activity suggested that glycolysis was accelerated during the treatments. Increased protease activity, lowering of FAA and the initially increased and subsequently decreased aminotransferase activities suggest an enhanced protein mobilization during early Cd(2+) exposure followed by a metabolic impairment during late exposure. Decreased hemolymph glucose level was observed in the crabs treated with 2.9mg·L(-1) Cd(2+) for 21d, suggesting an impaired gluconeogenesis. Ammonia level barely changed during the 14d Cd(2+) exposure most likely due to the increased urea and glutamine production; After 1.45 and 2.9mg·L(-1) Cd(2+) treatment for 21d, ammonia was observed increased followed by an exclusive increase in glutamine. Taken together, our results indicate that carbohydrate and protein are mobilized to a varying degree as a compensatory metabolism to response to the energy stress during acute Cd(2+) exposure. As the time lapsed, some symptoms on metabolism obstacle reflect the toxic effect of sublethal Cd(2+).     

Transition from anaerobic to aerobic growth conditions for the sulfate-reducing bacterium Desulfovibrio oxyclinae results in flocculation

A chemostat culture of the sulfate-reducing bacterium Desulfovibrio oxyclinae isolated from the oxic layer of a hypersaline cyanobacterial mat was grown anaerobically and then subjected to gassing with 1% oxygen, both at a dilution rate of 0.05 h(-1). The sulfate reduction rate under anaerobic conditions was 370 nmol of SO(4)(2-) mg of protein(-1) min(-1). At the onset of aerobic gassing, sulfate reduction decreased by 40%, although viable cell numbers did not decrease. After 42 h, the sulfate reduction rate returned to the level observed in the anaerobic culture. At this stage the growth yield increased by 180% compared to the anaerobic culture to 4.4 g of protein per mol of sulfate reduced. Protein content per cell increased at the same time by 40%. The oxygen consumption rate per milligram of protein measured in washed cell suspensions increased by 80%, and the thiosulfate reduction rate of the same samples increased by 29% with lactate as the electron donor. These findings indicated possible oxygen-dependent enhancement of growth. After 140 h of growth under oxygen flux, formation of cell aggregates 0.1 to 3 mm in diameter was observed. Micrometer-sized aggregates were found to form earlier, during the first hours of exposure to oxygen. The respiration rate of D. oxyclinae was sufficient to create anoxia inside clumps larger than 3 microm, while the levels of dissolved oxygen in the growth vessel were 0.7 +/- 0.5 microM. Aggregation of sulfate-reducing bacteria was observed within a Microcoleus chthonoplastes-dominated layer of a cyanobacterial mat under daily exposure to oxygen concentrations of up to 900 microM. Desulfonema-like sulfate-reducing bacteria were also common in this environment along with other nonaggregated sulfate-reducing bacteria. Two-dimensional mapping of sulfate reduction showed heterogeneity of sulfate reduction activity in this oxic zone.     

A gain-of-function screen identifies wdb and lkb1 as lifespan-extending genes in Drosophila

The aim of this work was to study the time course of the oxidative metabolism in mice lung after exposure to ambient particles (ROFA). Swiss mice were intranasally instilled with a ROFA suspension (0.20 mg/kg). Animals were sacrificed 1 or 3 h after the exposure. Eighty percentage of increased oxygen consumption was observed in tissue cubes after 1 h of exposure. This observation was accompanied by an increased NADPH oxidase activity (40%) and mitochondrial oxygen consumption in state 3 (19%). NO production by lung homogenates was found to be increased by 43% after 3 h of exposure. Phospholipid oxidation in lung homogenates showed a 29% increase after 1 h of exposure, while a 30% increase in the carbonyl content was found only after 3 h of exposure. Our data show the relative importance of different sources of reactive oxygen species (NADPH oxidase activity and mitochondrial respiration) to the increased tissue oxygen consumption, oxidative damage and antioxidant status observed in an acute model of ROFA particles exposure.     

夜间低温胁迫对番茄叶片活性氧代谢及AsA-GSH循环的影响

以番茄品种‘辽园多丽’为试材,利用人工气候室模拟设施生产中的夜间低温胁迫环境,研究9℃和6℃夜低温对番茄叶片活性氧代谢和AsA-GSH循环的影响。结果显示:9℃和6℃夜间低温胁迫3～9d可诱导番茄叶片中超氧阴离子(O2.-)产生速率、过氧化氢(H2O2)和丙二醛(MDA)含量上升;抑制过氧化物酶(POD)、过氧化氢酶(CAT)的活性,增加超氧化物歧化酶(SOD)和AsA-GSH循环中抗坏血酸过氧化物酶(APX)、脱氢抗坏血酸还原酶(DHAR)、谷胱甘肽还原酶(GR)的活性,并提高还原型抗坏血酸(AsA)、还原型谷胱甘肽(GSH)、氧化型谷胱甘肽(GSSG)的含量。研究表明,在夜间低温胁迫过程中,增加的番茄叶片中SOD活性和AsA-GSH循环清除活性氧的能力并未与氧还原的速率一致,从而导致番茄叶片中活性氧的累积,使细胞膜系统受到一定破坏,在6℃处理的植物中尤为明显。     

Metabolic and cardiorespiratory responses of summer flounder Paralichthys dentatus to hypoxia at two temperatures

To quantify the tolerance of summer flounder Paralichthys dentatus to episodic hypoxia, resting metabolic rate, oxygen extraction, gill ventilation and heart rate were measured during acute progressive hypoxia at the fish's acclimation temperature (22° C) and after an acute temperature increase (to 30° C). Mean ±s.e. critical oxygen levels (i.e. the oxygen levels below which fish could not maintain aerobic metabolism) increased significantly from 27 ± 2% saturation (2·0 ± 0·1 mg O(2) l(-1) ) at 22° C to 39 ± 2% saturation (2·4 ± 0·1 mg O(2) l(-1) ) at 30° C. Gill ventilation and oxygen extraction changed immediately with the onset of hypoxia at both temperatures. The fractional increase in gill ventilation (from normoxia to the lowest oxygen level tested) was much larger at 22° C (6·4-fold) than at 30° C (2·7-fold). In contrast, the fractional decrease in oxygen extraction (from normoxia to the lowest oxygen levels tested) was similar at 22° C (1·7-fold) and 30° C (1·5-fold), and clearly smaller than the fractional changes in gill ventilation. In contrast to the almost immediate effects of hypoxia on respiration, bradycardia was not observed until 20 and 30% oxygen saturation at 22 and 30° C, respectively. Bradycardia was, therefore, not observed until below critical oxygen levels. The critical oxygen levels at both temperatures were near or immediately below the accepted 2·3 mg O(2) l(-1) hypoxia threshold for survival, but the increase in the critical oxygen level at 30° C suggests a lower tolerance to hypoxia after an acute increase in temperature.     

Effects of KCN and NaN3 Pretreatment on the Cyanide-Resistant Respiration in Tobacco Callus

The effects of KCN (0.5mmol/L) and NaN3 (0.01 mmol/L) pretreatment on the operation of the alternative pathway in subcultured tobacco (Nicotiana rustica L. cv. Gansu yellow flower) callus were analyzed. After treatment with KCN and NaN3 for 12 h, the total respiration rate (Vt) decreased by 12% and 17%, whereas oxygen consuption by the cytochrome pathway decreased by 22% and 28% respectively. The capacity of the alternative pathway (Valt) remained constant, while the activity of the alternative pathway (ρ· Valt ) inreased slightly. This changing pattern led to a declined contribution of the cytochrome pathway to the total respiration rate and an increased activity of the alternative pathway. Treatment with KCN for 24 h brought about a slight rise of oxygen consumption by the cytochrome pathway as compared with that in callus treated for 12 h, but the oxygen consumption was still lower than that in the untreated callus. Treatment with NaN3 for 24 h resulted in a profound decrease of the cytochrome pathway operation and a continuing increase of the alternative pathway operation. These data indicated that the enhanced operation of the alternative pathway played a compensatory role to the total respiration when the cytochrome pathway was partially inhibited in tobacco callus.     

The effects of high intensity training upon respiratory gas exchanges during fixed term maximal incremental exercise in man

The response of respiratory gas exchanges to a 6 week high intensity training program was examined in 5 healthy males during fixed term maximal incremental treadmill exercise. Training was performed 3 d.wk-1 and consisted of a progressive series of repeated 15 sec and 30 sec maximal runs, and weight training exercises for the leg extensor muscles. Respiratory gases during the tests were continuously monitored using an on-line system. Muscle biopsy samples were obtained from the m. vastus lateralis before and after training for histochemical determination of fibre distribution based on myosin ATP-ase activity, and fibre cross-sectional area based on NADH-Tetrazolium Reductase activity. Training significantly increased the proportion of type IIa fibres (+5.9 +/- 2.0%, p less than 0.001) and decreased type I fibres (-6.3 +/- 2.0%, p less than 0.001), the distribution of type IIb fibres remained unchanged (+0.4 +/- 0.9%). Muscle cross-sectional area also showed a significant increase after training in type I (+318 +/- 215 microns 2, p less than 0.05), IIa (+652 +/- 207 microns 2, p less than 0.001) and IIb (+773 +/- 196 microns 2, p less than 0.001) fibres. During fixed term maximal incremental exercise the mean carbon dioxide output (VCO2) and mean respiratory exchange ratio (R = VCO2/VO2) were significantly increased (p less than 0.01) after training. The R-time relationship was at all times shifted to the left after training, being significantly (p less than 0.01) so over the final five min of exercise. No changes in mean exercise oxygen uptake (VO2), maximum oxygen uptake (VO2max) and maximum heart rate (FHRmax) were observed between tests.(ABSTRACT TRUNCATED AT 250 WORDS)     

The effect of glucocorticoids on the myosin heavy chain isoforms' turnover in skeletal muscle

The purpose of this study was to find the effect of dexamethasone on the myosin heavy chain (MyHC) isoforms' composition in different skeletal muscles and glycolytic (G) fibres in relation with their synthesis rate and degradation of MyHC isoforms by alkaline proteinases. Eighteen-week-old male rats of the Wistar strain were treated with dexamethasone (100 microg/100 g bwt) during 10 days. The forelimb strength decreased from 9.52 to 6.19 N (P<0.001) and hindlimb strength from 15.54 to 8.55 N (P<0.001). Daily motor activity decreased (total activity from 933 to 559 and ambulatory activity from 482 to 226 movements/h, P<0.001). The degradation rate of muscle contractile proteins increased from 2.0 to 5.9% per day (P<0.001), as well as the myosin heavy chain IIB isoform degradation with alkaline proteinase in fast-twitch (F-T) muscles (12 +/- 0.9%; P<0.05) and glycolytic muscle fibres (15 +/- 1.1%; P<0.001). The synthesis rate of MyHC type II isoforms decreased in Pla muscles (P<0.05) and MyHC IIA (P<0.05) and IIB in EDL muscle and G fibres (P<0.001). The relative content of MyHC IIB isoform decreased in F-T muscles (P<0.001) and in G fibres (P<0.01), and the relative content of IIA and IID isoforms increased simultaneously. Dexamethasone decreased the MyHC IIB isoform synthesis rate and increased the sensibility of MyHC IIB isoform to alkaline proteinase, which in its turn led to the decrease of MyHC IIB isoform relative content in F-T muscles with low oxidative potential and G muscle fibres.     

Effects of Low Salinity on Adult Behavior and Larval Performance in the Intertidal Gastropod Crepipatella peruviana (Calyptraeidae)

Shallow-water coastal areas suffer frequent reductions in salinity due to heavy rains, potentially stressing the organisms found there, particularly the early stages of development (including pelagic larvae). Individual adults and newly hatched larvae of the gastropod Crepipatella peruviana were exposed to different levels of salinity stress (32(control), 25, 20 or 15), to quantify the immediate effects of exposure to low salinities on adult and larval behavior and on the physiological performance of the larvae. For adults we recorded the threshold salinity that initiates brood chamber isolation. For larvae, we measured the impact of reduced salinity on velar surface area, velum activity, swimming velocity, clearance rate (CR), oxygen consumption (OCR), and mortality (LC50); we also documented the impact of salinity discontinuities on the vertical distribution of veliger larvae in the water column. The results indicate that adults will completely isolate themselves from the external environment by clamping firmly against the substrate at salinities ≤24. Moreover, the newly hatched larvae showed increased mortality at lower salinities, while survivors showed decreased velum activity, decreased exposed velum surface area, and decreased mean swimming velocity. The clearance rates and oxygen consumption rates of stressed larvae were significantly lower than those of control individuals. Finally, salinity discontinuities affected the vertical distribution of larvae in the water column. Although adults can protect their embryos from low salinity stress until hatching, salinities <24 clearly affect survival, physiology and behavior in early larval life, which will substantially affect the fitness of the species under declining ambient salinities.     

The consequences of acute cold exposure on protein oxidation and proteasome activity in short-tailed field voles,microtus agrestis

During cold exposure, animals upregulate their metabolism and food intake, potentially exposing them to elevated reactive oxygen species (ROS) production and oxidative damage. We investigated whether acute cold (7 +/- 3 degrees C) exposure (1, 10, or 100 h duration) affected protein oxidation and proteasome activity, when compared to warm controls (22 +/- 3 degrees C), in a small mammal model, the short-tailed field vole Microtus agrestis. Protein carbonyls and the chymotrypsin-like proteasome activity were measured in plasma, heart, liver, kidney, small intestine (duodenum), skeletal muscle (gastrocnemius), and brown adipose tissue (BAT). Trypsin-like and peptidyl-glutamyl-like proteasome activities were determined in BAT, liver, and skeletal muscle. Resting metabolic rate increased significantly with duration of cold exposure. In skeletal muscle (SM) and liver, protein carbonyl levels also increased with duration of cold exposure, but this pattern was not repeated in BAT where protein carbonyls were not significantly elevated. Chymotrpsin-like proteasome activity did not differ significantly in any tissue. However, trypsin-like activity in SM and peptidyl-glutamyl-like activity in both skeletal muscle and liver, were reduced during the early phase of cold exposure (1-10 h), correlated with the increased carbonyl levels in these tissues. In contrast there was no reduction in proteasome activity in BAT during the early phase of cold exposure and peptidyl-glutamyl-like activity was significantly increased, correlated with the lack of accumulation of protein carbonyls in this tissue. The upregulation of proteasome activity in BAT may protect this tissue from accumulated oxidative damage to proteins. This protection may be a very important factor in sustaining uncoupled respiration, which underpins nonshivering thermogenesis at cold temperatures.     

Extracellular superoxide dismutase inhibits innate immune responses and clearance of an intracellular bacterial infection

Reactive oxygen species and reactive nitrogen species play important roles during immune responses to bacterial pathogens. Extracellular superoxide dismutase (ecSOD) regulates extracellular concentrations of reactive oxygen species and reactive nitrogen species and contributes to tissue protection during inflammatory insults. The participation of ecSOD in immune responses seems therefore intuitive, yet is poorly understood. In the current study, we used mice with varying levels of ecSOD activity to investigate the involvement of this enzyme in immune responses against Listeria monocytogenes. Surprisingly, our data demonstrate that despite enhanced neutrophil recruitment to the liver, ecSOD activity negatively affected host survival and bacterial clearance. Increased ecSOD activity was accompanied by decreased colocalization of neutrophils with bacteria, as well as increased neutrophil apoptosis, which reduced overall and neutrophil-specific TNF-α production. Liver leukocytes from mice lacking ecSOD produced equivalent NO· compared with liver leukocytes from mice expressing ecSOD. However, during infection, there were higher levels of peroxynitrite (NO(3)·(-)) in livers from mice lacking ecSOD compared with livers from mice expressing ecSOD. Neutrophil depletion studies revealed that high levels of ecSOD activity resulted in neutrophils with limited protective capacity, whereas neutrophils from mice lacking ecSOD provided superior protection compared with neutrophils from wild-type mice. Taken together, our data demonstrate that ecSOD activity reduces innate immune responses during bacterial infection and provides a potential target for therapeutic intervention.     

虎斑乌贼的胚胎耗氧率

为了探究虎斑乌贼胚胎不同发育时期的耗氧率变化和几种生态因子对胚胎发育过程耗氧率的影响,试验采用封闭静水装置,对不同发育时期(12期)的耗氧率进行测定,并研究不同盐度(21、24、27、30、33)、温度(18、21、24、27、30 ℃)和pH(7.0、7.5、8.0、8.5、9.0)对胚胎4个主要发育时期(受精卵期、原肠胚期、器官形成期和内骨骼形成期)耗氧率的影响.结果表明: 胚胎各个发育时期耗氧率不同,随着发育的进程而增大,受精卵期为0.082 mg·(100 eggs)^-1·h^-1,而到原肠胚期的耗氧率显著升高,为0.279 mg·(100 eggs)^-1·h^-1,到孵化期时,耗氧率达到1.367 mg·(100 eggs)^-1·h^-1;盐度对器官形成期和内骨骼形成期的耗氧率均有显著影响(P<0.05),对受精卵期和原肠胚期影响不显著(P>0.05),当盐度为30时,4个发育时期耗氧率均达到最大值,分别为0.082、0.200、0.768和1.301 mg·(100 eggs)^-1·h^-1;温度对原肠胚期、器官形成期和内骨骼形成期的耗氧率有显著影响(P<0.05),对受精卵期无显著性影响(P>0.05),在27 ℃时,胚胎4个发育时期均达到最大值,分别为0.082、0.286、0.806和1.338 mg·(100 eggs)^-1·h^-1;而pH对4个发育时期的耗氧率均无显著性影响(P>0.05),受精卵期在pH 8.0时达到最大值,为0.116 mg·(100 eggs)^-1·h^-1,原肠胚期、器官形成期、内骨骼形成期在pH 8.5时达到最大值,分别为0.281 、0.799和1.130 mg·(100 eggs)^-1·h^-1.     

虎斑乌贼的胚胎耗氧率

为了探究虎斑乌贼胚胎不同发育时期的耗氧率变化和几种生态因子对胚胎发育过程耗氧率的影响,试验采用封闭静水装置,对不同发育时期(12期)的耗氧率进行测定,并研究不同盐度(21、24、27、30、33)、温度(18、21、24、27、30 ℃)和pH(7.0、7.5、8.0、8.5、9.0)对胚胎4个主要发育时期(受精卵期、原肠胚期、器官形成期和内骨骼形成期)耗氧率的影响.结果表明: 胚胎各个发育时期耗氧率不同,随着发育的进程而增大,受精卵期为0.082 mg·(100 eggs)^-1·h^-1,而到原肠胚期的耗氧率显著升高,为0.279 mg·(100 eggs)^-1·h^-1,到孵化期时,耗氧率达到1.367 mg·(100 eggs)^-1·h^-1;盐度对器官形成期和内骨骼形成期的耗氧率均有显著影响(P<0.05),对受精卵期和原肠胚期影响不显著(P>0.05),当盐度为30时,4个发育时期耗氧率均达到最大值,分别为0.082、0.200、0.768和1.301 mg·(100 eggs)^-1·h^-1;温度对原肠胚期、器官形成期和内骨骼形成期的耗氧率有显著影响(P<0.05),对受精卵期无显著性影响(P>0.05),在27 ℃时,胚胎4个发育时期均达到最大值,分别为0.082、0.286、0.806和1.338 mg·(100 eggs)^-1·h^-1;而pH对4个发育时期的耗氧率均无显著性影响(P>0.05),受精卵期在pH 8.0时达到最大值,为0.116 mg·(100 eggs)^-1·h^-1,原肠胚期、器官形成期、内骨骼形成期在pH 8.5时达到最大值,分别为0.281 、0.799和1.130 mg·(100 eggs)^-1·h^-1.     

Acute severe carbon monoxide exposure in the rat: effects of hyperglycemia and hypoglycemia on mortality, recovery, and neurologic deficit.

Human and animal studies suggest a poorer outcome in the presence of abnormal blood glucose concentration during cerebral hypoxia-ischemia. It is unknown whether this is also the case in acute severe carbon monoxide poisoning. Using Levine-prepared rats, three groups were established and exposed to CO to answer this question: (1) hyperglycemics resulting from the administration of a 50% glucose solution, (2) hypoglycemics resulting from the administration of normal saline, and (3) untreated controls. The rats inhaled 2400 ppm CO for 90 min in the absence of anesthesia. Blood glucose was raised to a mean value of 402 mg/dL just prior to CO exposure in group 1. This resulted in an increased mortality rate (i.e., 54%), and during 4 h of room air recovery an impaired ability to regain body temperature, an increased plasma lactate dehydrogenase activity, and an increased neurologic deficit as compared with group 3. Hypoglycemia, which developed during CO exposure in group 2 (mean minimum glucose after 90 min, 44 mg/dL), resulted in an increased mortality rate (i.e., 46%), and during 4 h of room air recovery an impaired ability to regain body temperature and an increased neurologic deficit as compared with group 3. Blood glucose concentration in the rats in groups 2 and 3 that died during or shortly after CO exposure was significantly depressed relative to the survivors of those groups. Plasma insulin activity was elevated during CO exposure in group 1 as compared with group 3, but fell during recovery; insulin remained low throughout CO exposure and recovery in group 2. The results demonstrate the deleterious effects of both a very high and a very low blood glucose concentration during acute CO exposure.     

The cerebral critical oxygen threshold of ventilated preterm lambs and the influence of antenatal inflammation

Perinatal inflammation is associated with adverse neurodevelopmental outcomes, which may be partly due to changes in the cerebral oxygen delivery/consumption relationship. We aimed to determine the critical oxygen delivery threshold of the brain of preterm, ventilated lambs and to determine whether the critical threshold is affected by exposure to inflammation in utero. Pregnant ewes received intra-amniotic injection of lipopolysaccharide or saline at 125 or 127 days of gestation. Pulmonary and systemic flow probes and catheters were surgically positioned in the fetus immediately before delivery at 129 days of gestation. After delivery, lambs were ventilated for 90 min using a positive end-expiratory pressure recruitment strategy. Cardio-respiratory variables and blood gases were measured regularly. Systemic and cerebral oxygen delivery, consumption (Fick), and extraction were calculated, and the relationship between cerebral delivery and consumption analyzed. Linear regression was used to define the transition or "critical" oxygen threshold as the point at which the slope of the oxygen delivery/consumption curve changed to be > 10°. Four subgroups were defined according to the calculated critical threshold. A total of 150 measurements were recorded in 18 lambs. Fetal cerebral oxygen consumption was increased by antenatal lipopolysaccharide (P < 0.05). The postnatal critical oxygen threshold was 3.6 ml·kg?1·min?1, corresponding to cerebral oxygen consumption of 0.73 ml·kg?1·min?1. High oxygen delivery and consumption were associated with increased pulmonary and carotid blood flow and systemic extraction compared with low oxygen delivery and consumption. No postnatal effect of antenatal inflammation was observed. Inflammation in utero increases fetal, but not postnatal, cerebral oxygen consumption. Adverse alterations to pulmonary blood flow can result in reduced cerebral blood flow, oxygen delivery, and consumption. Regardless of exposure to inflammation, there is a consistent postnatal relationship between cerebral oxygen delivery and consumption.     

Hydrogen peroxide mediates the radiation-induced mutator phenotype in mammalian cells

Chronic oxidative stress has been associated with genomic instability following exposure to ionizing radiation. However, results showing direct causal linkages between specific ROS (reactive oxygen species) and the ionizing radiation-induced mutator phenotype are lacking. The present study demonstrates that ionizing radiation-induced genomically unstable cells (characterized by chromosomal instability and an increase in mutation and gene amplification frequencies) show a 3-fold increase in steady-state levels of hydrogen peroxide, but not superoxide. Furthermore, stable clones isolated from parallel studies showed significant increases in catalase and GPx (glutathione peroxidase) activity. Treatment of unstable cells with PEG-CAT (polyethylene glycol-conjugated catalase) reduced the mutation frequency and mutation rate in a dose-dependent fashion. In addition, inhibiting catalase activity in the stable clones using AT (3-aminotriazole) increased mutation frequency and rate. These results clearly demonstrate the causal relationship between chronic oxidative stress mediated by hydrogen peroxide and the mutator phenotype that persists for many generations following exposure of mammalian cells to ionizing radiation.     

Compensatory and adaptive rearrangement in the human respiratory system under acute hypoxic conditions

Relationships between the parameters of external respiration (minute volume and respiration rate) and those of internal, tissue respiration (oxygen consumption, arteriovenous oxygen difference and efficiency of oxygen uptake) were studied during a period of acute hypoxia and upon its completion. The subjects were exposed to hypoxia for 25 min using oxygen-nitrogen hypoxic gas mixtures (HGMs) differing in oxygen content (8 and 12%, HGM-8 and HGM-12, respectively). From the third to the fifth minutes of exposure to HGM-8, the respiration minute volume (RMV) was found to increase by 51 ± 33% as compared to the background value; however, the body’s oxygen consumption (OC) was 35 ± 22% reduced. Afterwards, OC grew to reach, from the 20th to the 25th min of hypoxia, 108 ± 21% of the background value and 181% of the value determined from the third to the fifth minutes of hypoxia. OC growth was accompanied by an insignificant RMV increase (by 12%) as compared to the level determined from the third to the fifth minutes of hypoxia, whereas the efficiency of oxygen uptake from the arterial blood increased by 75% for the same period. RMV growth from the third to the fifth minutes of hypoxia occurred as expense result of a higher breathing depth; at the same time, the respiration rate decreased as compared to the background value. By the period from the 20th to the 25th min of exposure to HGM-8, the respiration rate increased by 21% as compared to the period from the third to the fifth minutes of hypoxia. The efficiency of oxygen uptake from the arterial blood remained higher than the background value for at least 5 min after completion of the exposure to HGM-8. During the same period, the ventilation equivalent, an indicator of the efficiency of external respiration, i.e., of oxygen supply to the body, was significantly lower than the background value. During the exposure to HGM-12, RMV increased to a lesser extent than on exposure to HGM-8, however, the efficiency of oxygen uptake was higher during exposure to HGM-12; therefore, OC was also higher in the latter case. Therefore, the assumption that, during hypoxia, intensified external respiration (ventilatory response) itself compensates oxygen deficiency in inhaled air is revised. Ventilatory response is only a portion of the entire functional system of respiration (both external and tissue respiration). The role of ventilatory response is important for conditioning the tissue respiration rearrangement to eliminate deficiency of oxygen consumption during hypoxia. The retained higher oxygen uptake from the arterial blood during the period after completion of hypoxic treatment testifies to the adaptive implication of changes in tissue respiration; the same is confirmed by a reduced ventilation equivalent after hypoxia, which is indicative of the growing efficiency of external respiration, i.e., of an improved oxygen supply to the body.     

不同光照条件下外源水杨酸对浒苔响应紫外辐射胁迫的影响

为研究不同光照条件下,外源水杨酸(SA)和紫外辐射(UV)对海洋绿藻浒苔的复合效应,在两个光照强度(高光:160 μmol·m^-2·s^-1;低光:70 μmol·m^-2·s^-1)条件下,设置对照(CK)、SA、UV及UV+SA处理(UV=3.2 W·m^-2、SA=10 μg·mL^-1),处理3 d后测定浒苔生长、叶绿素荧光参数、光合放氧速率、超氧化物歧化酶活性、可溶性糖和可溶性蛋白含量等的变化,探讨光照强度、UV及SA的复合效应.结果表明: 低光无UV条件下,SA会促进浒苔生长,降低浒苔叶绿素a(Chl a)和可溶性蛋白含量;高光无UV条件下, SA会抑制其生长,但显著提高了Chl a含量、呼吸速率、光合放氧速率、可溶性糖和可溶性蛋白含量;高光和UV条件下, UV+SA显著促进浒苔生长,提高Chl a和可溶性糖含量;低光和UV条件下,与UV相比,UV+SA提高了浒苔最大光化学效率(F_v/F_m)和可溶性蛋白含量,涨幅分别为139.8%和32.2%.外源SA的加入在一定程度上缓解了UV对浒苔的胁迫作用,且在高光条件下的效果更为显著.     

Increased biosynthesis of pyruvate kinase under hypoxic conditions in mammalian cells

The rate of biosynthesis of pyruvate kinase (ATP:pyruvate 2-O-phosphotransferase, EC 2.7.1.40) was compared in cells maintained under normoxic or hypoxic conditions. L8 cells (a myoblast cell line) were pulse-labeled with [3H]leucine and incorporation of radioactivity into pyruvate kinase was measured after quantitative affinity separation with anti-pyruvate kinase monoclonal antibody. During chronic hypoxia there is an increased rate of biosynthesis of pyruvate kinase leading to an increase in enzyme content and augmented glycolytic capacity. An inhibitor of the electron transport chain, antimycin A, was used to determine whether changes in pyruvate kinase content occurring during hypoxia are a result of reduction in molecular oxygen directly or an indirect consequence of oxygen depletion. Pyruvate kinase activity increased during chronic antimycin A exposure under normoxic conditions. The increase was quantitatively accounted for by an increase in cellular pyruvate kinase enzyme content. This suggested that decreases in the levels of molecular O2 are not the direct stimulus for the increased content of pyruvate kinase. It is more likely that the increased pyruvate kinase content results from depressed rates of electron transport through the mitochondrial electron transport chain.