Short-term UV-B radiation effects on morphology,physiological traits and accumulation of bioactive compounds in Prunella vulgaris L.

Prunella vulgaris plants (full-bloom stage) were subjected to short-term (15 days) UV-B radiation in a growth chamber. UV-B radiation was effective at enhancing morphological and biomass characteristics and decreasing chlorophyll contents of P. vulgaris. Treatment of P. vulgaris with artificial UV-B radiation significantly increased peroxidase (POD), superoxide dismutase (SOD) and glutathione (GSH) activities compared to the control treatment. UV-B radiation significantly increased the levels of hydrogen peroxide (H₂O₂), malondialdehyde (MDA) and proline in leaves of P. vulgaris compared to those of control plants. In addition, the contents of total flavonoids, rosmarinic acid, caffeic acid and hyperoside significantly increased under UV-B radiation. The total phenolic levels also increased under UV-B treatment. These results demonstrated that short-term UV-B radiation can enhance production of secondary metabolites in P. vulgaris, resulting in increased spica yield compared to that of control plants.     

The effects of solar ultraviolet-B radiation on the growth and yield of barley are accompanied by increased DNA damage and antioxidant responses

There is limited information on the impacts of present-day solar ultraviolet-B radiation (UV-B) on biomass and grain yield of field crops and on the mechanisms that confer tolerance to UV-B radiation under field conditions. We investigated the effects of solar UV-B on aspects of the biochemistry, growth and yield of barley crops using replicated field plots and two barley strains, a catalase (CAT)-deficient mutant (RPr 79/4) and its wild-type mother line (Maris Mink). Solar UV-B reduced biomass accumulation and grain yield in both strains. The effects on crop biomass accumulation tended to be more severe in RPr 79/4 (≈ 32% reduction) than in the mother line (≈ 20% reduction). Solar UV-B caused measurable DNA damage in leaf tissue, in spite of inducing a significant increase in UV-absorbing sunscreens in the two lines. Maris Mink responded to solar UV-B with increased CAT and ascorbate peroxidase (APx) activity. No effects of UV-B on total superoxide dismutase (SOD) activity were detected. Compared with the wild type, RPr 79/4 had lower CAT activity, as expected, but higher APx activity. Neither of these activities increased in response to UV-B in RPr 79/4. These results suggest that growth inhibition by solar UV-B involves DNA damage and oxidative stress, and that constitutive and UV-B-induced antioxidant capacity may play an important role in UV-B tolerance.     

Antioxidant actions of plant foods: Use of oxidative DNA damage as a tool for studying antioxidant efficacy

Plant-food-derived antioxidants and active principles such as flavonoids, hydroxycinnamates (ferulic acid, chlorogenic acids, vanillin etc.), β-carotene and other carotenoids, vitamin E, vitamin C, or rosemary, sage, tea and numerous extracts are increasingly proposed as important dietary antioxidant factors. In this endeavor, assays involving oxidative DNA damage for characterizing the potential antioxidant actions are suggested as in vitro screens of antioxidant efficacy. The critical question is the bioavailability of the plant-derived antioxidants.     

增强UV-B对蛋白核小球藻中NO释放的影响

研究了蛋白核小球藻在增强UV—B辐射下NO信号的产生。结果表明：NO释放量与UV—B的强度相关。在藻类细胞培养液中加入NOS的竞争性抑制剂硝基精氨酸(LNNA),不能抑制NO的释放。加入NO清除剂乙酰半胱氨酸(NAC),能明显减少NO的释放。在无氮和有氮培养基中NO同样的释放。这些结果说明NO生成途径不经过依赖L-精氨酸的NOS和依赖NO3^-和硝酸还原酶,NO的底物不是L-精氨酸和NO3^-在无氮和有氮培养基中同样有NO3^-的形成,NAC减少NO2^-的释放,说明生成了NO2^-有可能是NO释放后生成的。     

紫外辐射诱导烟草原生质体中DNA损伤的彗星电泳检测

以烟草原生质体为材料,采用彗星电泳检测用0.5W·m^-2紫外线以不同时间（0、5、10、30、60和120s）诱导的烟草原生质体中DNA的损伤。结果表明,在0～10s的时间内代表DNA损伤程度的尾矩、Olive尾矩等参数与紫外线照射时间具有良好的时间依赖关系。本文建立的烟草原生质体体系采用彗星电泳技术,可以快速而灵敏地检测紫外线对植物细胞的损伤程度。     

紫外线-B辐射对植物DNA及蛋白质的影响

大气平流层中的臭氧衰减,导致太阳辐射中的紫外辐射量有明显的增加,其中UV-B辐射对植物会产生不同程度的影响。分子生态学理论认为,UV-B辐射对植物造成的损伤,首先伤害植物的生物大分子,即进行光化学修饰。本文就臭氧衰减对生态环境和植物的影响途径进行了讨论,重点论述了UV-B辐射对植物蛋白质合成的抑制和DNA的损伤修复途径。并应用分子生物学技术研究植物对UV-B辐射的抗性机理和DNA修复技术的前景进行了展望。     

UVA‐induced reset of hydroxyl radical ultradian rhythm improves temporal lipid production in Chlorella vulgaris

We report for the first time that the endogenous, pseudo‐steady‐state, specific intracellular levels of the hydroxyl radical (si‐OH) oscillate in an ultradian fashion (model system: the microalga, Chlorella vulgaris), and also characterize the various rhythm parameters. The ultradian rhythm in the endogenous levels of the si‐OH occurred with an approximately 6 h period in the daily cycle of light and darkness. Further, we expected that the rhythm reset to a shorter period could rapidly switch the cellular redox states that could favor lipid accumulation. We reset the endogenous rhythm through entrainment with UVA radiation, and generated two new ultradian rhythms with periods of approximately 2.97 h and 3.8 h in the light phase and dark phase, respectively. The reset increased the window of maximum lipid accumulation from 6 h to 12 h concomitant with the onset of the ultradian rhythms. Further, the saturated fatty acid content increased approximately to 80% of total lipid content, corresponding to the peak maxima of the hydroxyl radical levels in the reset rhythm. © 2014 American Institute of Chemical Engineers Biotechnol. Prog., 30:673–680, 2014     

Is UV-B radiation affecting charophycean algae in shallow freshwater systems?

The objective of this study was to determine the effects of UV-B radiation on charophycean algae under natural conditions, since charophytes enhance water transparency in freshwater systems and levels of UV-B radiation have increased by ozone depletion. Potential and actual UV-B effects were studied by combining a glasshouse experiment in which plants were exposed to various levels of UV-B radiation and field measurements in two freshwater systems dominated by charophytes in the Netherlands. The glasshouse experiment showed that charophytes were sensitive to UV-B radiation. UV-B radiation negatively affected growth, while it increased levels of DNA damage in Chara aspera. Moreover, the charophytes did not seem to develop UV-B screens to protect against UV-B radiation since no increase in UV-B absorbing compounds was found. At field conditions, both spectroradiometrical measurements and DNA dosimeters showed that UV-B radiation was attenuated quickly in both freshwater systems, indicating that UV-B does not reach the submerged charophyte vegetation. However, specific conditions, like fluctuating water tables, may result in UV-B exposure to charophytes for certain periods annually.     

Hydroperoxide-induced DNA damage and mutations

Hydroperoxides (ROOH) are believed to play an important role in the generation of free radical damage in biology. Hydrogen peroxide (R=H) is produced by endogenous metabolic and catabolic processes in cells, while alkyl hydroperoxides (R=lipid, protein, DNA) are produced by free radical chain reactions involving molecular oxygen (autooxidation). The role of metal ions in generating DNA damage from hydroperoxides has long been recognized, and several distinct, biologically relevant mechanisms have been identified. Identification of the mechanistic pathways is important since it will largely determine the types of free radicals generated, which will largely determine the spectrum of DNA damage produced. Some mechanistic aspects of the reactions of low valent transition metal ions with ROOH and their role in mutagenesis are reviewed with a perspective on their possible role in the biological generation of DNA damage. A survey of hydroperoxide-induced mutagenesis studies is also presented. In vitro footprinting of DNA damage induced by hydroperoxides provides relevant information on sequence context dependent reactivity, and is valuable for the interpretation of mutation spectra since it represents the damage pattern prior to cellular repair. Efforts in this area are also reviewed.     

UV-B辐射增强对三种赤潮微藻DNA的伤害效应

运用生态毒理学和生物化学方法研究了UV-B辐射增强对赤潮异弯藻、亚历山大藻和中肋骨条藻DNA的伤害作用.结果表明,3种赤潮微藻的生长状况对UV-B辐射增强的敏感性不同;对UV-B辐射增强的敏感性由高到低依次是赤潮异弯藻、亚历山大藻和中肋骨条藻.随着UV-B辐射剂量的增加,3种赤潮微藻的DNA损伤程度提高,而且赤潮异弯藻DNA的损伤程度明显高于亚历山大藻和中肋骨条藻,亚历山大藻DNA的伤害程度又远远高于中肋骨条藻.UV-B辐射处理解除后,损伤DNA可明显恢复.赤潮异湾藻和亚历山大藻恢复培养6d,损伤DNA可明显恢复(P＜0.05);而中肋骨条藻恢复培养3d,损伤DNA可明显恢复(P＜0.05),说明3种赤潮微藻的DNA损伤水平不适合作为指示UV-B辐射增强的生物学指标.     

紫外辐射诱导植物叶片DNA损伤敏感性差异

单细胞凝胶电泳（彗星检测,cometassay）技术已广泛应用于动物细胞DNA损伤检测,但在植物细胞DNA损伤检测中的应用尚不多见。本研究通过对动物细胞彗星检测方法的改进,利用植物细胞原生质体作为材料,研究了不同发育期九里香（Murraya panicuata）叶片对UV-B诱导的DNA损伤的敏感性差异。彗星检测结果表明,九里香叶片DNA的损伤程度与UV-B辐射的剂量呈正相关：在相同UV—B辐射剂量下,九里香幼嫩叶片比成熟叶片的DNA损伤量大,表明其幼嫩叶片对UV-B辐射的敏感性比成熟叶片高。     

Enhanced UV-B radiation under field conditions increases anthocyanin and reduces the risk of photoinhibition but does not affect growth in the carnivorous plant Pinguicula vulgaris

The effects of enhanced UV-B radiation were investigated in the carnivorous plant Pinguicula vulgaris in a field experiment performed in Abisko, North Sweden (68° 21' N, 18° 49' E, 380 m above sea level). Potted plants were exposed to either ambient or ambient plus supplemental UV-B radiation, simulating a 15% ozone depletion. No effect was observed on either the epicuticular (external) or cellular (internal) UV absorbing capacity of the leaves. However, the anthocyanin content was more than doubled by supplemental UV-B radiation. In laboratory experiments, the anthocyanin rich, UV-B treated leaves were less susceptible to a low temperature/high light photoinhibitory treatment, as judged by in vivo chlorophyll fluorescence measurements. Yet, this potential benefit did not considerably affect the growth of the plant in the field (leaf area and dry mass, reproductive dry mass, flowering frequency, senescence rates, dry mass of winter buds). However, there was a marginally significant increase in root dry mass and in the root to shoot ratio, which may underlie the significant increase in the nitrogen content of the leaves. We suggest that P. vulgaris is resistant against UV-B radiation damage and that the possible negative effects of additional UV-B radiation on the growth of these plants may have been effectively counterbalanced by the lower risk of photoinhibition, due to the concomitant increase in anthocyanins.     

Selection in vitro for UV-tolerant sugar beet (Beta vulgaris) somaclones

With a reduced stratospheric ozone concentration, the generation of UV-tolerant plants may be of particular importance. Among different crop plants there is large variation in sensitivity to UV-B radiation. This study was undertaken to investigate the possibilities of using somaclonal variation and selection in vitro for improving UV-B tolerance in sugar beet (Beta vulgaris L.). Sugar beet callus was exposed to UV radiation (280–320 nm, 0.863–5.28 kJ m^-2 day^-1, unweighted) and resultant shoots were selected from surviving cells. After establishment of the plants, they were grown under either visible radiation (114 μmol m^-2 s^-1 PAR) or with the addition of UV radiation (6.3 kJ m^-2 day^-1 biologically effective UV-B). Screening of regenerants in vivo for tolerance to UV radiation was undertaken 10 months after termination of the UV selection pressure. Screening was done visually and by using a number of physiological parameters, including chlorophyll fluorescence induction, ultraweak luminescence, pigment analysis and total content of UV-screening pigments. A clear difference between the unselected and the UV-selected somaclones was observed when visually studying the UV damage and other leaf injury. The observations were supported by the ultraweak luminescence measurements. Unselected plants showed significantly greater damage when subjected to subsequent UV radiation as compared to the selected plants. The clones subjected to UV selection pressure displayed a significantly higher concentration of UV-screening pigments under subsequent UV radiation. The unselected plants under subsequent UV treatment showed a lower carotenoid concentration when compared to selected plants. However, no significant difference between treatments was found for chlorophyll a/b, or F/F_max, a measure of photosynthetic quantum yield.     

Aging in vertebrates,and the effect of caloric restriction: a mitochondrial free radical production–DNA damage mechanism?

Oxygen is toxic to aerobic animals because it is univalently reduced inside cells to oxygen free radicals. Studies dealing with the relationship between oxidative stress and aging in different vertebrate species and in caloric-restricted rodents are discussed in this review. Healthy tissues mainly produce reactive oxygen species (ROS) at mitochondria. These ROS can damage cellular lipids, proteins and, most importantly, DNA. Although antioxidants help to control this oxidative stress in cells in general, they do not decrease the rate of aging, because their concentrations are lower in long- than in short-lived animals and because increasing antioxidant levels does not increase vertebrate maximum longevity. However, long-lived homeothermic vertebrates consistently have lower rates of mitochondrial ROS production and lower levels of steady-state oxidative damage in their mitochondrial DNA than short-lived ones. Caloric-restricted rodents also show lower levels of these two key parameters than controls fed ad libitum. The decrease in mitochondrial ROS generation of the restricted animals has been recently localized at complex I and the mechanism involved is related to the degree of electronic reduction of the complex I ROS generator. Strikingly, the same site and mechanism have been found when comparing a long- with a short-lived animal species. It is suggested that a low rate of mitochondrial ROS generation extends lifespan both in long-lived and in caloric-restricted animals by determining the rate of oxidative attack and accumulation of somatic mutations in mitochondrial DNA.     

Biochemical studies on the lethal effects of solar and artificial ultraviolet radiation on Staphylococcus aureus

The effects of UV-B radiation generated in the laboratory and as a component of sunlight on the viability and particular biochemical activities of the bacterium Staphylococcus aureus have been examined. UV-B radiation progressively inhibits protein synthesis (assayed as ³H-alanine incorporation) and kills cells. Cell respiration, and RNA and DNA synthesis (³H-uridine and ³H-thymidine incorporation) were not greatly affected by UV-B irradiation. The OH and ¹O₂-free radical scavengers protected cells against killing and inhibition of protein synthesis by UV-B, suggesting that such radicals mediate the effects of UV-B on this organism. A similar protective effect using a ferric ion chelator suggests an important role for metallic ions in UV-B lethality.Abbreviations VIS, UV-A, UV-B, UV-C radiation in the bands 400–750 nm, 315–400 nm, 280–315 nm, 200–280 nm respectively - DBCO diazabicyclooctane - OFR oxygen free radical - OH, ¹O₂, O _inf2 ^sup- hydroxyl free radical, singlet oxygen, superoxide radical respectively     

On the mechanisms of the reaction of dodecatungstophosphate with alkyl radicals in aqueous solutions

The reduced lacunary polyoxotungstate, [PW₁₁O₃₉]⁸⁻, reacts with the ^.CH₂CH(OH)CH₃ and ^.CH₂C(CH₃)₂OH radicals via a mechanism involving β-hydroxide elimination to yield propene and 2-methyl propene respectively, and [PW₁₁O₃₉]⁷⁻. [PW₁₁O₃₉]⁸⁻ is also oxidized by methyl radicals in a reaction which yields methane as the major product. It is proposed that the reactions proceed via the formation of short lived transients with W-C σ bonds.     

ERK activation promotes neuronal degeneration predominantly through plasma membrane damage and independently of caspase-3

Our recent studies have shown that extracellular-regulated protein kinase (ERK) promotes cell death in cerebellar granule neurons (CGN) cultured in low potassium. Here we report that the "death" phenotypes of CGN after potassium withdrawal are heterogeneous, allowing the distinction between plasma membrane (PM)-, DNA-, and PM/DNA-damaged populations. These damaged neurons display nuclear condensation that precedes PM or DNA damage. Inhibition of ERK activation either by U0126 or by dominant-negative mitogen-activated protein kinase/ERK kinase (MEK) overexpression results in a dramatic reduction of PM damaged neurons and nuclear condensation. In contrast, overexpression of constitutively active MEK potentiates PM damage and nuclear condensation. ERK-promoted cellular damage is independent of caspase-3. Persistent active ERK translocates to the nucleus, whereas caspase-3 remains in the cytoplasm. Antioxidants that reduced ERK activation and PM damage showed no effect on caspase-3 activation or DNA damage. These data identify ERK as an important executor of neuronal damage involving a caspase-3-independent mechanism.