Effects of Salt Stress on Carbohydrate Metabolism in Desert Soil Alga Microcoleus vaginatus Gom.

The effects of salt stress on carbohydrate metabolism in Microcoleus vaginatus Gom., a cyanobacterium isolated from desert algal crusts, were investigated in the present study. Extracellular total carbohydrates and exopolysaccharides （EPS） in the culture medium produced by M. vaginatus increased significantly during the growth phase and reached a maximum during the stationary phase. The production of extracellular carbohydrates also significantly increased under higher salt concentrations, which was attributed to an increase in low molecular weight carbohydrates. In the presence of NaCI, the production of cellular total carbohydrates decreased and photosynthetic activity was impaired, whereas cellular reducing sugars, water-soluble sugars and sucrose content and sucrose phosphate synthase activity increased, reaching a maximum in the presence of 200 mmol/L NaCI. These parameters were restored to original levels when the algae were transferred to a non-saline medium. Sodium and K＋ concentrations of stressed cells decreased significantly and H＋-ATPase activity increased after the addition of exogenous sucrose or EPS. The results suggest that EPS and sucrose are synthesized to maintain the cellular osmOtic equilibrium between the intra-and extracellular environment, thus protecting algal cells from osmotic damage, which was attributed to the selective exclusion of cellular Na＋ and K＋ by H＋-ATPase.     

Nitric oxide plays a role as second messenger in the ultraviolet-B irradiated green alga <Emphasis Type="Italic">Chlorella pyrenoidosa</Emphasis>

Nitric oxide (NO) stimulated the activity of plasma membrane H⁺-ATPase, 5′-nucleotidase, peroxidase, ascorbate peroxidase and glutathione reductase in ultraviolet B (UV-B) irradiated Chlorella pyrenoidosa. It also boosted the activity of nitrogen-metabolism enzymes such as nitrate reductase, nitrite reductase, glutamine synthetase, which were inhibited by UV-B irradiation. The chlorophyll fluorescence ratio (Fv/Fm) of the UV-B irradiated algae and decreased continuously after the cells were transferred to UV-B irradiation. A continuing decrease of the Fv/Fm was observed even after the cells were transferred to photosynthetically active radiation (PAR). After adaptation for 8 h under PAR (after treatment with nitric oxide), Fv/Fm recovered to 55 % of normal levels — without NO the value approached zero. Exogenous NO stopped the decay of chlorophyll and thylakoid membrane in cells exposed to UV-B irradiation. NO plays probably a key role in damage induced by UV-B irradiation in green algae.     

PARP-1 inhibition induces a late increase in the level of reactive oxygen species in cells after ionizing radiation

Poly(ADP-ribose) polymerase 1 (PARP1), an enzyme activated by DNA strand breaks, synthesizes polymers of poly(ADP-ribose) (PAR) that modify chromatin and other proteins and play a role in DNA repair. Inhibition of PARP1 activity is considered a potentially important strategy in clinical practice, especially to sensitize tumor cells to chemo- and radio-therapy. Here we examined the influence of inhibition of PARP1 on formation of reactive oxygen species (ROS) and on DNA repair in cells exposed to ionizing radiation (IR). K562 (human myelogenous leukaemia) cells were grown and exposed to 4 or 12Gy of ionizing radiation in presence or absence of the PARP inhibitor NU1025 (100μM). Intracellular ROS were assayed using the probe 2,7-dichlorofluorescein with detection by flow cytometry and the rejoining of DNA strand breaks were followed by alkaline single cell gel electrophoresis (comet) assays. In untreated cells a significant increase in PAR formation occurred during the first 5min after IR, followed by a gradual decrease up to 30min. Addition of a PARP inhibitor arrested the production of PAR almost completely and decreased the rate of rejoining of DNA strand breaks significantly; however, 3h after irradiation we observed no difference in the amount of DNA strand breaks between PARP inhibitor-treated and untreated cells. Twelve to 48h after irradiation, an increase of ROS concentration was observed in irradiated cells and ROS levels in PARP inhibitor-treated cells were significantly higher than in cells without inhibitor. Irradiated cells grown in the presence or absence of PARP inhibitor did not differ in the frequencies of apoptotic and necrotic cells or in the activity of caspases at 24, 48 and 72h after irradiation. Poly(ADP-ribosylation) and inhibition of PARP1 appeared to modulate DNA strand break rejoining and influence the concentration of ROS in irradiated cells.     

Chemical radiosensitization by misonidazole: production and repair of DNA single-strand breaks in Yoshida ascites tumor cells.

Formation of strand-breaks in DNA and its repair in Yoshida ascites tumor cells exposed to gamma radiation (100-400 Gy) in presence and absence of misonidazole (10 mM) were studied. The methodology involved pre-labelling of cellular DNA by 3H-thymidine during cell proliferation in rats, irradiation of cells in vitro and analysing sedimentation profile of DNA by ultracentrifugation in alkaline sucrose density gradients. Irradiation under euoxic conditions resulted in formation of about 1.5 times greater number of strand breaks as compared to those formed during irradiation under hypoxic conditions. Misonidazole (10 mM) by its presence along with the cells during irradiation under hypoxic conditions caused a 3-fold increase in the number of single strand breaks, but under euoxic conditions of irradiation the presence of misonidazole did not enhance the strand break formation. Incubation of cells irradiated in absence of misonidazole for 1 hr in tissue culture medium at 37 degrees C resulted in repair of substantial fraction of the strand breaks while there was no repair of the DNA strand breaks in cells irradiated in the presence of the chemical.     

干燥-再吸水条件下爪哇伪枝藻生理特性和超微结构特征

以典型荒漠丝状蓝藻爪哇伪枝藻为材料,在温室中设置水合(对照)、轻微干燥、中度干燥和极度干燥4种处理,研究干燥胁迫对藻体光合活性、膜脂过氧化、细胞可溶性物质含量、抗氧化酶活性以及细胞超微结构的影响,并采用不同促进剂和抑制剂对干燥藻体进行再吸水处理,测定藻体光合活性的恢复情况。结果显示:(1)爪哇伪枝藻在干燥胁迫下PSⅡ最大光化学效率(Fv/Fm)显著降低,并与其藻体水分含量之间呈极显著性相关(r=0.97、P<0.000 1);(2)随着干燥胁迫程度增加,藻体MDA含量、SOD和CAT活性随之升高,细胞可溶性蛋白和可溶性糖含量增加;(3)在藻体再吸水条件下,培养液(BG-110)、胞外多糖和蔗糖对藻体Fv/Fm的恢复具有重要作用,N-乙酰半胱氨酸和脯氨酸对Fv/Fm有一定的恢复效果,氯霉素和敌草隆则抑制Fv/Fm;(4)与水合状态下的细胞结构相比,干燥藻体细胞结构发生明显的变化,如细胞壁增厚,原生质粘稠浓缩、呈紧密分层排列,细胞内出现大量细小黑色颗粒物等。(5)采用不同外源物质对干燥藻体进行再吸水时,藻体的光合活性呈现不同的恢复效果。研究表明,干燥胁迫下爪哇伪枝藻的光合活性受到明显抑制,细胞质膜过氧化程度加剧,细胞出现可溶性小分子物质积累,抗氧化酶活性增强,并造成细胞结构出现适应性变化。     

UV-B辐射对雨生红球藻光合特性和虾青素含量的影响及其响应

实验研究了不同强度的UV-B(280-320 nm)辐射对雨生红球藻(Haematococcus pluvialis)的光合活性、生物量、色素含量、活性氧(ROS)含量和抗氧化酶活性等的影响, 以探讨利用UV-B辐射诱导虾青素生物合成增强的可能性。结果发现, 经UV-B辐射处理后,雨生红球藻的光合活性降低、生物量增长被抑制。UV-B辐射对叶绿素影响不大, 但会改变细胞的类胡萝卜素和虾青素含量:0.1和0.3 W/m2强度的UV-B辐射使细胞中的这两种色素含量升高, 0.5 W/m2组的色素含量短暂升高后恢复到对照水平。中低强度的UV-B可以促进雨生红球藻单细胞虾青素含量的增加, 但由于其对细胞生长的抑制作用, 并不能使虾青素大量积累。随辐射时间延长, 细胞内ROS含量未明显增加,但抗氧化酶(过氧化氢酶和超氧化物歧化酶)活性下降, 雨生红球藻可能主要依靠虾青素来淬灭ROS。以上结果表明, UV-B辐射对雨生红球藻的主要生理生化过程有抑制作用, UV-B辐射既可以诱导虾青素的合成又会消耗一部分虾青素, 对虾青素含量的影响与其强度有关, 而利用虾青素来清除细胞内的ROS可能是雨生红球藻抵御这种不利环境条件的最重要的途径。       

UV-B resistance as a criterion for the selection of desert microalgae to be utilized for inoculating desert soils

The adaption capability of microalgae species to intense UV-B radiation is an important feature for their survival under the harsh growth conditions they have to face when used for inoculating unconsolidated sand soils in desert areas. In this study, the responses of photosynthetic activity, reactive oxygen species (ROS) generation, and DNA strand breaks to UV-B radiation in four microalgae isolated from artificially induced biological soil crusts were investigated. It was found that low UV-B doses easily inhibited the photosynthetic activity and induced serious DNA damage in Chlorella vulgaris. Microcoleus vaginatus showed the capability to withstand only moderate doses of UV-B, while Nostoc was capable of facing high doses of UV-B due to its lower generation of ROS and higher capability to repair photosystem II (PSII) and DNA damages. On the other hand, Scytonema javanicum showed additional strategies to survive UV-B irradiance, namely the closure of PSII when ROS generation increased rapidly, in addition to a high repair ability of PSII and DNA damage. The results obtained point out different resistance and defense mechanisms of the four microalgae in response to UV-B irradiance and suggest that the strain of Nostoc sp. tested is the most suitable for surviving under the high UV irradiation levels typical of desertified areas.     

Protective effect of nitric oxide against oxidative stress under ultraviolet-B radiation.

The response of bean leaves to UV-B radiation was extensively investigated. UV-B radiation caused increase of ion leakage, loss of chlorophyll, and decrease of the maximum efficiency of PSII photochemistry (Fv/Fm) and the quantum yield of PSII electron transport (PhiPSII) of bean leaves. H2O2 contents and the extent of thylakoid membrane protein oxidation increased, indicated by the decrease of thiol contents and the increase of carbonyl contents with the duration of UV-B radiation. Addition of sodium nitroprusside, a nitric oxide (NO) donor, can partially alleviate UV-B induced decrease of chlorophyll contents, Fv/Fm and PhiPSII. Moreover, the oxidative damage to the thylakoid membrane was alleviated by NO. The potassium salt of 2-(4-carboxyphenyl)-4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide, a specific NO scavenger, arrested NO mediated protective effects against UV-B induced oxidative damage. Incubation of thylakoid membrane with increasing H2O2 concentrations showed a progressive enhancement in carbonyl contents. H2O2 contents were decreased in the presence of NO under UV-B radiation through increased activities of superoxide dismutases, ascorbate peroxidases, and catalases. Taken together, the results suggest that NO can effectively protect plants from UV-B damage mostly probably mediated by enhanced activities of antioxidant enzymes.     

UV-B 胁迫下NaHSO3 对红芸豆叶片的保护作用

为了减轻UV-B辐射对植物叶片的伤害, 本研究以离体红芸豆叶片为实验材料, 通过外源施加NaHSO3的方法探讨了UV-B辐射下NaHSO3 对离体红芸豆叶片的保护作用。结果表明：与未处理对照相比较, 用0.5 mmol.L-1 NaHSO3处理的离体红芸豆叶片表面褐色斑减少、边缘蜷曲及萎蔫程度降低;且能延缓叶片中叶绿素和类胡萝卜素含量的降低;使类黄酮含量升高; 叶片中过氧化物酶(POD)和抗坏血酸过氧化物酶(APX)活性升高, 过氧化氢(H2O2)含量降低。进一步研究发现NaHSO3处理能明显延缓PSⅡ原初光能转换效率的降低;增强PSⅡ的电子传递能力, 减少叶绿体内有害自由基的产生, 减缓叶绿体内光合机构遭受破坏的程度。以上结果表明NaHSO3可能通过提高POD和APX的活性、降低自由基产生及保护光合色素等来实现UV-B胁迫下对红芸豆叶片的保护作用。     

Deoxyribonucleoside triphosphate imbalance. 5-Fluorodeoxyuridine-induced DNA double strand breaks in mouse FM3A cells and the mechanism of cell death

The mechanism of cytotoxic action of 5-fluorodeoxyuridine (FdUrd) in mouse FM3A cells was investigated. We observed the FdUrd-induced imbalance of intracellular deoxyribonucleoside triphosphate (dNTP) pools and subsequent double strand breaks in mature DNA, accompanied by cell death. The imbalance of dNTP pools was maximal at 8 h after 1 microM FdUrd treatment; a depletion of dTTP and dGTP pools and an increase in the dATP pool were observed. The addition of FdUrd in culture medium induced strand breaks in DNA, giving rise to a 90 S peak by alkaline sucrose gradient sedimentation. The loss of cell viability and colony-forming ability occurred at about 10 h. DNA double strand breaks as measured by the neutral elution method were also observed in FdUrd-treated cells about 10 h after the addition. These results lead us to propose that DNA double strand breaks play an important role in the mechanism of FdUrd-mediated cell death. A comparison of the ratio of single and double strand breaks induced by FdUrd to that observed following radiation suggested that FdUrd produced double strand breaks exclusively. Cycloheximide inhibited both the production of DNA double strand breaks and the FdUrd-induced cell death. An activity that can induce DNA double strand breaks was detected in the lysate of FdUrd-treated FM3A cells but not in the untreated cells. This suggests that FdUrd induces the cellular DNA double strand breaking activity. The FdUrd-induced DNA strand breaks and cell death appear to occur in the S phase. Our results indicate that imbalance of the dNTP pools is a trigger for double strand DNA break and cell death.     

Attempted base excision repair of ionizing radiation damage in human lymphoblastoid cells produces lethal and mutagenic double strand breaks

A significant proportion of cellular DNA damages induced by ionizing radiation are produced in clusters, also called multiply damaged sites. It has been demonstrated by in vitro studies and in bacteria that clustered damage sites can be converted to lethal double strand breaks by oxidative DNA glycosylases during attempted base excision repair. To determine whether DNA glycosylases could produce double strand breaks at radiation-induced clustered damages in human cells, stably transformed human lymphoblastoid TK6 cells that inducibly overexpress the oxidative DNA glycosylases/AP lyases, hNTH1 and hOGG1, were assessed for their radiation responses, including survival, mutation induction and the enzymatic production of double strand breaks post-irradiation. We found that additional double strand breaks were generated during post-irradiation incubation in uninduced TK6 control cells. Moreover, overproduction of either DNA glycosylase resulted in significantly increased double strand break formation, which correlated with an elevated sensitivity to the cytotoxic and mutagenic effects of ionizing radiation. These data show that attempted repair of radiation damage, presumably at clustered damage sites, by the oxidative DNA glycosylases can lead to the formation of potentially lethal and mutagenic double strand breaks in human cells.     

Formation of strand breaks in the DNA ofγ-irradiated chromatin

Summary Strand breaks have been determined by sedimentation on sucrose gradients in the DNA of chromatin irradiated after isolation from Chinese hamster lung fibroblasts. The yields of double-strand and single-strand breaks are similar to those found in the DNA of irradiated mammalian cells. Irradiation of isolated chromatin in the presence of the radical scavenger tertiary butanol indicates that at least 65% of single-strand breaks and 56% of double-strand breaks can be attributed to the action of hydroxyl radicals. The results indicate the influence of chromosomal proteins in modifying radiation damage to DNA and suggest that the mechanisms for the induction of strand breaks in the DNA of isolated chromatin may be comparable to those operating in the intact cell.     

不同剂量UV-B辐射对冬小麦幼苗形态及生理指标的影响

UV-B辐射增强对植物的影响效果存在差异,即使是同一物种的不同品种之间也存在差异。本研究以对UV-B不同耐性的2个冬小麦品种科遗26和泰山269为材料,比较了品种间及UV-B的剂量间的形态指标、生物量及生理指标的差异。结果表明:高剂量UV-B处理抑制了株高、叶色、茎数、鲜质量、光反应系统Ⅱ(PSⅡ)最大光化学效率(Fv/Fm)和光合速率,促进了丙二醛、类黄酮含量的增加及相对电导率的提高,2个品种的趋势基本相同,但泰山269的变化幅度大于科遗26,说明泰山269比科遗26敏感;低剂量的UV-B对株高、叶色、茎数、鲜质量表现出促进的趋势,对类黄酮的促进作用较大,对Fv/Fm、丙二醛及相对电导率的影响相对较小。     

Influence of chromatin structure and radical scavengers on yields of radiation-induced 8-oxo-dG and DNA strand breaks in cellular model systems

Radiation-induced formation of 7,8-dihydro-8-oxo-2'-deoxyguanosine (8-oxo-dG) and DNA strand breaks was studied in cultured cells with normal or modified chromatin structure. Human fibroblasts were irradiated as cellular monolayers (intact cells), nuclear monolayers (permeabilized cells with intact chromatin structure), and nucleoid monolayers (permeabilized and salt-treated cells with histone-free DNA). 8-oxo-dG was assayed with reverse-phase HPLC coupled to an electrochemical detector and strand breaks with the alkali unwinding assay. Depletion of low-molecular-weight nuclear components increased the radiation-induced formation of 8-oxo-dG fivefold compared to twofold for the formation of strand breaks. Removal of both low-molecular-weight components and histones increased the yield of 8-oxo-dG 46-fold and the yield of strand breaks 43-fold. Removal of only the histones thus leads to a two times greater increase in the yield of strand breaks compared to 8-oxo-dG. Addition of radical scavengers to nuclear and nucleoid monolayers provided a significantly better protection against the formation of 8-oxo-dG relative to the formation of strand breaks. These results suggest that in intact cells, 8-oxo-dG is preferentially formed in histone-free structures of chromatin, indicating a larger role for the indirect effect of radiation in the formation of 8-oxo-dG than in the formation of strand breaks.     

In vitro sucrose concentration affects growth and acclimatization of <Emphasis Type="Italic">Alocasia amazonica</Emphasis> plantlets

Plantlets of Alocasia amazonica were regenerated on the MS medium supplemented with different concentrations (0–9%) of sucrose. An absence of sucrose in the growth medium induced generation of leaves, however, it decreased multiplication. On contrary, sucrose supply of 6% or 9% enhanced multiplication but hampered photoautotrophic growth (generation of leaves). Increasing sucrose supply also increased sugars and starch content and number of stomata and decreased water potential and size of stomata during in vitro growth period. During ex vitro acclimatization, shoot length, root length, leaf number and root number of Alocasia plantlets grown with 3% sucrose, were found to be better among the other studied sucrose concentrations. Under ex vitro acclimatization, number of stomata, contents of various carbohydrates in the leaves were increased but size of stomata decreased with increasing sucrose supply during in vitro growth period. Moreover, water potential of leaves of plantlets, which have been grown with a sucrose concentration other than 3%, was decreased. During in vitro growth, net CO₂ assimilation rate (P_N), transpiration (E), stomatal conductance (g_s) and variable fluorescence to maximum fluorescence ratio (Fv/Fm) were unaffected, however, during acclimatization these were changed and maximum P_N, E, and g_s were observed in the plantlets micropropagated with 3% sucrose. Fv/Fm was decreased severely in the plantlets micropropagated with 6% sucrose during acclimatization. Thus a sucrose concentration of 3% in the medium is appeared to be better among studied concentrations for both in vitro growth and ex vitro acclimatization of A. amazonica plantlets.     

Modulation of DNA damage by pentoxifylline and alpha-tocopherol in skin fibroblasts exposed to Gamma rays

Previous in vivo studies showed the combination pentoxifylline (PTX) and alpha-tocopherol was highly efficient in reducing late radiation-induced skin damage. The present work aimed at investigating the molecular and cellular mechanisms involved in the effects of this combination. Primary cultures of confluent dermal fibroblasts were gamma-irradiated in the presence of PTX and trolox (Tx), the water-soluble analogue of alpha-tocopherol. Drugs were added either before or after radiation exposure and were maintained over time. Their antioxidant capacity and their effect on radiation-induced ROS production was assessed together with cell viability and clonogenicity. DNA damage formation was assessed by the alkaline comet assay and by the micronucleus (MN) test. Cell cycle distribution was also determined. The combination of PTX/ Tx was shown to reduce both immediate and late ROS formation observed in cells after irradiation. Surprisingly, decrease in DNA strand breaks measured by the comet assay was observed any time drugs were added. In addition, the micronucleus test revealed that for cells irradiated with 10 Gy, a late significant increase in MN formation occurred. The combination of PTX/Tx was shown to be antioxidant and to decrease radiation-induced ROS production. The observed effects on DNA damage at any time the drugs were added suggest that PTX/Tx could interfere with the DNA repair process.     

beta-sitosterol decreases irradiation-induced thymocyte early damage by regulation of the intracellular redox balance and maintenance of mitochondrial membrane stability

Both radiation injury and oxidation toxicity occur when cells are exposed to ion irradiation (IR), ultimately leading to apoptosis. This study was designed to determine the effect of beta-sitosterol (BSS) on early cellular damage in irradiated thymocytes and a possible mechanism of effect on irradiation-mediated activation of the apoptotic pathways. Thymocytes were irradiated (6 Gy) with or without BSS. Cell apoptosis and apoptosis-related proteins were evaluated. BSS decreased irradiation-induced cell death and nuclear DNA strand breaks while attenuating intracellular reactive oxygen species (ROS) and increasing the activities of antioxidant enzymes, including superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx). BSS decreased the release of cytochrome c from mitochondria to the cytosol and the mitochondrio-nuclear translocation of apoptosis-inducing factor (AIF). Furthermore, BSS partially inhibited the radiation-induced increase of cleaved caspase 3 and cleaved PARP, and attenuated the activation of JNK and AP-1. In addition, evidence suggests that ROS generated by irradiation are involved in this course of cell damage. The results indicate that BSS confers a radioprotective effect on thymocytes by regulation of the intracellular redox balance which is carried out via the scavenging of ROS and maintenance of mitochondrial membrane stability.     

Seminal plasma reduces exogenous oxidative damage to human sperm, determined by the measurement of DNA strand breaks and lipid peroxidation

Exposure of spermatozoa to reactive oxygen species (ROS) has been associated with cellular injury, that includes DNA damage and lipid peroxidation. In addition, sperm preparation techniques such as centrifugation, commonly used prior to in vitro fertilization and scientific studies, are associated with the generation of ROS and an increase in the level of DNA damage. The preservation, therefore, of sperm in vitro that might decrease the potential for oxidative DNA damage to arise and allow for an improvement in semen quality used for artificial insemination, is of importance. Seminal plasma is a rich source of antioxidants, which, potentially, safeguards sperm from oxidative attack during storage and once ejaculated. We have investigated the protection of human spermatozoa from ROS afforded by seminal plasma. Sperm were exposed to exogenous ROS by incubating the cells with hydrogen peroxide in the presence of ferrous sulfate and ADP. Aliquots of seminal plasma were added to the incubation mixture in differing amounts, and the generation of DNA strand breaks and thiobarbituric acid reactive species (TBARS), indicative of lipid peroxidation, determined. Incubation of sperm with exogenous ROS resulted in a significant generation of DNA strand breaks and lipid peroxidation compared to basal levels of damage (P<0.05). Addition of seminal plasma to the incubation media produced a significant decrease in DNA strand breaks and TBARS (P<0. 05), when the amount of plasma added exceeded 60% v/v. The results indicate that spermatozoal oxidative damage induced by exogenous ROS, specifically DNA damage and lipid peroxidation, is reduced by the presence of seminal plasma.     

Influence of cellular differentiation on repair of ultraviolet-induced DNA damage in murine proadipocytes

The effects of cellular differentiation on the repair of DNA damage induced by uv radiation were investigated in the murine 3T3-T proadipocyte cell culture system. Upon exposure to human plasma, actively cycling 3T3-T cells (stem cells) undergo growth arrest, which is followed by terminal differentiation into lipid-laden adipocytes. In response to uv irradiation, the level of unscheduled DNA synthesis is significantly lower in adipocytes as compared to stem cells. The alkaline elution assay was used to monitor the appearance of repair-induced strand breaks in 3T3-T cells after uv irradiation. DNA strand breaks were detected in stem cells by 4 min post-uv with essentially no further increase after 8 min. When terminally differentiated adipocytes were irradiated and allowed to repair, however, more strand breaks were present at 4 min and, in marked contrast to stem cells, continued to accumulate in adipocytes for at least 16 min post-uv. Inhibition of repair-replication with hydroxyurea and cytosine arabinoside significantly increased accumulation of repair-induced strand breaks in stem cells, yet had little effect on this accumulation in adipocytes. For stem cells and adipocytes, incision activity was linear out to at least 10 Jm-2 without saturation. These data suggested that 3T3-T cell differentiation is accompanied by a defect in some postincision process of the excision-repair pathway.     

Black tea extract supplementation decreases oxidative damage in Jurkat T cells

The purpose of this study was to investigate the protective effect of black tea (BT) extract against induced oxidative damage in Jurkat T-cell line. Cells supplemented with 10 or 25 mg/L BT were subjected to oxidation with ferrous ions. Malondialdehyde (MDA) production as marker of lipid peroxidation, DNA single strand breaks as marker of DNA damage, and modification of the antioxidant enzyme activity, glutathione peroxidase (GPX) were measured. Results show the efficacy of BT polyphenols to decrease DNA oxidative damage and to affect GPX activity (P<0.05), while no effect was shown on MDA production. The succeeding investigation of the activity of caffeine and epigallocatechin gallate demonstrated their antioxidant potential with respect to the cellular markers evaluated. In conclusion, this study supports the protective effect of BT against ferrous ions induced oxidative damage to DNA and the ability of BT to affect the enzyme antioxidant system of Jurkat cells.