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1.
An in vitro oxidative stress test has been developed to assess pollutant tolerance in freshwater algae using Euglena gracilis as the test organism and FeSO4 and NaCl as the pollutants. The test evaluates free radical-mediated oxidative stress through the concomitant application of three biochemical assays: (1) the non-invasive, gas chromatographic-volatile headspace analysis of hydroxyl radicals (OH) using dimethyl-sulphoxide as a radical trap; (2) the spectroscopic determination of total antioxidant activity; (3) a fluorescent microscopy viability test. In vitro pollutant testing was devised to simulate contaminant loadings that impact urban retention ponds. E. gracilis was found to be tolerant to FeSO4 (2–10% (w/v)) and NaCl (10–5000 ppm) as indicated by high positive viabilities (ca. 100%) and low, or no OH production, as compared to controls. Total antioxidant activity increased with increasing pollutant loading suggesting that the organism has the capacity to enhance antioxidant defence in response to pollutant stress. This in vitro test provides a new approach to monitor the effects of water quality on the biological components of urban and/or polluted aquatic ecosystems. It also has a potential application in the identification of putative algal phytoremediators. 相似文献
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Reactive oxygen species and antioxidant machinery in abiotic stress tolerance in crop plants 总被引:24,自引:0,他引:24
Various abiotic stresses lead to the overproduction of reactive oxygen species (ROS) in plants which are highly reactive and toxic and cause damage to proteins, lipids, carbohydrates and DNA which ultimately results in oxidative stress. The ROS comprises both free radical (O2?, superoxide radicals; OH, hydroxyl radical; HO2, perhydroxy radical and RO, alkoxy radicals) and non-radical (molecular) forms (H2O2, hydrogen peroxide and 1O2, singlet oxygen). In chloroplasts, photosystem I and II (PSI and PSII) are the major sites for the production of 1O2 and O2?. In mitochondria, complex I, ubiquinone and complex III of electron transport chain (ETC) are the major sites for the generation of O2?. The antioxidant defense machinery protects plants against oxidative stress damages. Plants possess very efficient enzymatic (superoxide dismutase, SOD; catalase, CAT; ascorbate peroxidase, APX; glutathione reductase, GR; monodehydroascorbate reductase, MDHAR; dehydroascorbate reductase, DHAR; glutathione peroxidase, GPX; guaicol peroxidase, GOPX and glutathione-S- transferase, GST) and non-enzymatic (ascorbic acid, ASH; glutathione, GSH; phenolic compounds, alkaloids, non-protein amino acids and α-tocopherols) antioxidant defense systems which work in concert to control the cascades of uncontrolled oxidation and protect plant cells from oxidative damage by scavenging of ROS. ROS also influence the expression of a number of genes and therefore control the many processes like growth, cell cycle, programmed cell death (PCD), abiotic stress responses, pathogen defense, systemic signaling and development. In this review, we describe the biochemistry of ROS and their production sites, and ROS scavenging antioxidant defense machinery. 相似文献
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Production of minute concentrations of superoxide (O2−) and nitrogen monoxide (nitric oxide, NO) plays important roles in several aspects of cellular signaling and metabolic regulation. However, in an inflammatory environment, the concentrations of these radicals can drastically increase and the antioxidant defenses may become overwhelmed. Thus, biological damage may occur owing to redox imbalance—a condition called oxidative and/or nitrosative stress. A complex interplay exists between iron metabolism, O2−, hydrogen peroxide (H2O2), and NO. Iron is involved in both the formation and the scavenging of these species. Iron deficiency (anemia) (ID(A)) is associated with oxidative stress, but its role in the induction of nitrosative stress is largely unclear. Moreover, oral as well as intravenous (iv) iron preparations used for the treatment of ID(A) may also induce oxidative and/or nitrosative stress. Oral administration of ferrous salts may lead to high transferrin saturation levels and, thus, formation of non-transferrin-bound iron, a potentially toxic form of iron with a propensity to induce oxidative stress. One of the factors that determine the likelihood of oxidative and nitrosative stress induced upon administration of an iv iron complex is the amount of labile (or weakly-bound) iron present in the complex. Stable dextran-based iron complexes used for iv therapy, although they contain only negligible amounts of labile iron, can induce oxidative and/or nitrosative stress through so far unknown mechanisms. In this review, after summarizing the main features of iron metabolism and its complex interplay with O2−, H2O2, NO, and other more reactive compounds derived from these species, the potential of various iron therapies to induce oxidative and nitrosative stress is discussed and possible underlying mechanisms are proposed. Understanding the mechanisms, by which various iron formulations may induce oxidative and nitrosative stress, will help us develop better tolerated and more efficient therapies for various dysfunctions of iron metabolism. 相似文献
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Binhua Zhou Baojian Li Wei Yi Xianzhang Bu Lin Ma 《Bioorganic & medicinal chemistry letters》2013,23(13):3759-3763
A series of 2-arylbenzimidazole derivatives (3a–3p and 4a–4i) were synthesized and evaluated as potential antioxidant and antimicrobial agents. Their antioxidant properties were evaluated by various in vitro assays including hydroxyl radical (HO) scavenging, superoxide radical anion (O2?) scavenging, 1,1-diphenyl-2-picrylhydrazyl (DPPH) radical scavenging, and ferric reducing antioxidant power. Results demonstrated that compounds with hydroxyl group at the 5-position of benzimidazole ring had a comparable or better antioxidant activity in comparison to standard antioxidant tert-butylhydroquinone (TBHQ). Markedly, compound 4h that showed the highest HO scavenging activity (EC50 = 46 μM) in vitro had a significant reduction of 2,2′-azobis(2-amidinopropane) dihydrochloride (AAPH)-induced intracellular oxidative stress and H2O2-induced cell death. In addition, these compounds showed moderate to good inhibitory activity against Staphylococcus aureus selectively at noncytotoxic concentrations. 相似文献
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Jingli Liu Huili Sun Fang Dong Qinzhao Xue Gang Wang Song Qin Zhanyong Guo 《Carbohydrate polymers》2009,78(3):439-443
Various quaternized chitosans (QCSs) were synthesized according to previous method. Their reducing power and antioxidant potency against hydroxyl radicals (OH) and hydrogen peroxide (H2O2) were explored by the established systems in vitro. The QCSs exhibited markedly antioxidant activity, especially TCEDMCS, whose IC50 on hydroxyl radicals was 0.235 mg/mL. They showed 65–80% scavenging effect on hydrogen peroxide at a dose of 0.5 mg/mL. Generally, the antioxidant activity decreased in the order TCEDMCS > TBEDMCS > EDMCS > PDMCS > IBDMCS > Chitosan. Furthermore, the order of their OH and H2O2 scavenging activity was consistent with the electronegativity of different substituted groups in the QCSs. The QCSs showed much stronger antioxidant activity than that of chitosan may be due to the positive charge density of the nitrogen atoms in QCSs strengthened by the substituted groups. 相似文献
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Rongsong Li Zhi Ning Jeffery Cui Bhavraj Khalsa Lisong Ai Wakako Takabe Tyler Beebe Rohit Majumdar Constantinos Sioutas Tzung Hsiai 《Free radical biology & medicine》2009,46(6):775-782
Exposure to particulate air pollution is linked to increased incidences of cardiovascular diseases. Ambient ultrafine particles (UFP) from diesel vehicle engines have been shown to be proatherogenic in ApoE knockout mice and may constitute a major cardiovascular risk in humans. We posited that circulating nano-sized particles from traffic pollution sources induce vascular oxidative stress via JNK activation in endothelial cells. Diesel UFP were collected from a 1998 Kenworth truck. Intracellular superoxide assay revealed that these UFP dose-dependently induced superoxide (O2?) production in human aortic endothelial cells (HAEC). Flow cytometry showed that UFP increased MitoSOX red intensity specific for mitochondrial superoxide. Protein carbonyl content was increased by UFP as an indication of vascular oxidative stress. UFP also up-regulated heme oxygenase-1 (HO-1) and tissue factor (TF) mRNA expression, and pretreatment with the antioxidant N-acetylcysteine significantly decreased their expression. Furthermore, UFP transiently activated JNK in HAEC. Treatment with the JNK inhibitor SP600125 and silencing of both JNK1 and JNK2 with siRNA inhibited UFP-stimulated O2? production and mRNA expression of HO-1 and TF. Our findings suggest that JNK activation plays an important role in UFP-induced oxidative stress and stress response gene expression. 相似文献
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Ekanayake PM Kang HS De Zyosa M Jee Y Lee YH Lee J 《Comparative biochemistry and physiology. Part B, Biochemistry & molecular biology》2006,145(3-4):318-324
The mitochondrial enzyme manganese superoxide dismutase (mitMn-SOD) is one of the antioxidant enzymes involved in cellular defense against oxidative stress and catalyzes the conversion of O2− into the stabler H2O2. In this study, a putative gene encoding Mn-SOD from disk abalone (Haliotis discus discus, aMn-SOD) was cloned, sequenced, expressed in Escherichia coli K12(TB1) and the protein was purified using pMAL protein purification system. Sequencing resulted ORF of 681 bp, which corresponded to 226 amino acids. The protein was expressed in soluble form with molecular weight of 68 kDa including maltose binding protein and pI value of 6.5. The fusion protein had 2781 U/mg activity. The optimum temperature of the enzyme was 37 °C and it was active in a range of acidic pH (from 3.5 to 6.5). The enzyme activity was reduced to 50% at 50 °C and completely heat inactivated at 80 °C. The alignment of aMn-SOD amino acid sequence with Mn-SODs available in NCBI revealed that the enzyme is conserved among animals with higher than 30% identity. In comparison with human mitMn-SOD, all manganese-binding sites are also conserved in aMn-SOD (H28, H100, D185 and H189). aMn-SOD amino acid sequence was closer to that of Biomphalaria glabrata in phylogenetic analysis. 相似文献
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Georgia Tanou Athanassios Molassiotis Grigorios Diamantidis 《Journal of plant physiology》2009,166(17):1904-1913
We tested whether pre-treatments of roots with H2O2 (10 mM for 8 h) or sodium nitroprusside (SNP; 100 μM for 48 h), a donor of NO, could induce prime antioxidant defense responses in the leaves of citrus plants grown in the absence or presence of 150 mM NaCl for 16 d. Both root pre-treatments increased leaf superoxide dismutase (SOD), catalase (CAT), ascorbate peroxidase (APX) and glutathione reductase (GR) activities, and induced related-isoform(s) expression under non-NaCl-stress conditions. When followed by salinity, certain enzymatic activities also exhibited an up-regulation in response to H2O2 or SNP pre-exposure. An NaCl-stress-provoked decrease in the ascorbate redox state was partially prevented by both pre-treatments, whereas the glutathione redox state under normal and NaCl-stress conditions was increased by SNP. Real-time imaging of NO production was found in vascular tissues and epidermal cells. Furthermore, NaCl-induced inhibition in OH scavenging activity and promotion of OH-mediated DNA strand cleavage was partially prevented by SNP. Moreover, NaCl-dependent protein oxidation (carbonylation) was totally reversed by both pre-treatments as revealed by quantitative assay and protein blotting analysis. These results provide strong evidence that H2O2 and NO elicit long-lasting systemic primer-like antioxidant activity in citrus plants under physiological and NaCl-stress conditions. 相似文献
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The effect of seasonality on oxidative metabolism in Nacella (Patinigera) magellanica 总被引:1,自引:0,他引:1
Gabriela Malanga María Susana Estevez Jorge Calvo Doris Abele Susana Puntarulo 《Comparative biochemistry and physiology. Part A, Molecular & integrative physiology》2007,146(4):551
We studied the seasonal variation on aerobic metabolism and the response of oxidative stress parameters in the digestive glands of the subpolar limpet Nacella (P.) magellanica. Sampling was carried out from July (winter) 2002 to July 2003 in Beagle Channel, Tierra del Fuego, Argentina. Whole animal respiration rates increased in early spring as the animals spawned and remained elevated throughout summer and fall (winter: 0.09 ± 0.02 μmol O2 h− 1 g− 1; summer: 0.31 ± 0.06 μmol O2 h− 1 g− 1). Oxidative stress was assessed at the hydrophilic level as the ascorbyl radical content / ascorbate content ratio (A / AH−). The A / AH− ratio showed minimum values in winter (3.7 ± 0.2 10− 5 AU) and increased in summer (18 ± 5 10− 5 AU). A similar pattern was observed for lipid radical content (122 ± 29 pmol mg− 1 fresh mass [FW] in winter and 314 ± 45 pmol mg− 1 FW in summer), iron content (0.99 ± 0.07 and 2.7 ± 0.6 nmol mg− 1 FW in winter and summer, respectively) and catalase activity (2.9 ± 0.2 and 7 ± 1 U mg− 1 FW in winter and summer, respectively). Since nitrogen derived radicals are thought to be critically involved in oxidative metabolism in cells, nitric oxide content was measured and a significant difference in the content of the Fe–MGD–NO adduct in digestive glands from winter and summer animals was observed. Together, the data indicate that both oxygen and nitrogen radical generation rates in N. (P.) magellanica are strongly dependent on season. 相似文献
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Comparison of antioxidant abilities of magnolol and honokiol to scavenge radicals and to protect DNA 总被引:3,自引:0,他引:3
The antioxidant properties of magnolol and honokiol were evaluated in the experimental systems of reducing ONOO− and 1O2, bleaching β-carotene in linoleic acid (LH) emulsion, and trapping 2,2′-azinobis(3-ethylbenzothiazoline-6-sulfonate) cationic radical (ABTS+) and 2,2′-diphenyl-1-picrylhydrazyl radical (DPPH), and then were applied to inhibit the oxidation of DNA induced by Cu2+/glutathione (GSH) and 2,2′-azobis(2-amidinopropane hydrochloride) (AAPH). Magnolol and honokiol were active to reduce ONOO− and 1O2. Honokiol showed a little higher activity to protect LH and to inhibit Cu2+/GSH-induced oxidation of DNA than magnolol. In addition, honokiol exhibited higher activities to trap ABTS+ and DPPH than magnolol. In particular, honokiol trapped 2.5 radicals while magnolol only trapped 1.8 radicals in protecting DNA against AAPH-induced oxidation. The obtained results suggested that low antioxidant ability of magnolol may be related to the intramolecular hydrogen bond formed between di-ortho-hydroxyl groups, which hindered the hydrogen atom in hydroxyl group to be abstracted by radicals. Therefore, the antioxidant capacity of magnolol was lower than that of honokiol. 相似文献
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Metals such as CuI and FeII generate hydroxyl radical (OH) by reducing endogenous hydrogen peroxide (H2O2). Because antioxidants can ameliorate metal-mediated oxidative damage, we have quantified the ability of glutathione, a primary intracellular antioxidant, and other biological sulfur-containing compounds to inhibit metal-mediated DNA damage caused hydroxyl radical. In the CuI/H2O2 system, six sulfur compounds, including both reduced and oxidized glutathione, inhibited DNA damage with IC50 values ranging from 3.4 to 12.4 μM. Glutathione and 3-carboxypropyl disulfide also demonstrated significant antioxidant activity with FeII and H2O2. Additional gel electrophoresis and UV-vis spectroscopy studies confirm that antioxidant activity for sulfur compounds in the CuI system is attributed to metal coordination, a previously unexplored mechanism. The antioxidant mechanism for sulfur compounds in the FeII system, however, is unlike that of CuI. Our results demonstrate that glutathione and other sulfur compounds are potent antioxidants capable of preventing metal-mediated oxidative DNA damage at well below their biological concentrations. This novel metal-binding antioxidant mechanism may play a significant role in the antioxidant behavior of these sulfur compounds and help refine understanding of glutathione function in vivo. 相似文献
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Masatoshi Inden Yoshihisa Kitamura Aya Tamaki Takashi Yanagida Tomonori Shibaike Atsuko Yamamoto Kazuyuki Takata Hiroyuki Yasui Takahiro Taira Hiroyoshi Ariga Takashi Taniguchi 《Neurochemistry international》2009,55(8):760-767
Pramipexole, an agonist for dopamine (DA) D2/D3-receptors, has been used to treat both early and advanced Parkinson's disease (PD). In this study, we examined the effect of pramipexole on DA neurons in a PD model of C57BL/6 mice, which were treated with rotenone (30 mg/kg, p.o.) daily for 28 days. Pramipexole (1 mg/kg, i.p.) was injected daily 30 min before each oral administration of rotenone. Chronic oral administration of rotenone caused a loss of DA neurons in the substantia nigra pars compacta (SNpc), motor deficits and the up-regulation of α-synuclein immunoreactivity in some surviving DA neurons. Pramipexole inhibited rotenone-induced DA neuronal death and motor deficits, and reduced immunoreactivity for α-synuclein. In addition, pramipexole inhibited the in vitro oligomerization of human wild-type α-synuclein by H2O2 plus cytochrome c. To examine the neuroprotective effect of pramipexole against oxidative stress, we used a DJ-1-knockdown SH-SY5Y cell line and electron spin resonance (ESR) spectrometry. Simultaneous treatment with H2O2 and pramipexole resulted in the significant protection of DJ-1-knockdown cells against cell death in a concentration-dependent manner. A high concentration of pramipexole directly scavenged hydroxyl radical (OH) generated from H2O2 and Fe2+. Furthermore, pramipexole increased Bcl-2 immunoreactivity in DA neurons in the SNpc. These results suggest that pramipexole may protect DA neurons against exposure to rotenone by chronic oral administration, and this effect is mediated by multiple functions including scavenging of OH and induction of Bcl-2 protein. 相似文献
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Lisa K. Folkes Madia Trujillo Silvina Bartesaghi Rafael Radi Peter Wardman 《Archives of biochemistry and biophysics》2011,(2):193
Modification of tyrosine (TyrOH) is used as a marker of oxidative and nitrosative stress. 3,3′-Dityrosine formation, in particular, reflects oxidative damage and results from the combination of two tyrosyl phenoxyl radicals (TyrO). This reaction is in competition with reductive processes in the cell which ‘repair’ tyrosyl radicals: possible reductants include thiols and ascorbate. In this study, a rate constant of 2 × 106 M−1 s−1 was estimated for the reaction between tyrosyl radicals and glutathione (GSH) at pH 7.15, generating the radicals by pulse radiolysis and monitoring the tyrosyl radical by kinetic spectrophotometry. Earlier measurements have suggested that this ‘repair’ reaction could be an equilibrium, and to investigate this possibility the reduction (electrode) potential of the (TyrO,H+/TyrOH) couple was reinvestigated by observing the fast redox equilibrium with the indicator 2,2′-azinobis(3-ethylbenzothiazoline-6-sulphonate). Extrapolation of the reduction potential of TyrO measured at pH 9–11 indicated the mid-point reduction potential of the tyrosyl radical at pH 7, Em7(TyrO,H+/TyrOH) = 0.93 ± 0.02 V. This is close to the reported reduction potential of the glutathione thiyl radical, Em7 = 0.94 ± 0.03 V, confirming the ‘repair’ equilibrium constant is of the order of unity and suggesting that efficient reduction of TyrO by GSH might require removal of thiyl radicals to move the equilibrium in the direction of repair. Loss of thiyl radicals, facilitating repair of TyrO, can arise either via conjugation of thiyl with thiol/thiolate or oxygen, or unimolecular transformation, the latter important at low concentrations of thiols and oxygen. 相似文献
18.
《Harmful algae》2013
The dinoflagellate Lingulodinium polyedrum is a toxin producer that shows the ability of turning to resting cysts as a survival strategy when exposed to environmental unfavorable conditions, such as nitrogen and phosphorus depletion, abrupt changes in temperature or light, and chemical or mechanical stress. Algal adaptation to all these conditions involves hydrogen peroxide (H2O2) and nitric oxide (NO) as key redox signals for housekeeping cellular processes. Thus, we aim here to shed light on the role of H2O2 and NO (from aqueous decomposition of sodium nitroprusside, SNP) as prooxidant agents and putative redox signals for encystment of the dinoflagellate L. polyedrum. Harsh oxidative stress imposed by 500 μM H2O2 treatment forced L. polyedrum cells to rapidly encyst, in less than 30 min, whereas slower cyst formation was observed upon lower H2O2 doses. L. polyedrum encystment was marked by a significant increase in the antioxidant carotenoid peridinin, although other photosynthetic pigments (chlorophyll a and β-carotene) and light-harvesting complexes (peridinin complex protein, PCP) were all diminished in cyst forms. Although SOD activity (a frontline antioxidant enzyme) was severely inhibited by increasing doses of H2O2, a theoretical compensatory effect was provided by the dose-dependent increase of ascorbate peroxidase activity (APX), which resulted in significant lower levels of lipid peroxidation during cyst formation. Although SNP data cannot be fully compared to those found with H2O2 treatments, changes in APX activity and in biomarkers of lipid and protein oxidation matched the dose–responses found in H2O2 experiments, revealing similar biochemical and morphological responses against increasing oxidative conditions during cyst formation. Our data significantly contribute to a better understanding of the relationship between encystment, photosynthesis, and antioxidant responses triggered by H2O2 and NO in L. polyedrum, a harmful diarrhetic shellfish poisoning toxin (DSPs) producer. 相似文献
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Endothelial dysfunction causes an imbalance in endothelial NO and O2− production rates and increased peroxynitrite formation. Peroxynitrite and its decomposition products cause multiple deleterious effects including tyrosine nitration of proteins, superoxide dismutase (SOD) inactivation, and tissue damage. Studies have shown that peroxynitrite formation during endothelial dysfunction is strongly dependent on the NO and O2− production rates. Previous experimental and modeling studies examining the role of NO and O2− production imbalance on peroxynitrite formation showed different results in biological and synthetic systems. However, there is a lack of quantitative information about the formation and biological relevance of peroxynitrite under oxidative, nitroxidative, and nitrosative stress conditions in the microcirculation. We developed a computational biotransport model to examine the role of endothelial NO and O2− production on the complex biochemical NO and O2− interactions in the microcirculation. We also modeled the effect of variability in SOD expression and activity during oxidative stress. The results showed that peroxynitrite concentration increased with increase in either O2− to NO or NO to O2− production rate ratio (QO2−/QNO or QNO/QO2−, respectively). The peroxynitrite concentrations were similar for both production rate ratios, indicating that peroxynitrite-related nitroxidative and nitrosative stresses may be similar in endothelial dysfunction or inducible NO synthase (iNOS)-induced NO production. The endothelial peroxynitrite concentration increased with increase in both QO2−/QNO and QNO/QO2− ratios at SOD concentrations of 0.1–100 μM. The absence of SOD may not mitigate the extent of peroxynitrite-mediated toxicity, as we predicted an insignificant increase in peroxynitrite levels beyond QO2−/QNO and QNO/QO2− ratios of 1. The results support the experimental observations of biological systems and show that peroxynitrite formation increases with increase in either NO or O2− production, and excess NO production from iNOS or from NO donors during oxidative stress conditions does not reduce the extent of peroxynitrite mediated toxicity. 相似文献
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Grigory V. Andrievsky Vadim I. Bruskov Artem A. Tykhomyrov Sergey V. Gudkov 《Free radical biology & medicine》2009,47(6):786-793
Aqueous solutions of highly stable supramolecular donor–acceptor complexes of chemically nonmodified pristine C60 fullerene molecules with H2O molecules (hydrated C60 fullerene–C60HyFn) and their labile nano-sized clusters were examined for their antioxidant effects on removal of hydroxyl radicals (OH) and protecting DNA against oxidative damage induced by ionizing radiation in vitro. The suppressing influence of C60HyFn on the formation of OH-radicals in water exposed to X-rays at doses of 1–7 Gy was assessed by determination of oxidation levels of coumarin-3-carboxylic acid. C60HyFn demonstrates apparent antiradical activity in vitro in the range of concentrations of 10−11–10−6 M. Paradoxically, the OH-removing efficacy of C60HyFn was in reverse correlation with fullerene concentration. It was hypothesized that the antiradical action of C60HyFn in water medium generally is due to a “nonstoichiometric” mechanism, supposedly to a hydrated free radical recombination (self-neutralization), which is catalyzed by specific water structures ordered by C60HyFn. With the use of 8-oxoguanine as a marker of oxidative damage to DNA, it has been demonstrated that C60HyFn in concentrations of 10−7–10−6 M protects nucleic acids against radical-induced damage. The second part of the present study was aimed to evaluate the overall radioprotective efficacy of C60HyFn in doses of 0.1 or 1 mg/kg b.w. injected intraperitoneally to mice either 1 h before or 15 min after lethal dose exposure of the X-ray (7 Gy) irradiation. Survival rate of the mice was observed at 30 day intervals after irradiation, while the weight gains of experimental animals were monitored as well. The most significant protective effect was demonstrated when 1 mg/kg dosage of C60HyFn was administered before irradiation. The outcome of the substance testing is 15% survival rate of irradiated animals at 30 days of observation, and prevention of noticeable weight loss characteristic for radiation impact, versus unprotected control animals. In conclusion, results of the study obviate that the apparent protective action of C60HyFn in vivo is determined by its considerable ability to decrease X-ray-generated reactive oxygen species. Based on the results and that neat C60 is nontoxic, actually in the hydrated form, without side effects and with sufficient radioprotective effects in low doses, C60HyFn may be considered as a novel antioxidant agent, which substantially diminishes the harmful effects of ionizing radiation. 相似文献