ETHYLENE RESPONSE FACTOR 74 (ERF74) plays an essential role in controlling a respiratory burst oxidase homolog D (RbohD)-dependent mechanism in response to different stresses in Arabidopsis.

Recent studies indicate that the ETHYLENE RESPONSE FACTOR VII (ERF-VII) transcription factor is an important regulator of osmotic and hypoxic stress responses in plants. However, the molecular mechanism of ERF-VII-mediated transcriptional regulation remains unclear. Here, we investigated the role of ERF74 (a member of the ERF-VII protein family) by examining the abiotic stress tolerance of an ERF74 overexpression line and a T-DNA insertion mutant using flow cytometry, transactivation and electrophoretic mobility shift assays. 35S::ERF74 showed enhanced tolerance to drought, high light, heat and aluminum stresses, whereas the T-DNA insertion mutant erf74 and the erf74;erf75 double mutant displayed higher sensitivity. Using flow cytometry analysis, we found that erf74 and erf74;erf75 lines lack the reactive oxygen species (ROS) burst in the early stages of various stresses, as a result of the lower expression level of RESPIRATORY BURST OXIDASE HOMOLOG D (RbohD). Furthermore, ERF74 directly binds to the promoter of RbohD and activates its expression under different abiotic stresses. Moreover, induction of stress marker genes and ROS-scavenging enzyme genes under various stress conditions is dependent on the ERF74-RbohD-ROS signal pathway. We propose a pathway that involves ERF74 acting as an on-off switch controlling an RbohD-dependent mechanism in response to different stresses, subsequently maintaining hydrogen peroxide (H2 O2 ) homeostasis in Arabidopsis.

NAD Acts as an Integral Regulator of Multiple Defense Layers.

Pyridine nucleotides, such as NAD, are crucial redox carriers and have emerged as important signaling molecules in stress responses. Previously, we have demonstrated in Arabidopsis (Arabidopsis thaliana) that the inducible NAD-overproducing nadC lines are more resistant to an avirulent strain of Pseudomonas syringae pv tomato (Pst-AvrRpm1), which was associated with salicylic acid-dependent defense. Here, we have further characterized the NAD-dependent immune response in Arabidopsis. Quinolinate-induced stimulation of intracellular NAD in transgenic nadC plants enhanced resistance against a diverse range of (a)virulent pathogens, including Pst-AvrRpt2, Dickeya dadantii, and Botrytis cinerea Characterization of the redox status demonstrated that elevated NAD levels induce reactive oxygen species (ROS) production and the expression of redox marker genes of the cytosol and mitochondrion. Using pharmacological and reverse genetics approaches, we show that NAD-induced ROS production functions independently of NADPH oxidase activity and light metabolism but depends on mitochondrial respiration, which was increased at higher NAD. We further demonstrate that NAD primes pathogen-induced callose deposition and cell death. Mass spectrometry analysis reveals that NAD simultaneously induces different defense hormones and that the NAD-induced metabolic profiles are similar to those of defense-expressing plants after treatment with pathogen-associated molecular patterns. We thus conclude that NAD triggers metabolic profiles rather similar to that of pathogen-associated molecular patterns and discuss how signaling cross talk between defense hormones, ROS, and NAD explains the observed resistance to pathogens.

Radiation resistance in thermophiles: mechanisms and applications.

The study of prokaryotic life in high temperature environments viz., geothermal areas, hot, acidic geysers and undersea hydrothermal vents has revealed the existence of thermophiles (or hyperthermophiles). These microorganisms possess various stress adaptation mechanisms which enable them to bypass multiple physical and chemical barriers for survival. The discovery of radiation resistant thermophile Deinococcus geothermalis has given new insights into the field of radiation microbiology. The ability of radiation resistant thermophiles to deal with the lethal effects of ionizing radiations like DNA damage, oxidative bursts and protein damage has made them a model system for exobiology and interplanetary transmission of life. They might be an antiquity of historical transport process that brought microbial life on Earth. These radiation resistant thermophiles are resistant to desiccation as well and maintain their homeostasis by advance DNA repair mechanisms, reactive oxygen species (ROS) detoxification system and accumulation of compatible solutes. Moreover, engineered radioresistant thermophilic strains are the best candidate for bioremediation of radionuclide waste while the extremolytes produced by these organisms may have predicted therapeutic uses. So, the present article delineate a picture of radiation resistance thermophiles, their adaptive mechanisms to evade stress viz., radiation and desiccation, their present applications along with new horizons in near future.

Low-level laser therapy stimulates the oxidative burst in human neutrophils and increases their fungicidal capacity.

Low-level laser therapy (LLLT) is known to enhance mitochondrial electron transfer and ATP production; thus, this study asked whether LLLT could stimulate the oxidative burst in human neutrophils (PMN) and improve their ability to kill microorganisms. Blood from healthy human subjects was collected and PMN were isolated from the samples. PMN were treated in vitro with 660 nm or 780 nm CW laser light at 40 mW power and increasing energies up to 19.2 J and were subsequently incubated with Candida albicans cells. Generation of hydroxyl radicals, hypochlorite anions and superoxide anions by PMN were checked using fluorescent probes and chemiluminescence assays; a microbicidal activity assay against C. albicans was also performed. LLLT excited PMN to a higher functional profile, which was translated as superior production of reactive oxygen species (ROS) and increased fungicidal capacity. The most efficacious energy was 19.2 J and, interestingly, the 660 nm light was even more efficacious than 780 nm at increasing the respiratory burst of PMN and the fungicidal capacity. Human neutrophils (PMN) were stimulated in vitro with 660 nm or 780 nm CW laser light at 40 mW of power and a total energy of 19.2 J. Low-level laser therapy (LLLT) excited PMN to a higher functional profile, which was translated as a superior production of reactive oxygen species (ROS) such as hydroxyl radicals (HO• ) and hypochlorite anions (ClO- ) (Figure) and increased fungicidal capacity against Candida albicans cells.

Inflammatory-type responses after exposure to ionizing radiation in vivo: a mechanism for radiation-induced bystander effects?

Haemopoietic tissues exposed to ionizing radiation are shown to exhibit increased macrophage activation, defined by ultrastructural characteristics and increased lysosomal and nitric oxide synthase enzyme activities. Macrophage activation post-irradiation was also associated with enhanced respiratory burst activities and an unexpected neutrophil infiltration. Examination of p53-null mice demonstrated that macrophage activation and neutrophil infiltration were not direct effects of irradiation, but were a consequence of the recognition and clearance of radiation-induced apoptotic cells. Increased phagocytic cell activity was maintained after apoptotic bodies had been removed. These findings demonstrate that, contrary to expectation, recognition and clearance of apoptotic cells after exposure to radiation produces both a persistent macrophage activation and an inflammatory-type response. We also demonstrate a complexity of macrophage activation following radiation that is genotype dependent, indicating that the in vivo macrophage responses to radiation damage are genetically modified processes. These short-term responses of macrophages to radiation-induced apoptosis and their genetic modification are likely to be important determinants of the longer-term consequences of radiation exposure. Furthermore, in addition to any effects attributable to immediate radiation-induced damage, our findings provide a mechanism for the production of damage via a 'bystander' effect which may contribute to radiation-induced genomic instability and leukaemogenesis.

Effect of magnetic resonance imaging on human respiratory burst of neutrophils.

It is known that low intensity magnetic fields increase superoxide anion production during the respiratory burst of rat peritoneal neutrophils in vitro. We investigated whether the high intensity magnetic fields (1.5 T) during magnetic resonance imaging can influence the human neutrophil function under in vivo conditions. Blood samples were obtained from 12 patients immediately before and after magnetic resonance imaging (mean time 27.6(+/-11.4 min)). The induced respiratory burst was investigated by the intracellular oxidative transformation of dihydrorhodamine 123 to the fluorescent dye rhodamine 123 via flow cytometry. The respiratory burst was induced either with phorbol 12-myristate 13-acetate, Escherichia coli, N-formyl-methionyl-leucylphenylalanine or priming with tumor necrosis factor followed by FMLP stimulation. There was no significant difference between the respiratory burst before and after magnetic resonance imaging, irrespective of the stimulating agent. Short time exposure to a high intensity magnetic field during magnetic resonance imaging seems not to influence the production of radical species in living neutrophils.

Ionizing radiation at low doses induces inflammatory reactions in human blood.

Irradiation of whole blood with 137Cs gamma rays intensifies the oxidative burst. Oxidant production was used as an indicator of inflammatory cell reactions and was measured by luminol-amplified chemiluminescence after treatment with inflammatory activators including bacteria, the neutrophil taxin formyl-Met-Leu-Phe, the Ca2+ ionophore A23187, the detergent saponin, and the tumor promoter phorbol ester. The irradiation response is dose-dependent up to about 100 microGy, is detectable within minutes, persists at least 1 h, and is transmitted intercellularly by a soluble mediator. The response is completely inhibited by Ca2+ sequestration in the presence of A23187 or by adenosine, indicating its Ca2+ dependency, and by the phospholipase A2 blocker p-bromphenacyl bromide. However, inhibition by the cyclooxygenase blocker aspirin is sporadic or absent. Blood taken after diagnostic examination of lungs with X rays also exhibited intensified chemiluminescence. These reactions implicate a role for specific amplifying mediator pathways, especially metabolites of the arachidonic acid cascade, in the response: "damage and repair" to cells or DNA plays little or no role. Our results provide evidence for a new mechanism of radiation action with possible consequences for the homeostasis of reactions involving inflammation and second messengers in human health and early development.

Ultraviolet B irradiation modulates the immune system of fish (Rutilus rutilus, Cyprinidae). I. Phagocytes.

Roach (Rutilus rutilus) were irradiated with a single dose of ultraviolet B (UVB) radiation (0.4 J/cm2) in order to study the effects of UVB on the nonspecific immune defense mechanisms of fish. Neutrophils and macrophages were isolated from the head kidney of fish on days 1-14 postirradiation. Both random and directed migration of neutrophils, studied by migration under agarose assay, were suppressed on day 1 after UVB irradiation. The respiratory burst of phorbol 12-myristate 13-acetate-stimulated neutrophils and macrophages was also suppressed at days 1 and 2 after UVB irradiation. The suppression of migration and respiratory burst were restored or the responses were even enhanced later, but on the other hand spontaneous cytotoxicity of neutrophils toward 51chromium-labeled K562 target cells stayed suppressed throughout the 14 day follow-up. This study indicates that UVB radiation has the potential to suppress the functioning of phagocytes and to compromise the immune system of fish.

Ultraviolet B irradiation modulates the immune system of fish (Rutilus rutilus, Cyprinidae). II: Blood.

The effects of a single dose of ultraviolet B (UVB) radiation (0.4 J/cm2) on immunological functions by blood leukocytes and on hematological parameters was studied in roach (Rutilus rutilus), a teleostean fish. The respiratory burst of phorbol 12-myristate 13-acetate stimulated whole blood phagocytes increased significantly after UVB irradiation but spontaneous cytotoxicity of blood leukocytes toward 51chromium-labeled K562 target cells was not markedly altered. Differential cell counting revealed that UVB exposure significantly increased the proportion of granulocytes and significantly decreased the proportion of lymphocytes in the peripheral blood, whereas hematocrit and the total number of white and red blood cells were unchanged. Plasma cortisol concentration increased in UVB-exposed fish. Severe handling stress caused similar, although not as potent, effects on the measured parameters of fish blood as UVB irradiation. These observations suggest that in fish UVB brings about a stress response, which may account for the observed alterations in the immune parameters and leukocyte composition of blood. Exposure of fish to strong visible light induced no alterations in immunological or hematological parameters, making it unlikely that ultraviolet radiation mediates its effects through visual perception.

The effects of low-dose X-irradiation on the oxidative burst in stimulated macrophages.

PURPOSE: Local irradiation with a dose of around 0.5 Gy is an effective treatment of acute necrotizing inflammations. The hypothesis that low doses of X-rays modulate the oxidative burst in activated macrophages, which plays a major role in the acute inflammatory process, was tested. MATERIALS AND METHODS: Murine RAW 264.7 macrophages were stimulated with LPS/gammaIFN, PMA or zymosan and oxidative burst was measured using either DCFH-DA or by reduction of cytochrome-C. Radiation doses of 0.3-10 Gy were given shortly before or after stimulation. RESULTS: Low X-ray doses of <1 Gy significantly reduced the oxidative burst in activated macrophages, whereas higher doses had little effect on oxidative burst. CONCLUSIONS: The modulation of oxidative burst by low radiation doses may contribute to the therapeutic effectiveness of low-dose radiotherapy of acute necrotizing inflammations.

Differences in radiosensitivity of the respiratory burst generated in HL-60 cells via different signal transduction pathways.

Induced differentiation of the promyelocytic leukaemia cell line, HL-60, is associated with the acquisition of functional properties, like the expression of specific receptors and the competence to exert the respiratory burst (RB). In this system we evaluated the effects of ionizing radiation on the signal transduction processes involved in the activation of the respiratory burst/NADPH oxidase. HL-60 cells were X-irradiated with up to 1 Gy and induced towards granulocytic differentiation by treatment with 1.25% DMSO on day 0. The expression of the formyl peptide receptor (FPR), the development of responsiveness of the cells to its ligand (f-MLP) and to 4 beta-phorbol 12-myristate 13-acetate (PMA) were measured up to day 7 postinduction/irradiation. Using flow cytometry, fluorescinated formyl-hexapeptide or unlabelled f-MLP as ligands and dihydrorhodamine 123 (DHR 123) as an indicator of RB activity, respectively, the acquisition of functional responsiveness to both stimuli was determined. Immature FPR were identified at day 2 after induction which responded to the agonist from day 3 on. F-MLP receptor-mediated RB oxidase activation was completely radioresistant to 1 Gy, while protein kinase C (PKC)-stimulated triggering of the enzyme via PMA was inhibited by about 50% by 0.5 and 1.0 Gy. We conclude that different signal transduction pathways as triggered by f-MLP and PMA respectively exhibit differences in radiosensitivity, with PKC subspecies and downstream responses being possible sites of radiation damage.

Effects of ultraviolet light on immune parameters of the roach.

Ultraviolet B radiation penetrates into water and can affect fish health and the immune system, as is the case with mammals. Teleost fish, the roach, were exposed to UVB irradiation in aquariums and a panel of immune parameters was determined. In addition to altered blood picture and respiratory burst by blood leukocytes, changes were noted also in major lymphatic organs. Respiratory burst and natural cytotoxicity activity of head kidney granulocytes and mitogen-activated proliferation of splenic lymphocytes were suppressed. Although mostly transitory, some parameters remained suppressed for the following 2 weeks. Ultraviolet A radiation had only minor effects. The stress induced by UVB may be involved in the modulation of immune parameters.

Impairment of phagocytic cell respiratory burst by UVA in the presence of fluoroquinolones: an oxygen-dependent phototoxic damage to cell surface microvilli.

Fluoroquinolones are widely used clinically as broad-spectrum antimicrobial agents. One of their side effects is UVA-dependent photosensitivity, observed after the skin is exposed to sunlight. We have investigated five fluoroquinolones and have found that their phototoxicity is oxygen dependent. Human phagocytic leucocytes were stimulated with serum opsonized zymosan to produce superoxide radical (O2-) (respiratory burst) in the presence of a sensitive O2(-)-specific cypridina luciferin analogue, 2-methyl-6-(p-methoxyphenyl)-3,7-dihydroimidazol (1,2-alpha) pyrazin-one hydrochloride (MCLA), as chemiluminescence reagent with which O2- can react to induce photon emission. The photon count was used as a measure of respiratory burst activity. When leucocytes were irradiated with UVA for 10 min in the presence of 3 micrograms ml-1 lomefloxacin, ciprofloxacin or norfloxacin, a marked decrease in respiratory burst activity was observed; in this respect, ofloxacin and tosufloxacin were weak. Scanning electron microscopy revealed that the cell surface microvilli were destroyed. The phototoxicity of fluoroquinolones could be abolished if oxygen in the tests was replaced by nitrogen or if the aminothiol DL-cysteine (1.5 mg ml-1) was added prior to irradiation. It is suggested that an oxygen species derived from UVA-excited drug molecules and oxygen mediates the phototoxicity of these fluoroquinolones.

[The effect of N2-laser radiation on the kinetics of the generation of active forms of oxygen by the granulocytic-macrophagal cells in a whole-blood system]. / Issledovanie vliianiia izlucheniia N2-lazera na kinetiku generatsii aktivnykh form kisloroda granulotsitarno-makrofagal'nymi kletkami v sisteme tsel'noi krovi.

The report deals with the study on the kinetics of the generation of the reactive oxygen forms (ROF) by granulocyte-macrophage cells (GMC) in the whole blood. It was shown that the energy of N2-laser radiation promotes the modulation effect of the ROF generation. Its biological significance can be connected with the correction of GMC's functional activity. We suppose that the mechanism of the modulation effect of the ROF production induced by N2-laser radiation connected with the triggering role of NADP(H), the key molecule of "respiratory burst", which absorbs the light of 337 nm, N2-laser emission wavelength.

[Modulated extremely high frequency electromagnetic radiation of low intensity activates or inhibits respiratory burst in neutrophils depending on modulation frequency]. / Modulirovannoe élektromagnitnoe izluchenie kraine vysokikh chastot nizkoi intensivnosti aktiviruet ili ingibiruet respiratornyi vzryv v zavisimosti ot chastoty moduliatsii.

The influence of low-intensity modulated electromagnetic radiation of extremely high frequencies (EHF EMR) on synergistic reaction of calcium ionophore A23187 and phorbol ester PMA in activation of the respiratory burst of the peritoneal neutrophils of mice line NMRI was investigated. The production of reactive oxygen species by the neutrophils was estimated by luminol-dependent chemiluminescence technique. The cells were irradiated in the far field zone of the channel radiator for 20 min in the presence of A23187 and then were activated by PMA after switching off the irradiation. It was shown, that continuous EHF EMR (50 microW/cm2) inhibited quasi-resonantly the synergistic reaction. The maximum effect was about 25% at carrier frequency of 41.95 GHz. Modulated radiation with carrier frequency of 41.95 GHz and modulation frequency of 1 Hz activated the synergistic reaction, but at modulation frequencies of 0.1, 16 and 50 Hz inhibited one. At fixed modulation frequency of 1 Hz the nonlinear dependence of the effect on the carrier frequency was found. The synergistic reaction was activated in the frequency range of 41.95-42.05 GHz and was inhibited at the frequencies of 41.8-41.9 GHz. The effect was observed only at raised intracellular free calcium concentration and at calcium fluxes through plasma membrane. The obtained results prove the possibility of control over cell functioning by low-intensity modulated EHF EMR, presumably, manipulating by connected systems of enzyme reactions.

[Millemetre waves inhibit the synergistic effect of calcium ionophore A23187 and phorbol ester in neutrophil respiratory burst]. / Millimetrovye volny ingibiruiut sinergicheskii effekt kal'tsievogo ionofora A23187 i forbolovogo efira v aktivatsii respiratornogo vzryva neitrofilov.

The effect of extremely high frequency electromagnetic field (mm-waves) on respiratory burst of neutrophils was studied. The peritoneal evoked neutrophils of the mice (NMRI line) were used. The production of reactive oxygen species was estimated by luminol-dependent chemiluminescence technique. Cells were irradiated by the mm-waves of 41. 95 GHz in the far field zone of the channel radiator during 20 min. Absorbed energy flux density was 150 microW/cm2. The irradiation was carried out at different concentrations of calcium ionophore A23187 and then neutrophils were stimulated by phorbol 12-myristate 13-acetate (PMA) 1 microM, activator of PKC. At irradiation of neutrophils the synergistic action of A23187 and PMA was not changed at low concentration of ionophore 10 nM-0.5 microM and was suppressed at high concentrations 0.5-10 microM. The largest inhibition of about 60% was obtained at the concentration of A23187 20 microM. The effect of mm-waves was not found under exposure in Ca(2+)-free medium for all used A23187 concentrations. We suggest that the mm-wave effect on the production of reactive oxygen species by neutrophils is determined by the influx of extracellular Ca2+ and PKC.

[Role of phospholipase A2 and epoxygenase in inhibition of respiration burst in neutrophils by low intensity radiation of extremely high frequency]. / Rol' fosfolipazy A2 i époksigenazy v ingibirovanii respiratornogo vzryva neitrofilov nizkointensivnym élektromagnitnym izlucheniem kraine vysokoi chastoty.

The role of some components of the phospholipid metabolism in the activation of neutrophil respiratory burst and its inhibition by electromagnetic radiation (EMR) of extremely high frequencies (EHF) was studied. It was shown that EHF EMR has effect on cells with a high sensitivity to the inhibitor of phospholipase A2 4-bromophenacyl bromide. However, againsts the background of the inhibitor, the effect of EHF EMR was not observed on cells with either high or low sensitivity to the inhibitor. EHF EMR was also inefficient with cells pretreated with proadifen, an inhibitor of epoxygenase (cytochrome P-450). The results obtained suggest that the effect of EHF EMR manifests itself in cells with a high activity of phospholipase A2 and is realized with the participation of epoxygenase metabolites of arachidonic acid.

Impact of total-body irradiation on the response to a live bacterial challenge.

PURPOSE: Concern regarding radiation effects on human health continues to increase worldwide. Given that infection is a major cause of morbidity and mortality after exposure, the aim of this study was to evaluate decrements in immune cell populations using a mammalian model subjected to a live bacterial infection. MATERIALS AND METHODS: C57BL/6 mice were exposed to total-body irradiation (TBI) with 3 Gy protons (70 cGy/min). One, 2, 4, 8 or 16 days later, subsets of mice were injected intraperitoneally with live Escherichia coli [055:K59(B5)]. Control groups received no radiation and vehicle (no bacteria). The mice were euthanized for analyses 90-120 min after injection of the bacteria. RESULTS: There were no unexpected effects of radiation or E. coli alone. Despite dramatic radiation-induced decreases in all leukocyte populations in both the blood and spleen, irradiated mice were still able to respond to an immune challenge based on capacity to generate an oxidative burst and secrete inflammatory cytokines, i.e., tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6). However, these responses were generally elevated above control values. CONCLUSIONS: Together, these results suggest the possibility for enhanced inflammation-associated tissue injury and increased risk for chronic inflammation.

Protracted low-dose radiation priming and response of liver to acute gamma and proton radiation.

This study evaluated liver from C57BL/6 mice irradiated with low-dose/low-dose-rate (LDR) γ-rays (0.01 Gy, 0.03 cGy/h), with and without subsequent exposure to acute 2 Gy gamma or proton radiation. Analyses were performed on day 56 post-exposure. Expression patterns of apoptosis-related genes were strikingly different among irradiated groups compared with 0 Gy (p < 0.05). Two genes were affected in the Gamma group, whereas 10 were modified in the LDR + Gamma group. In Proton and LDR + Proton groups, there were six and 12 affected genes, respectively. Expression of genes in the Gamma (Traf3) and Proton (Bak1, Birc2, Birc3, Mcl1) groups was no longer different from 0 Gy control group when mice were pre-exposed to LDR γ-rays. When each combined regimen was compared with the corresponding group that received acute radiation alone, two genes in the LDR + Gamma group and 17 genes in the LDR + Proton group were modified; greatest effect was on Birc2 and Nol3 (> 5-fold up-regulated by LDR + Protons). Oxygen radical production in livers from the LDR + Proton group was higher in LDR, Gamma, and LDR + Gamma groups (p < 0.05 vs. 0 Gy), but there were no differences in phagocytosis of E. coli. Sections stained with hematoxylin and eosin (H&E) suggested more inflammation, with and without necrosis, in some irradiated groups. The data demonstrate that response to acute radiation is dependent on radiation quality and regimen and that some LDR γ-ray-induced modifications in liver response were still evident nearly 2 months after exposure.

Different sensitivity of carp (Cyprinus carpio) and rainbow trout (Oncorhynchus mykiss) to the immunomodulatory effects of UVB irradiation.

In order to study the sensitivity of two fish species, carp (Cyprinus carpio) and rainbow trout (Oncorhynchus mykiss), to the immunomodulatory effects of ultraviolet B (UVB) radiation, the fish were exposed to a single UVB dose of 50, 250, 500 or 1,000 mJ cm(-2). These species represent different phylogenetic groups of fish, and they differ also in their behaviour inhabitating often dark and turbid (carp) or clear and transparent waters (salmonids). Immune responses were studied on day 1 post-irradiation. Unexposed fish, and fish exposed to radiation depleted of UV wavelengths served as controls. UVB irradiation markedly enhanced the blood respiratory burst and cytotoxic activity in carp, but in the head kidney these parameters were significantly suppressed. Rainbow trout respiratory burst was affected only after exposure with the highest dose of UVB. Lymphopenia and granulophilia were noted in both fish blood after exposure. This study indicates that UVB irradiation modulates immune functions in both fish species studied, and that rainbow trout is more tolerant than carp against UVB. Fish are clearly adapted to the environmental UVB levels prevailing in their usual living habitats, but are also a target of undesired effects of UVB on immune functions whenever exposed to increased radiation levels.