Effect of temperature on the modification of spectral properties of tryptophan aqueous solutions induced by water previously treated with laser radiation

It was shown that preliminary exposure of a solvent (water) to low-intensity laser radiation reduces the tryptophan fluorescence intensity, and this fluorescence quenching effect is retained throughout the temperature range explored (from 8 up to 50 degrees C). The effects found are interpreted as resulting from changes in solvent properties induced by the action of electromagnetic radiation on interaction of water molecules with solute.     

Effects of quercetin and enhanced UV-B radiation on the soybean (Glycine max) leaves

The possible ameliorative effects of quercetin on soybean [Glycine max (L.) Merr.] leaves exposed to UV-B radiation were conducted in greenhouse. The symmetrical leaves supplied with quercetin solution (0.2%, 1%) were exposed to UV-B radiation (0, 3.5, 6.5 kJ m⁻² d⁻¹). 0.2% quercetin ameliorated leaf photosynthesis, improved leaf water content (LWC), and decreased lipid oxidation. The unfavorable effect on photosynthetic parameter was displayed in 1% quercetin treatment. The effect of quercetin on phenylalanine ammonia lyase (PAL) activity varied with the quercetin concentration, UV-B radiation intensity and leaf development. In the later development polyphenol oxidase (PPO) activity was increased significantly by quercetin treatments. We suggested that quercetin with suitable concentration could serve as UV-B protective agent partly due to its antioxidant capacity.     

Protection of DNA from high LET radiation by two OH radical scavengers,tris (hydroxymethyl) aminomethane and 2-mercaptoethanol

The effect of high linear energy transfer (LET) radiation on DNAin vitro, both in protective and non-protective environments was investigated. Two hydroxyl radical scavengers, tris(hydroxymethyl) aminomethane and 2-mercaptoethanol, were compared for their ability to protect SV40 DNA from radiation damage over a wide LET range. At comparable OH scavenging capacities, significant differences were found between these protective agents, indicating that other, radical scavenger-dependent processes affected the extent to which the DNA was protected. In general, a decrease in single-strand breaks (SSBs) relative to double-strand breaks (DSBs) was observed as LET increased. This effect was more pronounced when a radioprotector was present. Comparison of the relative biological efficiency (RBE) of radiation damage as LET increased showed a peak of DSB production in the mid-LET range. These data agree with measurements made by Christensen et al. (1972). An explanation for this increase in DSB production efficiency has been proposed based on the particle track structure of high-LET radiation.Correspondence to: G. Taucher-Scholz     

Effect of pulse electromagnetic radiation on erythrocyte ghosts

The pulse microwave radiation has been shown to increase the fluorescence intensity of 2-toluidinonaphthanene-6-sulfonate (2,6-TNS) and 1-anilinonaphthalene-8-sulfonate (1,8-ANS) built-in membranes of erythrocyte ghosts. In experiments with 2,6-TNS a frequency dependence of the effect of microwave radiation with maximum within the frequency range of 55-65 Hz has been found. It is suggested that the changes registered with fluorescent probes are induced by mechanical oscillations generated by the pulse microwave radiation.     

Effect of dihydroxyanthraquinone (DHAQ) and radiation on the survival of cultured Chinese hamster ovary cells

Dihydroxyanthraquinone (DHAQ) is currently being tested as a cancer chemotherapeutic agent because of its structural similarity to Adriamycin (ADR) and other DNA-intercalating antibiotics. The interaction of DHAQ and ionizing radiation on the induction of cell lethality was investigated in Chinese hamster ovary cells in culture. In asynchronous populations of cells, DHAQ produced a slight enhancement of radiation-induced cell lethality as evidenced by changes in both shoulder and slope of the radiation dose-survival curves. However, DHAQ had no effect on either the extent or time course of recovery from sublethal radiation damage. In synchronous populations of cells treated at various times before or after selection in mitosis, the combination of DHAQ and radiation produced greater cell killing than that predicted based on simple additivity of effect, with a decided enhancement for cells treated during S phase. These results indicate that DHAQ is similar to other DNA-intercalating antibiotics in regard to the interaction with ionizing radiation to produce cell lethality.     

Cellular transformation by radiation: Induction,promotion, and inhibition

Mammalian cell cultures offer powerful tools for evaluating qualitatively and quantitatively the oncogenic potential of radiation over a wide range of doses with particular importance at the low dose range that is relevant to human exposure and risk. Our studies have shown that early events in the process of radiation induced transformation in both rodent and human cells requires initial replication for fixation of transformation as a hereditary property of the cells and further clonal expansion for full expression. Early events (fixation) are inhibited by cell–cell contact and high cell density but can be modified at low temperature where repair processes are slowed. Cell–cell contact and communication in tissue organization may be in part responsible for our findings that radiation oncogenesis induced in utero in hamsters is expressed at a lower frequency than that induced in vitro. Quantitative studies carried out on hamster embryo cells indicate that neutrons are more effective in their carcinogenic potential than x-rays but also more toxic, that splitting the dose of x-rays at low doses leads to enhanced transformation, but that at high doses protracted radiation has a sparing effect. At all dose ranges survival was increased by protracting the radiation dose, thus suggesting that different repair processes must be involved for survival and transformation. Similar observations were seen when the protease inhibitor Antipain was found to enhance transformation in rodent and human cells when present at the time of radiation, but was protective when added after radiation. Survival was not modified under any of those conditions, and Antipain did not affect DNA replication and repair. In our qualitative studies, once cells are transformed by radiation, they exhibit a wide range of structural and functional phenotypic changes, some of which are membrane-associated and are expressed within days after induction. Our current studies on nutritional and hormonal influences on radiation transformation indicate the following: Pyrolysate products from broiled protein foods act in synergism with radiation to produce transformation, whereas vitamin A analogs are powerful, preventive agents. Retinoids inhibit both x-ray-induced transformation and its promotion by TPA: these modifications (enhancement by TPA, inhibition by retinoids) are not reflected in sister chromatid exchanges, but are reflected in the level of membrane associated enzymes Na/K ATPase. Whereas retinoids modify late events (expression, promotion), we find that thyroid hormone plays a crucial role in the early phases of radiation and chemically induced transformation. Under hypothyroid conditions no transformation is observed. The addition of triiodothyronine at physiological levels results in a transformation rate that is dose-related. Our recent success in transforming human skin fibroblasts will enable quantitative and qualitative studies of radiation carcinogenesis in a system relevant to man.     

Molecular hydrogen and radiation protection

Molecular hydrogen (dihydrogen, H(2)) acts as a therapeutic antioxidant by selectively reducing hydroxyl radicals (?OH) and peroxynitrite (ONOO-). It has been well-known that ionising radiation (IR) causes oxidative damage and consequent apoptosis mainly due to the production of ?OH that follows radiolysis of H(2)O. Our department reported the protective effect of H(2) in irradiated cells and mice for the first time, and this effect is well repeated by us and another laboratory in different experimental animal models. A randomised, placebo-controlled investigation also showed consumption of H(2) can improve the quality of life of patients treated with radiotherapy for liver tumours. These encouraging results suggested that H(2) has a potential as a radioprotective agent with efficacy and non-toxicity.     

Modification of damaging effect of ultraviolet radiation on peritoneal macrophage membranes in mice

Different factors modificating damaging effect of middle-wave ultraviolet radiation (lambda max = 306 nm) on mice peritoneal macrophage plasma membranes were studied. It was shown that damaging effect of ultraviolet declined when the cells were simultaneously treated by red light (lambda max = 713 nm). This protective effect increased when a red component of light became greater and achieved almost 100% when it consisted 28.6%. It was also found that the decrease in intra- and extracellular pH led to the decrease in damaging effect of UVR. The increase of pH bring to an elevation of UVR destructive effect.     

Effect of low intensity pulse-modulated electromagnetic radiation on activity of alkaline phosphatase in blood serum

The change in alkaline phosphotase activity in vitro with frequencies modulation at low intensity of pulse-modulated electromagnetic radiation was experimentally shown (EMR, 2375 MHz, intensity: 0.8, 8.0; 40.0 microW/cm2; range modulation: 30-310 Hz; time of interaction: 1-3 min). Revealed effects could be regarded as an evidence of informative character of interaction of modulated EMR.     

Health risks of low dose ionizing radiation in humans: a review

Radiobiologists have been struggling to estimate the health risks from low doses of radiation in humans for decades. Health risks involve not only neoplastic diseases but also somatic mutations that may contribute to other illnesses (including birth defects and ocular maladies) and heritable mutations that may increase the risk of diseases in future generations. Low dose radiation-induced cancer in humans depends on several variables, and most of these variables are not possible to correct for in any epidemiologic study. Some of the confounding factors include (i) interaction of radiation with other physical (UV light), chemical, and biological mutagens and carcinogens in a synergistic manner; (ii) variation in repair mechanisms that depend on dose; (iii) variation in sensitivity of bystander cells to subsequent radiation exposure that depends on whether they have been pre- or postirradiated; and (iv) variation in adaptive response that depends on radiation doses and protective substances (antioxidants). In our opinion, both the linear no-threshold-response and the threshold-response models might not be suitable in predicting cancer risk at low radiation doses in a quantitative sense. Low doses of ionizing radiation should not be considered insignificant for risks of somatic and heritable mutations and neoplastic and nonneoplastic diseases in humans.     

Variable interaction of heat and procaine in potentiation of radiation lethality in mammalian cells of neoplastic origin

Mild hyperthermia in conjunction with procaine HCl acts as a potentiator of radiation lethality in HeLa cells, with little toxicity for unirradiated cells. The majority of irradiated cells responds extensively within a four hour period of treatment with the two agents. Potentiation of radiation lethality by the combined treatment was also found in a line of human melanoma cells, and to a lesser extent in a line of human ovarian carcinoma cells. The interaction of heat and procaine in the process of potentiation of radiation lethality was assessed from a series of radiation survival curves, with temperatures ranging from 37 to 42 degrees C and procaine concentrations from 1 to 3 mM. The interactive factor was obtained from the ratio of the Dose Reduction Factor (DRF) due to procaine in heated cells, to the DRF due to procaine in unheated cells; a ratio larger than unity denotes interaction of heat and procaine. The largest interaction was observed when individual agents exerted only a minimal radiopotentiating effect, as if increased effectiveness of one agent pre-empted the effectiveness of the other agent.     

Effects of a protecting osmolyte on the ion atmosphere surrounding DNA duplexes

Osmolytes are small, chemically diverse, organic solutes that function as an essential component of cellular stress response. Protecting osmolytes enhance protein stability via preferential exclusion, and nonprotecting osmolytes, such as urea, destabilize protein structures. Although much is known about osmolyte effects on proteins, less is understood about osmolyte effects on nucleic acids and their counterion atmospheres. Nonprotecting osmolytes destabilize nucleic acid structures, but effects of protecting osmolytes depend on numerous factors including the type of nucleic acid and the complexity of the functional fold. To begin quantifying protecting osmolyte effects on nucleic acid interactions, we used small-angle X-ray scattering (SAXS) techniques to monitor DNA duplexes in the presence of sucrose. This protecting osmolyte is a commonly used contrast matching agent in SAXS studies of protein-nucleic acid complexes; thus, it is important to characterize interaction changes induced by sucrose. Measurements of interactions between duplexes showed no dependence on the presence of up to 30% sucrose, except under high Mg(2+) conditions where stacking interactions were disfavored. The number of excess ions associated with DNA duplexes, reported by anomalous small-angle X-ray scattering (ASAXS) experiments, was sucrose independent. Although protecting osmolytes can destabilize secondary structures, our results suggest that ion atmospheres of individual duplexes remain unperturbed by sucrose.     

Untargeted effects of ionizing radiation: implications for radiation pathology

The dogma that genetic alterations are restricted to directly irradiated cells has been challenged by observations in which effects of ionizing radiation, characteristically associated with the consequences of energy deposition in the cell nucleus, arise in non-irradiated cells. These, so called, untargeted effects are demonstrated in cells that have received damaging signals produced by irradiated cells (radiation-induced bystander effects) or that are the descendants of irradiated cells (radiation-induced genomic instability). Radiation-induced genomic instability is characterized by a number of delayed adverse responses including chromosomal abnormalities, gene mutations and cell death. Similar effects, as well as responses that may be regarded as protective, have been attributed to bystander mechanisms. Whilst the majority of studies to date have used in vitro systems, some adverse non-targeted effects have been demonstrated in vivo. However, at least for haemopoietic tissues, radiation-induced genomic instability in vivo may not necessarily be a reflection of genomically unstable cells. Rather the damage may reflect responses to ongoing production of damaging signals; i.e. bystander responses, but not in the sense used to describe the rapidly induced effects resulting from direct interaction of irradiated and non-irradiated cells. The findings are consistent with a delayed and long-lived tissue reaction to radiation injury characteristic of an inflammatory response with the potential for persisting bystander-mediated damage. An important implication of the findings is that contrary to conventional radiobiological dogma and interpretation of epidemiologically-based risk estimates, ionizing radiation may contribute to malignancy and particularly childhood leukaemia by promoting initiated cells rather than being the initiating agent. Untargeted mechanisms may also contribute to other pathological consequences.     

The protection of DNA in blood leukocytes from damaging action of ultraviolet radiation using the “Useful Sun” strategy

The damaging effects of light that was emitted by a DRSh250-3 mercury lamp on the DNA of mouse blood leukocytes was studied in vitro. It was shown that the main DNA damage is due to the action of UVB radiation (280–320 nm). Under the combined effects of the UV radiation and the orange–red fluorescent component it was found that the additional fluorescent light with the spectral maximum at 625 nm from nanoluminophore materials (quantum dots that are based on CdSe/ZnS, CdSe/CdS/ZnS) protected the cellular DNA from the damaging effect of UV radiation. Using nanomolar concentrations of hydrogen peroxide, the hypothesis of the role of reactive oxygen species in the protective effects of the red–orange light was tested in vitro. It was shown for the first time that the mechanisms of the protective effects are associated with the induction of an adaptive response by nanomolar concentrations of hydrogen peroxide that are induced by the orange–red light.     

Tissue Raman spectroscopy for the study of radiation damage: brain irradiation of mice

Radiotherapy is routinely employed in the treatment of head and neck cancers. Acute cell death, radiation-activated chemical cascades, and the induction of genes coding for protective factors like cytokines are considered to be the major processes involved in radiation damage and repair. It should be possible to follow these processes by monitoring the biochemical interactions initiated by radiation. We have carried out Raman spectroscopy studies on tissue from mice subjected to brain irradiation to identify the biochemical changes occurring in tissue and brain as a result of radiation injury. These studies show that brain irradiation produces drastic spectral changes even in tissue far removed from the irradiation site. The changes are very similar to those produced by the stress of inoculation and restraint and the administration of an anesthetic drug. While the changes produced by stress or anesthetics last for only a short time (a few hours to 1 or 2 days), radiation-induced changes persist even after 1 week. The spectral changes can be interpreted in terms of the observation of new spectra that are dominated by bands due to proteins. The results thus support the hypothesis that various protective factors are released throughout the body when the central nervous system (CNS) is exposed to radiation.     

Antistress cross-protection of UV irradiated yeast cells with participation of extracellular peptide factors

Antistress effect of extracellular peptides on UV irradiated yeast of different phylogenetic groups was studied. Yeast from different ecotopes and taxonomic groups exposed to UV radiation of a lethal intensity showed a protective effect and reactivating effect with participation of extracellular peptides. The highest protective activity was found in peptide reactivation factors (RFs) of bakery yeast-Saccharomyces cerevisiae, Kluyveromyces fragilis, and Candida utilis; the highest reactivating activity was exhibited by factors of the above-mentioned cultures and Debariomyces hansenii. Cross-protective and reactivating effects of RFs of yeast belonging to different taxonomic groups were demonstrated. Cross-protection increased two to three times after preexposure of reactivation factors to UV light (activation) in contrast to their reactivating effect.     

Immunocorrective action of tuftsin during exposure to ionizing radiation

The effect of the tetrapeptide tuftcin (Thr-Lys-Pro-Arg) on the humoral immune response in CBA mice exposed to sublethal irradiation in a dose of 450 sGy was studied. The drug was injected intraperitoneally for 5 days before (series I) or after (series II) radiation exposure. It has been shown that taftcin has no protective action but decreases considerably the immune response lowering due to radiation.     

In vivo spin trapping of free radicals generated in brain, spleen, and liver during gamma radiation of mice

Spin trapping techniques combined with electron spin resonance spectroscopy were used to capture and detect free radicals generated in vivo during exposure to ionizing radiation. Tissue extracts of mice given an intraperitoneal or intragastric dose of the spin trap, alpha-phenyl-t-butyl nitrone prior to exposure to gamma radiation (2 to 5 Gy), contained a radical adduct with hyperfine splitting constants characteristic of spin adducts of carbon-centered lipid radicals. Considerably more radicals were trapped in tissues when the trap was given 3 h before radiation as compared to 30 min before exposure. The radicals observed may either be secondary species resulting from an attack on cellular components by products of water radiolysis, or primary radicals resulting from direct interaction of the radiation with biological molecules. The results indicate that the spin trapping agent is able to penetrate well into animal tissues, and to capture radical species under conditions where the latter would be expected to occur.     

Response of transformed and normal mouse cell lines to anti-melanin compounds, hyperthermia, and radiation.

Five cell lines (one parental, two transformed melanin producing, and two transformed non-melanin producing) were evaluated for the responses to 2- and 4-hydroxyanisole (2HA, 4HA) alone or combined with hyperthermia or radiation. All cells exhibited a non-specific toxic response to the two compounds and the effect was exposure time and concentration dependent and was greater for 4HA compared to 2HA. In addition, the two melanin-producing cell lines were more sensitive, demonstrating specific toxicity to such cell lines. The treatment with either 2HA or 4HA combined with heat and radiation resulted mostly in additive or antagonistic effects, except for one combination of 2HA plus radiation in the melanin-producing R25 cells. Thus, while these compounds may be useful in therapy for pigmented melanomas, combined treatment with radiation is not recommended.