[en] The immune system comprises one aspect of the host's defense mechanism against potentially harmful agents. It has become recognized as an important factor in light radiation sensitivity and light-mediated disease. The interaction of light radiation with the immune system has formed the basis for the evolving discipline of photoimmunology. A description of the multicomponent immune system, its modification by light radiation, and a discussion of how photoimmunological studies may provide data important for understanding the mechanisms involved in photosensitivity are presented in this review. Photosensitivity may be either acquired or may be genetic in nature. Acquired photosensitivity involves an individual's reaction to either light alone or light in conjunction with topically or systemically administered photosenitizing agents. The outcome of such a reaction can be benign or severe, depending on a number of factors. Genetic photosensitivity includes the reactions to light radiation of individuals carrying the genetic information for inherited diseases such as Ataxia telangiectasia (AT) and Xeroderma pigmentosum (XP). Factors associated with these conditions can lead to enhanced sensitivity to radiation-related diseases, such as cancer. In addition, there are conditions which cannot be readily placed in either of the categories just described but, nevertheless, have been correlated with immune system dysfunction. These include photoallergy, photosensitivity associated with autoimmunity, and light-induced skin cancer. Immunological studies have provided information which may aid in elucidating the problem of photosensitivity and in the development of suitable radioprotective measures

[en] Cells of most, if not all, animal species contain information for type C retraviruses. This information is normally repressed, but may be derepressed after cellular exposure to a variety of agents. This phenomenon of virus induction can be utilized to investigate the phenomenon of gene derepression, since control of type C virus induction is thought to be under regulatory processes affecting cellular genes. Properties of type C retraviruses, results of virus induction studies, and discussion of a possible mechanism(s) for virus induction are presented in this review. Utilizing the Al-2 nonproducer cell line, originally derived from cells of the BALB/c mouse, quantitative and kinetic dose-response data have been obtained for type C virus induction by uv radiation, chemicals, and biological agents. Studies showing that protease inhibitors suppress induction suggest the presence of a common mechanism for controlling virus induction; i.e., a protein repressor(s) which acts to control virus gene derepression. Since protease inhibitors suppress induction of prophage in E. coli, similar processes may control virus induction in animal and bacterial systems

[en] Two strains of murine leukemic lymphoblasts, L5178Y-R and L5178Y-S, are inversely cross-sensitive to uv radiation and x rays. They also show considerable difference in tumorigenicity: L5178Y-R cells form ascitic tumors in DBA/2 mice with high efficiency, whereas L5178Y-S cells only very rarely form solid tumors. L5178Y-R cells maintain their characteristics when passaged in vivo. Upon prolonged cultivation in vitro, they undergo conversion into L5178Y-S cells. The obtained results strongly suggest that increase of x-ray sensitivity, decrease of uv sensitivity, and loss of tumorigenicity occur simultaneously in the conversion

[en] A non-lethal concentration of H₂O₂ (0.05 percent) greatly enhances near-ultraviolet (NUV) inactivation of phage T7. Simultaneous treatment with H₂O₂ and NUV reduces the amount of DNA injected into the bacterial host, but not the number of phage adsorbed. In genetic crosses a gradient of recombination results; markers injected first are reduced to a lesser extent than those injected last. Based on biochemical experiments, we conclude that normal injection of T7 phage DNA is prevented because of DNA-protein crosslinks. Such crosslinks could be important lesions in NUV cellular damage in general, as supported by experiments with NUV + H₂O₂ irradiated L-929 fibroblasts and B-16 melanoma cells. Further tests show that the synergistic action of NUV + H₂O₂ may be via alteration of -SH on cysteine to yield a new chromophore that has lambda/sub max/ above 305 nm. Without H₂O₂, NUV alters a different chromophore, as determined in control experiments

[en] The survival curves of uv-irradiated herpes simplex virus assayed in uv- or x-irradiated rat cells were analyzed with regard to radiation-enhanced reactivation (RER) and other processes produced by cell irradiation. Results in rat mammary tumor cells (which express RER) and in rat embryo cells (which do not express RER) were compared. Irradiation of the cells caused a change in virus survival in both cell types, which was partially expressed as a decrease in the extrapolation of the second component of the virus survival curve. RER was expressed as a change in the D₀(1/slope) of the survival curves and reached a plateau level by 6 J/m² or 10 Gy of cell irradiation. These two types of changes in the virus survival curves are apparently independent. An additional process occurred in heavily uv-irradiated tumor cells which cannot be easily interpreted. A brief analysis of methods to quantitate RER indicates that the D₀ of the virus survival curve is more useful than the commonly used reactivation factor

[en] The effect of 8-methoxypsoralen (8-MOP) and ultraviolet radiation (UV) of different wavelengths in the region 300 nm to 400 nm on the activation of latent tumor virus from SV40 transformed cells was investigated. Results indicate that 8-MOP and UV treatment may activate as much as 1000-fold more virus than UV alone at these wavelengths. A preliminary action spectrum for this effect is given. (author)

[en] The effect of ultraviolet (uv) radiation (235 to 313 nm) on cell killing and induction of mutants in L5178Y mouse lymphoma cells was compared to the effect of uv radiation (240 to 313 nm) on induction of pyrimidine dimers in Syrian hamster embryo cells. A very strong similarity among the three action spectra was found, suggesting that uv-induced pyrimidine dimer formation is a step common to both cell killing and mutagenesis in mammalian cells

[en] Cellular transformation in vitro has been used to test for the carcinogenic potential of chemical and physical insults including light. This report discusses the measurement of transformation, and reviews studies done on the effects of exposure to artificial light on cellular transformation or on cellular transformation by a virus. To date, cool-white lamps have been found to cause cellular transformation, while germicidal lamps and sunlamps have been found to cause cellular transformation and to enhance virally produced transformation

[en] Knowledge of both acute and chronic biological effects is currently used to evaluate light safety. In some cases, a quantitative basis for avoiding exposures greater than a certain value can be stated. In other cases, however, only a qualitative estimate of the hazard is available. In a discussion that uses mercury vapor lamps as an example, the interplay between the two types of data leading to action is described

[en] Exposure of L5178Y-S (but not L5178Y-R) cells to uv-fluences below 4 J/m² causes enhancement of both cell growth rate and cloning efficiency. No measurable increase in production of 6-thioguanine resistant mutants was observed when cells were stimulated by exposure to 0.5 J/m², however, a significant increase in mutation frequency accompanied growth stimulation caused by 2.5 J/m²