Action spectra for inactivation of normal and xeroderma pigmentosum human skin fibroblasts by ultraviolet radiations.
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Biomedical subjects
Publications and source records attributed to S H Moss.
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The wavelengths of sunlight considered to be responsible for erythema and skin cancer formation are in the range 290-340 nm. Formulated sunscreens usually contain an agent that absorbs in this wavelength region, and one of the most widely used is para-aminobenzoic acid (PABA). Previous work has demonstrated the sensitization by PABA of the lethal and mutagenic effects of near-ultraviolet (UV) radiation in a model bacterial system. Experiments with the mouse lymphoma L5178Y cell line have now demonstrated sensitization by PABA of the lethal effect of near-UV radiation, the extent of which, after correction for absorption of UV radiation by PABA, bears a direct relationship to PABA concentration. The limitations of these results in predicting the response of human skin to the presence of PABA during exposure to UV radiation is emphasized.
We assessed the clinical, serologic, and renal abnormalities of two patients with the syndrome of hypocomplementemia, vasculitis, and urticaria. Both patients presented with recurrent urticaria and were found subsequently to have glomerulonephritis. Both manifested depletion of the early complement (C) components, and their Cl inhibitor levels were normal. Circulating immune complexes were detected by two of three assays in both patients. One patient had a high titer of Sm antibodies. The detectable immune complexes were of high molecular weight, and were more suggestive of classical lupus erythematosus than the low molecular weight (7S) Clq precipitins which characterize some cases of hypocomplementemia-vasculitis-urticaria syndrome. Biopsy of the skin lesions in both patients revealed leukocytoclastic vasculitis with immunoglobulin and C deposits at the dermal-epidermal junction. Renal biopsy specimens showed segmental or diffuse proliferative mesangial glomerulonephritis. The results suggest that patients with this syndrome do not conform to a discrete entity but rather exhibit a spectrum of diseases ranging from systemic lupus erythematosus to the syndrome of urticaria, hypocomplementemia, and low molecular weight Clq precipitins.
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The mechanism of formation of photoreactivable damage in deoxyribonucleic acid (DNA) by ionizing radiation in a dark repair deficient strain of Escherichia coli (uvrA recA) has been investigated. By altering the ratio of damage produced directly (by ionization) to that formed indirectly (by Cerenkov ultraviolet (U.V.) radiation by 137Cs gamma-rays, it has been demonstrated that the major portion of the photoreactivable damage is produced by Cerenkov U.V. radiation. The amount of photoreactivable damage produced by 50 kVp X-rays, which cannot generate Cerenkov radiation, is similar to that component of photoreactivable damage produced by 137Cs gamma-rays that is not attributed to Cerenkov radiation. It is suggested that the second mechanism of formation of photoreactivable damage in DNA by ionizing radiation is the direct excitation of DNA. The possible role of Cerenkov U.V. radiation in ionizing radiation mutagenesis is discussed.
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The enhancement of gamma-radiation-induced damage in bacteria by the presence of oxygen during irradiation has been attributed to changes in the rate of formation, or alternatively in the repair, of single-strand breaks. This paper presents data which support the hypothesis that the observed effect of oxygen of modifying viability after irradiation is in part associated with lesions other than DNA single-strand breaks. In particular, the influence of oxygen during gamma-irradiation on the subsequent efficiency of photo-reactivation and excision repair is used to demonstrate that oxygen enhancement is due to a reduction in the excision repair of non-photo-reactivable damage.
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Investigation of the effect of photoreactivation, excision, and recombination repair, individually and in combination, on the survival of ultraviolet-irradiated Escherichia coli K-12 mutants has led to a possible explanation of the loss of photoreactivability and of the complex changes in viability observed during liquid-holding. It is suggested that at higher ultraviolet light doses the excision repair mechanism becomes saturated due to overlapping of excised regions on opposite strands of the deoxyribonucleic acid helix. The results also provide support for the existing hypothesis that states that the shape of shouldered survival curves of ultraviolet-irradiated bacteria can be described in terms of the probability of occurrance of overlapping excised regions. Using the data obtained with repair-deficient mutants with closely related genetic makeup, we present a mathematical model that accurately predicts the shape of the observed survival curves and provides an estimate of the number of nucleotides in each fragment of deoxyribonucleic acid removed by the excision repair mechanism.
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