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At least 703 records · Page 39Linked to original sources
PubMed1969

Association of microcyst formation in Spirillum itersonii with the spontaneous induction of a defective bacteriophage.

Mitomycin C and ultraviolet light were found to induce the formation of microcysts in Spirillum itersonii. These forms, as well as spontaneously occurring microcysts in this species, were found to contain phage tail parts, rhapidosomes, and a granular substance not seen in normal cells. It is suggested that microcysts are formed as the result of the induction of a defective phage. The production of phage lysozyme within the cell could lead to the formation of spherical forms as the cells lose their structural mucopeptide layer. Complete virus particles were not seen, nor was any biological activity demonstrated when the induced cultures were tested against two other strains of S. itersonii. The other strains of this bacterium also formed microcysts and phage tail parts when induced with mitomycin. Attempts to isolate an organism lacking the defective phage have been unsuccessful.

Bacteriophages↗
PubMed1985

An ultrastructural study of corneal incisions induced by an excimer laser at 193 nm.

Far ultraviolet light (193 nm) produced by an excimer laser has been used to produce a variety of incisions in the corneas of anaesthetised rabbits. Tissue was lost from the site of irradiation but the nature of the underlying molecular interactions responsible for such tissue erosion remain obscure. Ultrastructural analysis of the walls of the ablated areas show damage to the adjacent structures to be confined to a zone 60 to 200 nm in width. These dimensions could either be attributed to photochemical processes in which high energy photons directly break organic molecular bond, or to thermal reactions which result in limited heat flow and damage confined to the absorption depth at 193 nm of less than 1 micron. In non-penetrating incisions that reached within 40 micron of Descemet's membrane, endothelial cells were lost beneath the line of the irradiation. This spalling of cells seemed to be generated by shock or acoustic waves.

Animals↗
PubMed1994

Immunochemical detection of cyclobutane thymine dimers in epidermal Langerhans cells of ultraviolet B-irradiated hairless mice.

An immunocytochemical method was developed to study in vivo induction and removal of DNA damage in a specific cell population in the epidermis of hairless mice after ultraviolet B (UVB) exposure: the immunocompetent antigen-presenting Langerhans cells. To this aim, Ia+ cells, which are representative for epidermal Langerhans cells, were compared with the bulk of epidermal cells with respect to the nuclear level of cyclobutane thymine dimers. Mouse Langerhans cells were identified with a membrane-located immunoperoxidase stain, whereas DNA and DNA damage were revealed with fluorescent nuclear stains. After a low dose of UVB (approximately 1 minimal erythema dose), dimer levels were determined both in all murine epidermal cells and in Ia+ cells separately. At 24 h after irradiation, dimer removal was still incomplete, with a persistence of approximately 50% of the initially induced dimers in epidermal cells in general, and of approximately 75% in Langerhans cells. Possible applications of the method developed and the results presented here are discussed in relation to the immunosuppressive effect of UV.

Animals↗
PubMedDate not supplied

Short-term and long-term UVB-induced immunosuppression in human skin exhibit different ultrastructural features.

Short-term ultraviolet B light (UVB)-induced immune suppression was established by the ability of UVB to inhibit induction of allergic contact dermatitis (ACD) to dinitrochlorobenzene (DNCB). The long-term effect was assessed by a dramatic reduction of the mixed-epidermal cell lymphocyte reaction (MECLR) responses. Immuno electron microscopic (IEM) investigation of HLA class II localization on epidermal Langerhans cells (LC) (pivotal for the immune response of the skin) showed no difference in HLA class II expression after UVB-exposure compared to control skin, both after short-term and long-term UVB-exposure. Ultrastructural examination of the epidermis revealed a normal appearance of the epidermal cells after long-term UVB-exposure. However, after short-term UVB-exposure the epidermis exhibited many abnormalities, ranging from the stratum corneum to the basal membrane. So although both short- and long-term UVB exposures were able to cause immune suppression in the skin, those processes were not accompanied with identical morphological epidermal features.

Dermatitis, Allergic Contact↗
PubMed1983

Malignant transformation of guinea pig cells after exposure to ultraviolet-irradiated guinea pig cytomegalovirus.

Guinea pig cells were malignantly transformed in vitro by ultraviolet (uv)-irradiated guinea pig cytomegalovirus (GPCMV). When guinea pig hepatocyte monolayers were infected with uv-irradiated GPCMV, three continuous epithelioid cell lines which grew in soft agarose were established. Two independently derived GPCMV-transformed liver cells and a cell line derived from a soft agarose clone of one of these lines induced invasive tumors when inoculated subcutaneously or intraperitoneally into nude mice. The tumors were sarcomas possibly derived from hepatic stroma or sinusoid. Transformed cell lines were also established after infection of guinea pig hepatocyte monolayers with human cytomegalovirus (HCMV) or simian virus 40 (SV40). These cell lines also formed colonies in soft agarose and induced sarcomas in nude mice. It is concluded that (i) GPCMV can malignantly transform guinea pig cells; (ii) cloning of GPCMV-transformed cells in soft agarose produced cells that induced tumors with a shorter latency period but with no alteration in growth rate or final tumor size; and (iii) the tumors produced by GPCMV-and HCMV-transformed guinea pig cells were more similar to each other in growth rate than to those induced by SV40-transformed guinea pig cells.

Animals↗
PubMed1968

Alterations in the morphology of Bacillus subtilis after exposure to beta-lysin and ultraviolet light.

Viable counts, turbidities, and electron micrographs of Bacillus subtilis exposed to beta-lysin and ultraviolet light (UV), singly or in combination, were compared in an attempt to relate death with changes in morphology. The decreases in survival of both the beta-lysin- and UV-treated cells were rapid and preceded decreases in turbidity, as well as the changes in morphology. No significant differences were observed in turbidity reduction or morphological alterations of control cells from those of cells exposed to UV light. These cells developed prominent subcell wall spaces during incubation in the hypertonic stabilizing medium. No observable damage in either the cell wall or the cell membrane had taken place during 4 hr, but by 20 hr extensive damage of these two structures was apparent. The control and UV-treated cells exposed to beta-lysin did not develop prominent subcell wall spaces. Within 2 hr, lesions were observable in their cell walls, and the cytoplasmic membranes were permeable to phosphotungstic acid. The damage to these structures became more extensive with time. Although the visible changes of control and UV-treated cells were evident much later than those induced by beta-lysin, the morphological alterations in all cells were similar. It appeared that beta-lysin caused an accelerated release of an autolytic enzyme which digested the cell walls.

Bacillus subtilis↗
PubMed1987

Histogenesis of UV light-induced blister formation.

Histological examination of ultraviolet light (UVL)-induced blister formation in guinea pig skin is reported. Light and electron-microscopic examination was performed on skin exposed to single and multiple exposures of a large dose of UVB. In light microscopy, intracellular edema was prominent, especially in the lower part of the epidermis, where it developed into a blister. It seemed to be a subepidermal bulla. The PAS-positive basement membrane was observed at the floor of the blister. The positive Nikolsky's sign seemed to be due to a separation between the degenerated and regenerated epidermis. Electron microscopy revealed a marked intercellular as well as intracellular edema and well-preserved desmosomes. The basal lamina was always located at the floor of the blister. The difference in UVL-induced blister formation between normal and pathological conditions is discussed.

Animals↗
PubMed2004

Hornet flight is generated by solar energy: UV irradiation counteracts anaesthetic effects.

The Oriental hornet Vespa orientalis (Hymenoptera, Vespinae) flies outside its nest only in the daytime and never in the dark. Oriental hornets can be anaesthetized by means of diethyl ether, following which they awake spontaneously within about > or =1 h. However, when the anaesthetized hornets are exposed to direct irradiation they awake much faster and immediately fly out and this is within the temperature range for their normal activities (20-40 degrees C). Light exerts an effect not only on intact hornets, but also on their main body parts, be they the head, thorax or gaster, or a torso without a head or without a gaster. These body parts also 'awake' from ether anaesthesia when illuminated, especially by ultraviolet (UV) B or shorter light wavelengths, but a body without a gaster awakes much later than normal. As for flight activity, headless hornets do not fly at all, while hornets devoid of a gaster flutter their wings when illuminated but are incapable of rising in the air. When vespan cuticular regions are coated with paint that blocks the passage of light, such as UVB blockers, or with white Tipp-Ex, the awakening from anaesthesia is delayed. The vespan cuticle evinces photovoltaic activity, even in dead specimens, so that upon exposure to light it is possible to record levels of 30-180 mV, both in a wakeful hornet and in one that has undergone anaesthesia. We conjecture that in the awake hornet the voltage that its cuticle generates under the influence of light is transported within the cuticular interlamellar membranes to be utilized as flight energy by the muscles attached to them; however, in the narcotized hornet, the diethyl ether apparently decreases or disrupts membranal order, blocking any ionic channel activity and thereby inducing the anaesthesia. Presumably, this state of phase transition is remedied spontaneously, albeit in a lengthy process, or else the light energy in UV speeds up restoration of the ionic channel activity and the synaptic transmission and thereby contributes to a more rapid awakening. In this regard, the hornet gaster is an extensive region for absorbing light, which explains why its absence considerably delays the awakening from anaesthesia.

Anesthetics, Inhalation↗
PubMed2006

UV-irradiation induces oxidative damage to mitochondrial DNA primarily through hydrogen peroxide: analysis of 8-oxodGuo by HPLC.

Roles of reactive oxygen species (ROS) in damage to mitochondrial DNA (mtDNA) following ultraviolet (UV)-irradiation were investigated in the human hepatoma cell line SK-HEP-1. We altered the intracellular status of ROS by the overexpression of manganese superoxide dismutase (MnSOD) and/or catalase. Using HPLC, we analyzed 8-oxo-7,8-dihydro-2'-deoxyguanosine (8-oxodGuo), known as a marker of damage to DNA molecules. UV-irradiation resulted in the accumulation of 8-oxodGuo in these cells. The overexpression of MnSOD enhanced the accumulation of 8-oxodGuo by UV. The co-overexpression of catalase inhibited the accumulation of 8-oxodGuo by UV in MnSOD-transfectants. The overexpression of MnSOD reduced the colony forming capacity in SK-HEP-1 cells and the co-overexpression of catalase with MnSOD stimulated the capacity compared to control. UV-irradiation inhibited the colony forming capacity in these cells; no difference was observed among the capacities of control, MnSOD- and catalase-transfectants. However, the overexpression of MnSOD/catalase significantly rescued the reduction of colony forming capacity by UV-irradiation. Our results suggest that the accumulation of hydrogen peroxide plays a key role in the oxidative damage to mtDNA of UV-irradiated cells, and also that the overexpression of both MnSOD and catalase reduces the mtDNA damage and blocks the growth inhibition by UV. Our results also indicate that the increased activity of MnSOD may lead to a toxic effect on mtDNA by UV-irradiation.

8-Hydroxy-2'-Deoxyguanosine↗
PubMed1985

Effects of ultraviolet radiation on human epidermal cell alloantigen presentation: initial depression of Langerhans cell-dependent function is followed by the appearance of T6- Dr+ cells that enhance epidermal alloantigen presentation.

The effects of ultraviolet radiation (UV) on the immune parameters of human epidermis were studied. We determined the effects of both in vitro and in vivo UV on human epidermal cell surface markers and on epidermal immune function in the allogeneic epidermal cell-lymphocyte reaction (ELR). Epidermal cells obtained immediately after in vitro and in vivo UV exposure exhibited a dose-dependent decrease in alloantigen-presenting function in the ELR. This was not the result of a decrease in the number of T6+ Dr+ Langerhans cells but was due to their being less efficient at alloantigen presentation than equivalent numbers of Langerhans cells from unirradiated skin. The reduced stimulation in the ELR immediately after UV was not reversible by the addition of exogenous IL 1 or indomethacin and thus appeared to be due to a direct effect of UV on the alloantigen-presenting function of Langerhans cells. In contrast to this suppression of the epidermal immune function when epidermal cells were obtained immediately after UV, epidermal cells harvested 24 hr or later after in vivo UV exhibited a dose-dependent enhancement of allostimulatory capacity in the ELR that peaked 3 days after UV. The time course of the enhancement of allostimulation in the ELR after in vivo UV coincided with a decrease in the percentage of Langerhans cells and the appearance within the epidermis of T6- Dr+ cells, which are derived from the bone marrow, as evidenced by their expression of the bone marrow derivation markers HLe 1 and T200. Removal of Dr+ cells but not of T6+ cells from epidermal cell suspensions harvested 3 days after in vivo UV abrogated allostimulation in the ELR, demonstrating that the T6- Dr+ cells were responsible for the observed UV-induced enhancement of alloantigen presentation. Taken together, the results indicate that the timing and dosage of UV exposure are critical factors determining whether suppression or enhancement of epidermal immune function follows UV.

Amputation, Surgical↗
PubMed1991

Killing of Burkitt-lymphoma-derived Daudi cells by ultraviolet-inactivated vaccinia virus.

Interaction of active and UV-inactivated vaccinia virus at high multiplicity caused cytological changes and inhibition in cellular protein and DNA synthesis, thus arresting the multiplication of Burkitt-lymphoma-derived Daudi cells and eventually killing the cells. Adsorption to the cells but the lack of penetration was evident by immunofluorescence, electron microscopy and [3H]thymidine-labeled virus incorporation. Viral DNA synthesis or virus replication was not demonstrated. Thus, it appears that the massive adsorption of viral particles, active or UV-inactivated, or possibly a "toxic" component that resides in the virion, damages the plasma membrane and may be responsible for killing the cells by a mechanism of lysis from without.

Animals↗
PubMed1986

Malorientation and abnormal segregation of chromosomes during recovery from colcemid and nocodazole.

Reversal of meiotic arrest in crane-fly spermatocytes by U. V. irradiation of Colcemid-arrested cells or by rinsing Nocodazole-arrested cells in fresh buffer results in the induction of chromosome malorientation. Malorientations observed among Colcemid-recovering and Nocodazole-recovering spermatocytes at frequencies higher than normally observed in untreated cells included associations of sister kinetochores of half-bivalents with both spindle poles (amphitely), in contrast with associations of sisters with only one pole (syntely) as is usually found during the first meiotic division. In several cases, prior to anaphase onset, maloriented bivalents appeared unusually tilted with respect to the spindle axis, and during anaphase they gave rise to laggard half-bivalents that did not segregate during anaphase along with half-bivalents having proper syntelic orientation. The results parallel previous findings obtained during cold recovery, and the properties of the drugs used here suggest that their action on microtubules, although reversible, induces malorientation during recovery from meiotic arrest.

Animals↗