IMPACT OF UVB and 03 ON THE OXYGEN FREE RADICAL SCAVENGING SYSTEM IN Arabidopsis thaliana GENOTYPES DIFFERING IN FLAVONOID BIOSYNTHESIS

Abstract— The effect of UVB and ozone (O₃) on growth and ascorbate-glutathione cycle were investigated in Arabidopsis thaliana wild-type Landsberg erecta (LER) and its transparent testa ( tt 5) mutant differing in UVB sensitivity. Ultraviolet-B radiation decreased dry matter production of tt5, while the dry weight of LER remained unaltered. Ozone exposure decreased dry weight of both genotypes. Ultraviolet-B radiation decreased the F_v/F_m ratio in tt5 but not in LER plants, while O₃ exposure decreased the F_v/F_m ratio in both genotypes. Ultraviolet-B radiation enhanced total ascorbic acid, total glutathione and their redox state and superoxide dismutase and glutathione reductase activities in both genotypes and the increases were greater in tt5 compared to UVB-irradiated LER. Although O₃ exposure enhanced total ascorbic acid and total glutathione in both genotypes, the redox state was significantly higher in tt5. Ozone exposure enhanced superoxide dismutase and glutathione reductase activities in tt5 while there were no major changes in LER. These results suggested that (1) plants blocked in flavonoid biosynthesis are sensitive to UVB in spite of their ability to maintain efficient oxygen free radical scavenging systems and (2) plants sensitive to UVB are comparatively tolerant of O₃ compared to UVB-insensitive plants. The differential responses of plants are discussed with reference to their ability to maintain high redox states of ascorbate and glutathione.     

Ultraviolet Radiation Effects on a Microscopic Green Alga and the Protective Effects of Natural Dissolved Organic Matter

Abstract— The population and photosynthetic responses of a microscopic green alga ( Selenastrum capricornutum ) to realistic levels of UV radiation (UVA and UVB) were assessed in natural lake waters of different dissolved organic carbon (DOC) concentration. Specific growth rates and photosynthetic competence (as reflected by F_v/F_m [measure of maximal quantum efficiency of photosystem II] and t_1/2 [estimate of electrons transported to the plastoquinone pool] measured by in vivo variable chlorophyll a fluorescence) were compared between two exposure levels of UVR and two concentrations of DOC (2.5 mg C L⁻¹ 7.7 mg C L⁻¹). Exposure periods of 6–9 days (five to nine generations) were used. Exposure to UVA primarily affected the efficiency of photosystem II, as evidenced by significant decreases of F_v/F_m but not growth rates or t_1/2 Exposure to UVB, in the presence of UVA, did not cause significant additional decreases of F_v/F_m but did diminish growth rates. In the low DOC water, t_1/2 was also diminished, suggesting different proximate sites of action from those for UVA. The high DOC water decreased the effective exposure to both UVA and UVB and diminished the negative impact of UV radiation on the cells, but the apparent protection was not explicable solely by the shading action of the DOC. Control values for F_v/F_m, growth rates and t_1/2 were all lower in the high DOC water, suggesting a negative side effect to the apparent protective action of the DOC against UVB.     

Cell Cycle Kinetics Following UVA Irradiation in Comparison to UVB and UVC Irradiation

Abstract— There is limited information about the carcinogenic effect of longwave ultraviolet radiation (UVA: 315-400 nm). In particular very little is known about the relevant genotoxic damage caused by physiological doses of UVA radiation. A general response of cells to DNA damage is a delay or arrest of the cell cycle. Conversely, such cellular responses after UVA irradiation would indicate significant genotoxic damage. The aim of this study is to compare cell cycle kinetics of human fibroblasts after UVC (190-280 nm radiation), UVB (280-315 nm radiation) and UVA irradiation. Changes in the cell cycle kinetics were assessed by bivariate flow cytometric analysis of DNA synthesis and of DNA content. After UVC, UVB or UVA irradiation of human fibroblasts a suppression was seen of bromodeoxyuridine (BrdU) incorporation at all stages of S phase. The magnitude of this suppression appeared dose dependent. Maximum suppression was reached at 5-7 h after UVB exposure and directly after UVA exposure, and normal levels were reached 25 h after UVB and 7 h after UVA exposure. The lowered BrdU uptake corresponded with a lengthening of the S phase. No dramatic changes in percentages of cells in G₁, S and G₂/M were seen after the various UV irradiations. Apparently, UVA irradiation, like UVB and UVC irradiation, can temporarily inhibit DNA synthesis, which is indicative of genotoxic damage.     

Alterations in Skin Immune Response Throughout Chronic UVB Irradiation—Skin Cancer Development and Prevention by Naproxen

Skin exposure to UVB radiation has been reported to produce both a significant inflammatory response and marked immunosuppression. This work was aimed to evaluate whether the response of murine skin to an acute UVB dose was modified by pre-exposure to chronic UVB irradiation and by topical treatment with naproxen, a nonsteroidal anti-inflammatory drug. Moreover, the effect of naproxen on the incidence of UV-induced skin tumors was studied. Prostaglandin E₂ (PGE₂) and tumor necrosis factor alpha (TNF-α) levels were increased 96 h post-UVB in acutely irradiated animals and both mediators were modified by topical naproxen application—PGE₂ was decreased while TNF-α was increased. Such inflammatory response was suppressed when mice were chronically irradiated. Naproxen application on chronically irradiated mice reduced the incidence of tumor lesions. Taken together, our data suggest that chronic UVB irradiation generates an immunosuppressive state that prevents skin cells from responding normally to an acute irradiation challenge, thus impairing the protective effect of TNF-α against skin tumor development. Furthermore, reduction in the incidence of tumor lesions by naproxen may be due to its ability to increase TNF-α levels as well as to decrease PGE₂.     

TNO Institute of Environmental Sciences, Energy Research and Process Innovation, the Netherlands

Abstract— A radiative transfer model is used to study the effect of stratospheric ozone depletion and tropospheric pollution on UVB (280-315 nm) radiation in the troposphere at midiatitudes of the Northern Hemisphere. The difference in the vertical distribution of UVB radiation for a range of pollution conditions typical for remote clean and more polluted sites on cloudless summer days is shown. The changes in downward UVB irradiance, UVB actinic flux, DNA-weighted UV radiation and photodissociation frequency of ozone at the earth's surface are quantified in relation to stratospheric ozone depletion and typical ranges of tropospheric pollutants (ozone [O3], sulfur dioxide [SO₂] and aerosols) in nonurban polluted regions. The results show that near the earth's surface, in non-urban polluted regions, an increase of tropospheric pollution, which occurred over the last 50-100 years, has cancelled the effect of an increase of UVB radiation due to stratospheric ozone depletion that has occurred since the late 1970s. The results hold for summer conditions and the decrease of UVB radiation is most pronounced in the polluted boundary layer. At higher altitudes the effect of tropospheric pollution on UVB radiation is far less. Prior to 1970 it was mainly tropospheric pollution that altered UVB radiation at the surface of the earth. In addition, since the late 1970s enhanced UVB radiation reaching the top of the troposphere, due to stratospheric ozone depletion, also had an impact on UVB levels in the troposphere.     

HYDROGEN PEROXIDE MEDIATES UV-INDUCED IMPAIRMENT OF ANTIGEN PRESENTATION IN A MURINE EPIDERMAL-DERIVED DENDRITIC CELL LINE

Abstract— Ultraviolet-B (290–320 nm) radiation is known to impair the antigen-presenting cell (APC) function of Langerhans cells (LC), skin-specific members of the dendritic cell (DC) family. We sought to address mechanisms of this effect, focusing on the role played by hydrogen peroxide. For this purpose, we used a newly established murine DC line, XS52, which resembles epidermal LC in several respects. The APC capacity of XS52 cells, using two different CD4* T cell clones as responders, was inhibited significantly (>50%) by exposure to UV radiation (unfiltered FS20 sunlamps) at relatively small fluences (50–100 J/m²). Ultraviolet radiation also inhibited growth factor-dependent proliferation of XS52 cells. On the other hand, cell surface phenotype was relatively well preserved after irradiation; expression levels of B7-1 and B7-2 were reduced slightly, while other molecules ( e.g. Ia, CD54, CD1 la and CD18) were not affected. With respect to the role played by hydrogen peroxide, pretreatment with purified catalase (900 U/mL) prevented UV-induced inhibition of APC function. Short-term exposure to 3 miM H₂0₂ or f-butyl H₂0₂ mimicked UV radiation by inhibiting APC function. Finally, intrinsic catalase activity was substantially lower in XS52 cells compared with Pam 212 keratinocytes. These results indicate that the generation of hydrogen peroxide alone is sufficient to produce some, but not all, of the deleterious effects of UV radiation on DC derived from the skin.     

Solar UVB Dosimetry by Amplification of Short and Long Segments in Phage LD DNA

Abstract— DNA UVB dosimeters, consisting of minidots of dried bacteriophage DNA placed on a UV-transparent polymer film, were analyzed by polymerase chain reactions (PCR). Ultraviolet-B dosimetry obtained with amplification of phage LD DNA of segments of 1.08 kilobase pairs (kbp) and 2.24 kbp was compared with that obtained with amplification of a 0.5 kbp segment (H. Yoshida and J. D. Regan, 66, 82-88, Photochem. Photobiol 1997). The number of lesions in each segment induced by UV radiation is proportional to the size of the amplified segments; thus, the average lesion frequency per unit dose was greatest in the 2.24 kbp and least in the 0.5 kbp segment. The average lesion frequency per unit dose was 3.5 times 10_-2 and 11.9 times 10_-2 m₂ kJ_-1 for 1.08 kbp and 2.24 kpb, respectively, compared to that for 0.5 kbp of 1.7 times 10_-2 m₂ kJ_-1 at 50 ng DNA. Dependability of DNA dosimeters, containing 50 ng and 100 ng, was tested by placing the DNA dosimeters for a time period of either 1 or 2 days outdoors on 8-12 January at Melbourne, FL. The daily dose was obtained directly with amplification of the 2.24 kbp segment and the 2 day continuous dose was obtained with amplification of the 1.08 kbp segment. Although the average lesion frequencies were different, both 50 ng and 100 ng DNA dosimeters provided about the same UVB dose, equivalent to the dose applied with a solar UVB simulator. The total UVB dose for 4 days obtained by amplification of the 1.08 and 2.24 kbp segments was 19.4-20.8 kJ m_-2, which is within experimental error with the 4 day continuous dose obtained with 0.5 kbp segments. The average daily dose obtained by 0.5 kbp and 1.08 kbp agreed with the average daily dose directly obtained with 2.24 kbp.     

THE EFFECTS OF LIQUID HOLDING ON NEAR-UV(300–400 nm) IRRADIATED ESCHERICHIA COLI STRAINS DIFFERING IN NEAR AND FAR-UV RADIATION SENSITIVITY

Abstract— Stationary phase cells from four Escherichia coli strains differing in near- (nur vs. nur ₊) and far-UV (recAl vs. recA₊) radiation sensitivity were subjected to near-UV radiation (NUV) in 0.85% saline. Although the NUV-irradiated cultures yielded increased colony numbers following 24 h of liquid holding (LH), a fluctuation test for each experiment showed that the observed increases were not due to recovery but were in fact due to cell multiplication. The decline in viability observed after NUV with liquid holding using the fluctuation test was equivalent in strains RT2, 3 and 4 while the decline observed with RT1 was less marked. The discrepancy between LH involving cell densities of 10₈-10₉ and 1–4 cells/m/ can be resolved by assuming that with dense cell suspensions, NUV-induced membrane damage leads to leakage or lysis, supplying sufficient nutrients to allow growth of undamaged, surviving cells.     

Effect of UVB Radiation on Utilization of Inorganic Nitrogen by Antarctic Microalgae

Abstract— The impact of UVB (280-315 nm) radiation (WG 305) on uptake of ¹⁵N-ammonium and ¹⁵N-nitrate of marine phytoplankton from station 219 (47°W, 61.5°S) and sea ice-algae from station 265 (22.6°W, 73.29°S) was studied during the Polarstern Cruise (EPOS III, Leg 3) to the Weddell Sea, Antarctica 1989. Uptake rates of ¹⁵NH₄⁺ were higher and more affected by UVB radiation than those of ¹⁵N0₃-. Pool sizes of the main amino acids changed in response to the used inorganic nitrogen source and UV exposure. Pools of glutamine, serine and glycine decreased, whereas those of alanine, asparagine and glutamate increased after UVB irradiation. The ¹⁵N-incorporation into the amino acids was reduced as a result of UVB exposure of phytoplankton and ice algae. Results are discussed with reference to an inhibitory effect on the enzymes of both carbon and nitrogen metabolism as well as to adaptation strategies.     

Alternation in Photosynthetic Characteristics of Anabaena doliolum Following Exposure to UVB and Pb

Abstract— Anabaena doliolum , when exposed to either ultraviolet-B (UVB) radiation or Pb, showed reduced growth rate, carbon fixation, O₂-evolution, photosynthetic electron transport activity and ATP pool size. The rate of respiration was found to increase in UVB-treated cells; this increase was more pronounced in the cells exposed to UVB and Pb simultaneously. The UVB-induced inhibition of 2,6-dichlorophenol indophenol (DCPIP) photoreduction and lowering of chlorophyll a fluorescence could not be reversed by artificial electron donors (diphenyl carbazide, NH₂OH and MnCl₂). These electron donors, however, substantially reversed the inhibition caused by Pb, thereby suggesting that UVB primarily inhibits the photosys-tem II (PS II) reaction center and Pb arrests the electron flow at the water splitting site. Nevertheless, the suppressed fluorescence intensity and the reduced emission and excitation peaks of phycobilisomes indicate the involvement of Pb in inhibition of PS II. All combinations of UVB and Pb inhibited the different metabolic processes in a synergistic manner.     

Cis-UROCANIC ACID SYNERGIZES WITH HISTAMINE FOR INCREASED PGE2 PRODUCTION BY HUMAN KERATINOCYTES: LINK TO INDOMETHACIN-INHIBITABLE UVB-INDUCED IMMUNOSUPPRESSION

Abstract— There is considerable evidence that suppression of the immune system by UVB (280–320 nm UV) irradiation is initiated by UVB-dependent isomerization of a specific skin photoreceptor, urocanic acid (UCA), from the trans to the cis form. Previous studies have confirmed that cis -UCA administration to mice 3–5 days prior to hapten sensitization at a distant site, suppresses the contact hypersensitivity (CHS) response upon challenge. This study demonstrates in mice that cis -UCA, like UVB, suppresses CHS to trinitrochlorobenzene by a mechanism partly dependent on prostanoid production. In vitro experimentation showed that human keratinocytes, isolated from neonatal foreskin, increased prostaglandin E₂ (PGE₂) production in response to histamine but not UCA alone. However, cis -UCA synergized with histamine for increased PGE₂ production by keratinocytes. cis -urocanic acid also increased the sensitivity of keratinocytes for PGE₂ production in response to histamine. Prostaglandin E₂ from keratinocytes exposed to cis -UCA and histamine may contribute directly, or indirectly, to the regulation of CHS responses by UVB irradiation.     

Amplified Degradation of Photosystem II D1 and D2 Proteins under a Mixture of Photosynthetically Active Radiation and UVB Radiation: Dependence on Redox Status of Photosystem II

Abstract— Plants exposed to a mixture of photosynthetically active radiation (PAR) and UVB radiation exhibit a marked boost in degradation of the D1 and D2 photosysteni II (PS II) reaction center proteins beyond that predicted by the sum of rates in PAR and UVB alone (amplified degradation). Becausee degradation driven by visible or UVB radiation alone is uncoupled from PS II redox status, it was therefore assumed that the mixed-light-amplified component of degradation would behave similarly. Surprisingly, amplified degradation proved to be coupled tightly to the redox status of PS II. We show that inactivation of the PS II water oxidation by heat shock or oxidation of the plastosemiquinone (Q_A-) by silicomolybdate nullifies only the amplified component of degradation but not the basic rates of degradation under PAR or UVB alone. The data are interpreted to indicate that formation of plastosemiquinone or an active water-oxidizing Mn₄ cluster, is the UVB chromophore involved in amplified degradation of the D1 and D2 proteins. Furthermore, accumulation of Q_A-by 3-(3,4-dichlorophenyl)-1,1-dimethylurea or 2-bromo-3-methyl-6-isopropyl-4-nitrophenol stimulated the mixed-light-amplified degradation component. Thus, amplified degradation of the D1 and D2 proteins in mixed radiance of PAR plus UVB (which simulates naturally occurring radiance) proceeds by a mechanism clearly distinct from that involved in degradation under PAR or UVB alone.     

CHANGES IN TRANSMISSION CHARACTERISTICS OF POLYMETHYLMETHACRYLATE AND CELLULOSE (III) ACETATE DURING EXPOSURE TO ULTRAVIOLET LIGHT

Abstract— Ultraviolet-transparent polymethylmethacrylate (PMMA) and cellulose (III) acetate (CA) (often used as a cut-off filter in UVB [280–320 nm] biological effect studies) were exposed to a 20 W Philips TL 12 lamp to examine changes in transmission characteristics due to UVB exposure. Transmission of UVB and biologically weighted UVB (UV_BE(DNA)) through PMMA were similar, 88.3 and 83.5%, respectively. The absorption characteristics of PMMA did not change with time at any of the UV irradiance levels applied. However, transmission of UVB and UVB_BE(DNA)) through new CA differed considerably: 59% versus only 11%, respectively. Also, spectral absorption characteristics changed with time due to degradation of CA, at a rate that was dependent on the incident UVB irradiance. The decrease in transmission through CA of both UVB and UV_BE(DNA) can be described by exponential functions. The CA that was wrapped around the UV lamp showed dramatic changes in UV absorption over the first few hours of use. However, when CA was placed at a longer distance from the light source initial degradation was less. It is concluded that PMMA can be applied in UV effect studies as a reasonable alternative for quartz. The CA should, however, be used with care, because the large transmission decreases that were observed strongly hamper an accurate calculation of (biologically weighted) UVB dose rates.     

THE EFFECT OF THE ANTIPSORIATIC DRUG METABOLITE ETRETIN (Ro 10-1670) ON UVB IRRADIATION INDUCED CHANGES IN THE METABOLISM OF ARACHIDONIC ACID IN HUMAN KERATINOCYTES IN CULTURE

[¹⁴C]Arachidonic acid was avidly incorporated into human keratinocytes in culture and following exposure to UVB irradiation of 9 mJ/cm² (erythemally effective, EE) substantial amounts of ¹⁴C-radiolabel were released from the cells. The release of radiolabel was accompanied by a decrease in the labelling of phosphatidylethanolamine whereas the labelling of triacylglycerols and cholesteryl esters was increased. Keratinocytes produced significant amounts of prostaglandin E₂ (PGE₂) and following UVB irradiation of 9 mJ/cm² (EE) the formation of prostaglandin E₂ was increased.
Etretin (Ro 10-1670), the active metabolite of the antipsoriatic drug etretinate (Ro 10-9359), affected significantly neither the total release of radiolabel induced by UVB nor the formation of prostaglandin E₂. However, in the presence of etretin the UVB irradiation induced transfer of [^l4C]arachidonic acid into triacylglycerols and cholesteryl esters was not increased as much as in the corresponding experiments without etretin. On the basis of the present study it appears that etretin does not interfere with the release of arachidonic acid in amounts which could be related to the therapeutic effects of the combination of retinoids with UVB irradiation (Re-UVB) in the treatment of psoriasis.     

THE ACTION OF ULTRAVIOLET RADIATION ON THE CELL PROLIFERATION OF TWO-CELL MOUSE EMBRYOS

Abstract— The two-cell mouse embryo has a unique cell cycle of a short DNA synthesis (S) phase and an extremely long post-DNA synthesis (G₂) phase. An attempt was made to investigate the radiation biology of the long G₂ phase using UV radiation as a probe. Two cell mouse embryos, at various positions in the cell cycle, were UV-irradiated in phosphate-buffered saline. The embryos were cultured for a few hours to 3 days to assay for their cell proliferative characteristics. The embryos were most sensitive to the killing action of UV radiation in the late G₂ phase. The embryos divided more than two times after low UV fluences before dying and experienced G₂ phase delays.
These results can be contrasted to the situation in somatic cells, in which the action of UV radiation is S phase selective. One possibility is that the target for the action of UV radiation is different in two-cell mouse embryos from that in somatic cells and that the target is similar to that for X-ray effects.     

NON-NUCLEAR DAMAGE AND CELL LYSIS ARE INDUCED BY UVA, BUT NOT UVB OR UVC, RADIATION IN THREE STRAINS OF L5178Y CELLS

The potential to induce non-nuclear changes in mammalian cells has been examined for (1) UVA1 radiation (340–400 nm, UVASUN 2000 lamp), (2) UVA + UVB (peak at 313 nm) radiation (FS20 lamp), and (3) UVC (254 nm) radiation (GI5T8 lamp). The effects of irradiation were monitored in vitro using three strains of L5178Y (LY) mouse lymphoma cells that markedly differ in sensitivity to UV radiation. Comparisons were made for the effects of approximately equitoxic fluences that reduced cell survival to 1–15%. Depending on the cell strain, the fluences ranged from 830 to 1600 kJ/m² for the UVASUN lamp, 75 to 390 J/m² for the FS20 lamp and 3.8 to 17.2 J/m² for the G15T8 lamp. At the exposure level used in this study, irradiation with the UVASUN, but not the FS20 or G15T8, lamp induced a variety of non-nuclear changes including damage to cytoplasmic organelles and increased plasma membrane permeability and cell lysis. Cell lysis and membrane permeabilization were induced by the UVA1 emission of the UVASUN lamp, but not by its visible + IR components (>400 nm). The results show that the plasma membrane and other organelles of LY cells are highly sensitive to UVA1 but not to UVB or UVC radiation. Also UVA1, but not UVB or UVC radiation, causes rapid and extensive lysis of LY cells. In conclusion, non-nuclear damage contributes substantially to UVA cytotoxicity in all three strains of LY cells.     

THE EFFECT OF CHRONIC LOW-DOSE UVB RADIATION ON LANGERHANS CELLS, SUNBURN CELLS, UROCANIC ACID ISOMERS, CONTACT HYPERSENSITIVITY and SERUM IMMUNOGLOBULINS IN MICE

Abstract— C3H mice were irradiated three times a week for up to 6 weeks with either 500 J/m² or 1000 J/m² broadband UVB (270–350 nm) or 3000 J/m² narrowband UVB (311–312 nm; TL01 source). Each dose was suberythemal to the mouse strain used. The number of Langerhans cells (LC) in the epidermis was reduced by over 50% after 2 weeks of irradiation with the UVB source and by 20% following TL01 irradiation. Continued irradiation for up to 6 weeks resulted in no further decrease in LC numbers in the case of the UVB source but a steady decline to 40% in the case of the TL01 source. Sunburn cells were detected following irradiation with both sources but the numbers were very low in comparison with acute exposure. Ultraviolet-B exposure resulted in doubling of the thickness of the epidermis throughout the 6 weeks of irradiation while TL01 exposure did not alter epidermal thickness. Conversion of trans- to ew-urocanic acid (UCA) was observed with both UVB and TL01 sources. The percentage of cis -UCA started to return to normal after 4 weeks of TL01 exposure despite continued irradiation. As observed following a single exposure, the contact hypersensitivity (CH) response was significantly reduced following 6 weeks of UVB irradiation but was unaffected by TL01 exposure, indicating no correlation between cis -UCA levels and CH response. Total serum immunoglobulin levels remained unchanged throughout the 6 weeks of UVB or TL01 irradiation but IgE titers significantly increased in all cases in the first 2 weeks of irradiation, indicating a possible shift to a T_H2 cytokine profile. The IgE levels started to return to normal at later times. Thus chronic broadband UVB exposure induces a number of cutaneous and systemic responses that are likely to be dose dependent, while chronic TL0I exposure induces only some of the these responses.     

PROTECTION OF Ustilago violacea FROM TOLUIDINE BLUE PHOTOSENSITIZATION and HYDROGEN PEROXIDE INDUCED KILLING and MITOTIC RECOMBINATION BY CAROTENES

Abstract— The accumulation of (J-carotene in the ph/ph ⁺ y diploid strain of the smut fungus Ustilago violacea was associated with reduced killing and lower levels of induced mitotic recombination compared to the β-carotene lacking ph/ph⁺ w strain in response to both incandescent photosensitization and treatment with H₂0₂. The ph/ph⁺ y strain was only slightly more resistant to killing by exogenous toluidine blue (TB) photosensitization. The ph/ph⁺ y strain exhibited significantly greater levels of survival when exposed to incandescent radiation and 1.5 μ.M TB for 15 min, as well as 3.0. 0.3, 0.03, 0.003% H₂0₂ in the dark. The ph/ph⁺ y strain also exhibited lower levels of mitotic recombination after endogenous TB photosensitization and the latter two H₂0₂ treatments. Similar survival results were obtained for the carotene accumulating haploid strain l.C2y and the carotene lacking haploid strain l.C2iv in response to H₂0₂ exposure.     

ALTERATIONS OF PROTEOGLYCANS IN ULTRAVIOLET-IRRADIATED SKIN

Abstract— The effect of UVB exposure on the distribution and synthesis of dermal proteoglycans was measured in the skin of hairless mice. Two groups of mice were included: one was irradiated for 10 weeks; the other was kept as control. After intraperitoneal injection of sodium ³⁵S-sulfate, punch biopsies were taken for histology and proteoglycans were extracted from the remaining skin with 4 M guanidinium chloride, containing 3–[(3-cholamidopropyl)dimethylammonio]-1-propanesulfonate (0.5%, weight per volume). Following proteolytic digestion, the glycosaminoglycan constituents were isolated and analyzed by quantitative cellulose acetate electrophoresis and enzymatic digestibility.
Under the influence of UVB radiation, newly synthesized proteoglycans measured by ³⁵SO₄ uptake increased as much as 60%. In addition, the irradiated skin had a higher average content of proteoglycan than had control skin (4981 μg vs 4134 μg/g dry weight). This could be ascribed to an increase in heparin (1400 vs 533 μ g/g dry weight) and heparan sulfate (472 vs 367 μg/g dry weight), whereas no change in the concentration of hyaluronic acid (1243 vs 1372 μg/g dry weight) and dermatan sulfate (1866 vs 1863 μg/g dry weight) was observed. The irradiated animals also exhibited a marked increase in the synthesis of heparan sulfate and heparin (62% and 71%, respectively). These results demonstrate that chronic doses of UVB altered proteoglycan metabolism through both quantitative and qualitative changes.     

THE REACTION OF METHYLENE WITH HYDROGEN

Abstract— An investigation has been made of the reaction between methylene, formed by the photolysis of ketene, and hydrogen. Ethane, ethylene and methane are the major hydrocarbon products, and it has been shown that the formation of these products may be adequately described by the sequence of processes
CH₂CO + hv → CH₂+ CO (1)
CH₂+ H₂→ CH₃+H (2)
2CH₃→ C₂H₆ (3)
CH₃+ H₂+ CH₄+ H (4)
CH₂+ CH₂CO → C₂H₄+ CO (7)
In particular, the relative rates of ethane and methane formation are consistent with the known rate constants for reactions (3) and (4), and it is not therefore necessary to postulate the participation of an 'insertion' process
CH₂+ H₂→ CH₄ (6) to account for the formation of methane.
Decrease of the energy possessed by the methylene, either by increase of the wavelength of ketene photolysis, or by increase of gas pressure, is shown to result in an increase in the reactivity of the methylene towards ketene relative to its reactivity towards hydrogen (i.e. the ratio k₂/k₂ increases).