AIM: To establish whether d-limonene can protect against induction of cyclobutane pyrimidine dimers(CPDs) and sunburn in ultraviolet irradiation(UVR) irradiated mouse skin. METHODS: The d-limonene was given in 4 daily...AIM: To establish whether d-limonene can protect against induction of cyclobutane pyrimidine dimers(CPDs) and sunburn in ultraviolet irradiation(UVR) irradiated mouse skin. METHODS: The d-limonene was given in 4 daily oral 20 μL aliquots at different concentrations as follows: 100%, 10% or 1% in liponate and 100% liponate as control. One day after the final d-limonene treatment, the mice were anesthetized with i.p. sodium pentobarbital and placed in boxes to allow a rectangular(2 cm × 4 cm) region of dorsal skin to be irradiated with a single, ultraviolet radiation dose of 1.5 kJ /m2. Skin samples from UVR irradiated area were obtained at 5 min after UVR exposure for CPD detection, at 6 d after UVR exposure, skin samples were obtained for in situ analysis for N-myc downstream regulating gene 1(NDRG1)(a stress response gene), proliferating cell nuclear antigen(PCNA)(an S-phase marker) and filaggrin(a barrier integrity gene). Based on immunohistochemistry staining, the number of CPD, NDRG1 and PCNA positive cells, as well as unstained cells was counted in 3 different individually selected areas and percentage of positive cells was established. RESULTS: CPD reduction occurred as follows: liponate only-none; 1% d-limonene-54.3% reduction of CPDs; 10% d-limonene-73.4% reduction of CPDs; 100% d-limonene-86.1% reduction of CPDs, the latter equivalent to a UV dose of only 0.21 k J/m2. Sunburn was also dose-dependently reduced by d-limonene. The NDRG1 protein was strongly induced by UVR(70.0% ± 10.4% positive cells), but 1% d-limonene reduced the response to 64.6% ± 9.2%, 10% d-limonene reduced the response to 16.2% ± 3.4% and 100% d-limonene reduced the response to 6.3% ± 1.7%. Similarly, PCNA was 52.4% ± 9.9% positive in UVR exposed skin, and 1% d-limonene reduced it to 42.9% ± 8.1%, 10% d-limonene reduced it to 36.2% ± 6.7% and 100% d-limonene reduce it to 13.8% ± 3.4%. NDRG1 and PCNA were increased by d-limonene or UVR separately, but combined they produced less than either agent separately owing to the protective effect of pre-exposure to d-limonene. CONCLUSION: Overall d-limonene acted to protect against ultraviolet B-induced DNA photodamage and sunburn in UVR exposed skin.展开更多
Utilizing a pulse radiolysis equipment with time-resolved optical detector, kinetic processes of electron-induced splitting of cis-syn 1,3-dimethyluracil cyclobutane dimer (DMUD) in aqueous solution were investigated ...Utilizing a pulse radiolysis equipment with time-resolved optical detector, kinetic processes of electron-induced splitting of cis-syn 1,3-dimethyluracil cyclobutane dimer (DMUD) in aqueous solution were investigated in the presence or absence of riboflavin (RF) or flavin adenine dinucleotide (FAD). It has been observed that the cyclobutane pyrimidine dimer reacting with hydrated electron splits spontaneously to give a monomer and a monomer radical anion, and the anion transfers one electron to RF or FAD. From the buildup kinetics of radical species, the rate constants of electron transfer from the monomer radical anion to RF and FAD have been determined. On the basis of comparison of the interactions between DMUD and hydrated electron in the presence and absence of RF or FAD, a chain reaction process in the absence of RF or FAD has been demonstrated.展开更多
The oxidative splitting process of cis-syn 1,3-dimethyluracil cyclobutane dimer (DMUD) in aqueous solution was investigated using pulse radiolysis technique. The results indicated that DMUD can be splitted into 1,3-...The oxidative splitting process of cis-syn 1,3-dimethyluracil cyclobutane dimer (DMUD) in aqueous solution was investigated using pulse radiolysis technique. The results indicated that DMUD can be splitted into 1,3-dimethyluracil (DMU) by OH radicals (OH ·) and Br_2 radical anions (Br ·-_2), but not by azide radicals (N ·_3). The oxidative mechanisms that an H-abstracted from DMUD for OH · oxidative splitting and an electron transfer from DMUD to Br ·-_2, were suggested. Related kinetic parameters were determined.展开更多
DNA damage in the form of cyclobutane pyrimidine dimers(CPDs) and (6-4) photoproducts(6-4PPs) induced by UV-B radiation in Arabidopsis thaliana at different temperatures was investigated using ELISA with specific mono...DNA damage in the form of cyclobutane pyrimidine dimers(CPDs) and (6-4) photoproducts(6-4PPs) induced by UV-B radiation in Arabidopsis thaliana at different temperatures was investigated using ELISA with specific monoclonal antibodies. CPDs and 6-4PPs increased during 3 h UV-B exposure, but further exposure led to decreases. Contrary to the commonly accepted view that DNA damage induced by UV-B radiation is temperature-independent because of its photochemical nature, we found UV-B-induction of CPDs and 6-4PPs in Arabidopsis to be slower at a low than at a high temperature. Photorepair of CPDs at 24℃ was much faster than that at 0℃ and 12℃, with 50% CPDs removal during 1 h exposure to white light. Photorepair of 6-4PPs at 12℃ was very slow as compared with that at 24℃, and almost no removal of 6-4PPs was detected after 4 h exposure to white light at 0℃. There was evidence to suggest that temperature-dependent DNA damage and photorepair could have important ecological implications.展开更多
基金Supported by NCI Center Grant CA16087(NYU Kaplan Cancer)NIEHS Center Grant(Nelson Institute of the NYU Schoolof Medicine)Biokeys for Flavors,LLC,No.ES00260
文摘AIM: To establish whether d-limonene can protect against induction of cyclobutane pyrimidine dimers(CPDs) and sunburn in ultraviolet irradiation(UVR) irradiated mouse skin. METHODS: The d-limonene was given in 4 daily oral 20 μL aliquots at different concentrations as follows: 100%, 10% or 1% in liponate and 100% liponate as control. One day after the final d-limonene treatment, the mice were anesthetized with i.p. sodium pentobarbital and placed in boxes to allow a rectangular(2 cm × 4 cm) region of dorsal skin to be irradiated with a single, ultraviolet radiation dose of 1.5 kJ /m2. Skin samples from UVR irradiated area were obtained at 5 min after UVR exposure for CPD detection, at 6 d after UVR exposure, skin samples were obtained for in situ analysis for N-myc downstream regulating gene 1(NDRG1)(a stress response gene), proliferating cell nuclear antigen(PCNA)(an S-phase marker) and filaggrin(a barrier integrity gene). Based on immunohistochemistry staining, the number of CPD, NDRG1 and PCNA positive cells, as well as unstained cells was counted in 3 different individually selected areas and percentage of positive cells was established. RESULTS: CPD reduction occurred as follows: liponate only-none; 1% d-limonene-54.3% reduction of CPDs; 10% d-limonene-73.4% reduction of CPDs; 100% d-limonene-86.1% reduction of CPDs, the latter equivalent to a UV dose of only 0.21 k J/m2. Sunburn was also dose-dependently reduced by d-limonene. The NDRG1 protein was strongly induced by UVR(70.0% ± 10.4% positive cells), but 1% d-limonene reduced the response to 64.6% ± 9.2%, 10% d-limonene reduced the response to 16.2% ± 3.4% and 100% d-limonene reduced the response to 6.3% ± 1.7%. Similarly, PCNA was 52.4% ± 9.9% positive in UVR exposed skin, and 1% d-limonene reduced it to 42.9% ± 8.1%, 10% d-limonene reduced it to 36.2% ± 6.7% and 100% d-limonene reduce it to 13.8% ± 3.4%. NDRG1 and PCNA were increased by d-limonene or UVR separately, but combined they produced less than either agent separately owing to the protective effect of pre-exposure to d-limonene. CONCLUSION: Overall d-limonene acted to protect against ultraviolet B-induced DNA photodamage and sunburn in UVR exposed skin.
基金This work was supported by the National Natural Science Foundation of China(Grant No.30000036)Special Fund for Doctoral Program fromthe Ministry of Education of China and Foundation of University of Science and Technology of China.
文摘Utilizing a pulse radiolysis equipment with time-resolved optical detector, kinetic processes of electron-induced splitting of cis-syn 1,3-dimethyluracil cyclobutane dimer (DMUD) in aqueous solution were investigated in the presence or absence of riboflavin (RF) or flavin adenine dinucleotide (FAD). It has been observed that the cyclobutane pyrimidine dimer reacting with hydrated electron splits spontaneously to give a monomer and a monomer radical anion, and the anion transfers one electron to RF or FAD. From the buildup kinetics of radical species, the rate constants of electron transfer from the monomer radical anion to RF and FAD have been determined. On the basis of comparison of the interactions between DMUD and hydrated electron in the presence and absence of RF or FAD, a chain reaction process in the absence of RF or FAD has been demonstrated.
基金ProjectsupportedbytheNationalNaturalScienceFoundationofChina (No .30 0 0 0 0 36)andDoctoralProgrammefromtheStateEducationCom missionofChina .
文摘The oxidative splitting process of cis-syn 1,3-dimethyluracil cyclobutane dimer (DMUD) in aqueous solution was investigated using pulse radiolysis technique. The results indicated that DMUD can be splitted into 1,3-dimethyluracil (DMU) by OH radicals (OH ·) and Br_2 radical anions (Br ·-_2), but not by azide radicals (N ·_3). The oxidative mechanisms that an H-abstracted from DMUD for OH · oxidative splitting and an electron transfer from DMUD to Br ·-_2, were suggested. Related kinetic parameters were determined.
文摘DNA damage in the form of cyclobutane pyrimidine dimers(CPDs) and (6-4) photoproducts(6-4PPs) induced by UV-B radiation in Arabidopsis thaliana at different temperatures was investigated using ELISA with specific monoclonal antibodies. CPDs and 6-4PPs increased during 3 h UV-B exposure, but further exposure led to decreases. Contrary to the commonly accepted view that DNA damage induced by UV-B radiation is temperature-independent because of its photochemical nature, we found UV-B-induction of CPDs and 6-4PPs in Arabidopsis to be slower at a low than at a high temperature. Photorepair of CPDs at 24℃ was much faster than that at 0℃ and 12℃, with 50% CPDs removal during 1 h exposure to white light. Photorepair of 6-4PPs at 12℃ was very slow as compared with that at 24℃, and almost no removal of 6-4PPs was detected after 4 h exposure to white light at 0℃. There was evidence to suggest that temperature-dependent DNA damage and photorepair could have important ecological implications.
