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At least 19 recordsLinked to original sources

PubMed1991

Inhibition of cis-diammine-1,1-cyclobutane dicarboxylatoplatinum(II)-induced DNA interstand cross-link removal and potentiation of cis-diammine-1,1-cyclobutane dicarboxylatoplatinum(II) cytotoxicity by hydroxyurea and 1-beta-D-arabinofuranosylcytosine.

1-beta-D-Arabinofuranosylcytosine (ara-C) and hydroxyurea (HU) were investigated as potential DNA repair inhibitors with cis-diammine-1,1-cyclobutane dicarboxylatoplatinum(II) (CBDCA). HU plus ara-C, known inhibitors of DNA excision-repair, had previously been found to produce cytotoxic synergy and delayed removal of DNA interstrand cross-links with cis-diamminedichloroplatinum(II) (DDP). Since CBDCA and DDP share a common active intermediate, it should be possible to reproduce this interaction with CBDCA. However, the stable dicarboxylate chelate ring structure of CBDCA results in kinetics that differ significantly from those of DDP, due to slower hydrolysis to the active species. DNA adducts form more slowly, with interstand cross-links peaking approximately 12-h later and disappearing more gradually than in the case of DDP. It was therefore expected that a longer antimetabolite exposure might be required for repair inhibition with CBDCA. The 12-h exposure to HU plus ara-C previously found effective with DDP produced no cytotoxic synergy with a 2-h CBDCA exposure. Lengthening the antimetabolite treatment to 24 h resulted in approximately 1 log of synergistic toxicity, while a 24-h simultaneous exposure to HU, ara-C, and CBDCA resulted in 2 logs. Cells exposed to all three drugs showed a 2- to 3-fold greater level of interstrand cross-links after 36- to 48-h of incubation following drug removal, compared to CBDCA alone. Taken together, these findings suggest that HU plus ara-C modulates the repair of platinum-DNA adducts and establishes an effective in vitro schedule at clinically achievable concentrations for the use of those antimetabolites with CBDCA.

Animals↗

PubMed2004

The cyclobutane dimers of 5-methylcytosine and their deamination products.

The photochemical reactions of 5-methylcytosine (m(5)C), a minor component of mammalian DNA, have been studied at a concentration of 2 mM in frozen 10 mM aqueous NaCl solution at dry ice temperature (194.5 K). For these studies, low-pressure lamps emitting mainly UVB radiation were used. We have isolated and characterized three cyclobutane dimers, namely the cis-anti(c,a) the cis-syn(c,s) and the trans-syn(t,s) forms. While the c,a and the t,s cyclobutane dimers are relatively stable towards deamination upon standing in solution at 277 K, the c,s isomer is gradually converted into the corresponding c,s m(5)C-thymine (Thy) mixed dimer; this latter reaction occurs considerably faster at 310 K. The t,s cyclobutane dimer is converted into the corresponding m(5)C-Thy mixed dimer upon incubation at 373 K, while the c,a dimer is converted into a mixture of m(5)C and c,a mixed dimer when incubated at 310 K. Irradiation of equimolar mixtures of Thy (1 mM) and m(5)C (1 mM) under similar conditions yields each of the three m(5)C cyclobutane dimers, as well as significant amounts of c,a, c,s and t,s m(5)C-Thy mixed cyclobutane dimers. These m(5)C-Thy dimers undergo decompositions similar in nature to the processes undergone by m(5)C cyclobutane dimers. Pseudo-first order rate constants for deamination of the c,s m(5)C homodimer and c,s m(5)C-Thy heterodimer at various temperatures and at pH 7.7 have been measured and the enthalpies and entropies of activation have been evaluated for the deamination processes for these two compounds. The two dimers have half-lives of about 14 and 22 h, respectively, at 310 K; however, at 273 K, the corresponding half-lives can be evaluated as being around 30 and 36 days, respectively.

5-Methylcytosine↗

PubMed1992

Effect of intermolecular triplex formation on the yield of cyclobutane photodimers in DNA.

We have studied the effect of intermolecular triplexes formation on the yield of cyclobutane photodimers in DNA. DNA duplex within the pyrimidine-purine-pyrimidine triplex d(TC)nd(GA)nd(CT)n is protected from the formation of cyclobutane photodimers in the case of the stabilization of this triplex by acid pH, and in the case of supplementary stabilization by Mg2+ or Zn2+. We have studied pH-independent pyrimidine-purine-purine triplexes stabilized by bivalent cations. In such triplexes, the protection from the formation of [6-4] photodimers is observed, whereas the protection from cyclobutane dimer formation does not take place. The formation of the d(TC)nd(GA)nd(GA)n triplex leads to an inversion of the intensities of cyclobutane CT and TC photodimers. We observed a sharp decrease in photoreactivity with respect to cyclobutane dimers in the duplex tract d(C)18d(G)18 in the presence of Ba2+, Cd2+, Co2+, Mn2+, Zn2+ and Ni2+. The formation of the d(C)nd(G)nd(G)n triplex leads to 'antifootprinting', i.e. an increase in the yield of cyclobutane photodimers.

Base Sequence↗

PubMed1993

Heat-shock treatment selectively affects induction and repair of cyclobutane pyrimidine dimers in transcriptionally active genes in ultraviolet-irradiated human fibroblasts.

The effect of hyperthermia on induction and repair of UV-radiation-induced cyclobutane pyrimidine dimers was investigated in the genome overall and in transcriptionally active and inactive genes in confluent human fibroblasts. Hyperthermia treatment (30 min, 45 degrees C) of human fibroblasts resulted in an increase in the protein content of isolated nuclei (protein aggregation) similar to that observed for HeLa S3 cells. The faster rate of disaggregation of nuclear proteins and the higher survival rate of heated fibroblasts in comparison with those for HeLa cells provide further evidence for a possible role of protein aggregation in heat-induced cell killing. Determination of the frequencies of cyclobutane pyrimidine dimers in the genome overall and in restriction fragments of the active adenosine deaminase (ADA) gene and inactive 754 locus revealed that hyperthermia selectively inhibits the induction of cyclobutane pyrimidine dimers in transcriptionally active DNA. Removal of cyclobutane pyrimidine dimers from the ADA gene was strongly delayed during the first 8 h in 10 J/m2 UV-irradiated fibroblasts. Such inhibition of repair of cyclobutane pyrimidine dimers was not observed for the 754 gene, indicating that inhibition of repair by hyperthermia is generally not mediated by inactivation of repair enzymes. It is proposed that the inhibition of induction and repair of cyclobutane pyrimidine dimers in active genes by hyperthermia is related to the heat-induced aggregation of proteins with the nuclear matrix, proximal to which active genes are located. Our results are consistent with a functional compartmentalization of DNA repair at the nuclear matrix.

DNA Repair↗

PubMed1999

An NMR and conformational investigation of the trans-syn cyclobutane photodimers of dUpdT.

Both trans-syn cyclobutane-type photodimers of 2'-deoxyuridylyl (3'-5') thymidine (dUpdT) were formed by deamination of the corresponding trans-syn cyclobutane photodimers of 2'-deoxycytidylyl (3'-5') thymidine (dCpdT) and were examined by 1H-, 13C-, and 31P-nmr spectroscopy. One- and two-dimensional nmr experiments provided a nearly complete assignment of the 1H, 13C, and 31P resonances. Scalar and nuclear Overhauser effect contacts were used to determine the conformation of the deoxyribose rings, exocyclic bonds, cyclobutane rings, and glycosidic linkages. Isomer I (S-type class; CB-; SYN-ANTI) and isomer II (N-type class; CB+; ANTI-SYN) exhibit markedly different conformational features. 31P chemical shifts show that the relative flexibility is dUpdT > isomer II > isomer I. The conformations of these species are very similar to those of other previously examined trans-syn photodimers. Among bipyrimidine photodimers of a given diastereomeric form (i.e., trans-syn I or II), the nmr-derived conformational parameters are nearly invariant, regardless of base substitution pattern. This contrasts with the substituent-dependent variation of cyclobutane ring conformation observed by Kim et al. (Biopolymers, 1993, Vol. 33, pp. 713-721) for an analogous series of cis-syn photodimers. Steric crowding of cyclobutane ring substituents is offered as an explanation for the difference in substituent effects between the families of cis-syn and trans-syn photodimers.

Dinucleoside Phosphates↗

PubMed1997

Antigen structural requirements for recognition by a cyclobutane thymine dimer-specific monoclonal antibody.

A monoclonal antibody (TDM-2) specific to a UV-induced cyclobutane pyrimidine dimer (T[cis-syn]T) has previously been established; however,the immunization had used UV-irradiated calf-thymus DNA containing a heterogeneous mixture of photoproduct sites. We investigated here the structural requirements of antigen recognition by the antibody using chemically synthesized antigen analogs. TDM-2 bound with cis-syn,but not trans-syn thymine dimer,and could bind strongly with four nucleotide analogs in which the cis-syn pyrimidine dimer was located in the center. Antigen analogs containing abasic linkers at the 5'- or 3'-side of the cis-syn cyclobutane pyrimidine dimer were synthesized and tested for binding to TDM-2. The results indicated that TDM-2 recognizes not only the cyclobutane ring but also both the 5'- and 3'-side nucleosides of the cyclobutane dimer. Furthermore,it was proved that either the 5'- or 3'-side phosphate group at a cyclobutane dimer site was absolutely required for the affinity to TDM-2. The antibody showed a strong binding to single stranded DNA but indicated little binding to double stranded DNA.

Animals↗

PubMed1990

Formation of cyclobutane thymine dimers photosensitized by pyridopsoralens: a triplet-triplet energy transfer mechanism.

The 365 nm irradiation of thymine thin films in the presence of pyridopsoralens is shown to induce the formation of cyclobutane thymine dimers, in contrast to other compounds such as 8- and 5-methoxypsoralen. In order to elucidate the mechanism of such a photosensitized reaction, we have determined the energy of the lowest triplet state (T1) of these compounds, using phosphorescence spectroscopy and CNDO/S quantum chemistry calculations. The T1 energy values were found to be significantly higher for pyridopsoralens--up to 0.3 eV--than for 8- and 5-methoxypsoralen (approximately 2.8 eV), which are not able to photoinduce cyclobutane thymine dimers. The determination of the relative efficiency of cyclobutane thymine dimer formation was performed using chromatographic analysis. A good correlation was found between the energy of the T1 state of the psoralen derivatives and the related cyclobutane thymine dimer formation. Moreover, the photosensitized cyclobutane thymine dimer formation appeared to be temperature-dependent. Our results are consistent with a mechanism involving a triplet energy transfer from the pyridopsoralen to thymine.

Energy Transfer↗

PubMed1991

Simultaneous establishment of monoclonal antibodies specific for either cyclobutane pyrimidine dimer or (6-4)photoproduct from the same mouse immunized with ultraviolet-irradiated DNA.

Six new monoclonal antibodies (TDM-2, TDM-3, 64M-2, 64M-3, 64M-4 and 64M-5) specific for ultraviolet (UV) induced DNA damage have been established. In the antibody characterization experiments, two TDM antibodies were found to show a dose-dependent binding to UV-irradiated DNA (UV-DNA), decrease of binding to UV-DNA after cyclobutane pyrimidine dimer photoreactivation, binding to DNA containing cyclobutane thymine dimers, and unchanged binding to UV-DNA after photoisomerization of (6-4)photoproducts to Dewar photoproducts. These results indicated that the epitope of TDM monoclonal antibodies was the cyclobutane pyrimidine dimer in DNA. On the other hand, four 64M antibodies were found to show a dose-dependent binding to UV-DNA, unchanged binding to UV-DNA after cyclobutane pyrimidine dimer photoreactivation, undetectable binding to DNA containing thymine dimers, and decrease of binding to UV-DNA after photoisomerization of (6-4)photoproducts. These results indicated that the epitope of 64M antibodies was the (6-4)photoproduct in DNA. This is the first report of the simultaneous establishment of monoclonal antibodies against the two different types of photolesions from the same mouse. By using these monoclonal antibodies, we have succeeded in measuring both cyclobutane pyrimidine dimers and (6-4)photoproducts in the DNA from human primary cells irradiated with physiological UV doses.

Animals↗

PubMed1986

UV light-induced cyclobutane pyrimidine dimers are mutagenic in mammalian cells.

We used a simian virus 40-based shuttle vector plasmid, pZ189, to determine the role of pyrimidine cyclobutane dimers in UV light-induced mutagenesis in monkey cells. The vector DNA was UV irradiated and then introduced into monkey cells by transfection. After replication, vector DNA was recovered from the cells and tested for mutations in its supF suppressor tRNA marker gene by transformation of Escherichia coli carrying a nonsense mutation in the beta-galactosidase gene. When the irradiated vector was treated with E. coli photolyase prior to transfection, pyrimidine cyclobutane dimers were removed selectively. Removal of approximately 90% of the pyrimidine cyclobutane dimers increased the biological activity of the vector by 75% and reduced its mutation frequency by 80%. Sequence analysis of 72 mutants recovered indicated that there were significantly fewer tandem double-base changes and G X C----A X T transitions (particularly at CC sites) after photoreactivation of the DNA. UV-induced photoproducts remained (although at greatly reduced levels) at all pyr-pyr sites after photoreactivation, but there was a relative increase in photoproducts at CC and TC sites and a relative decrease at TT and CT sites, presumably due to a persistence of (6-4) photoproducts at some CC and TC sites. These observations are consistent with the fact that mutations were found after photoreactivation at many sites at which only cyclobutane dimers would be expected to occur. From these results we conclude that UV-induced pyrimidine cyclobutane dimers are mutagenic in DNA replicated in monkey cells.

Animals↗

PubMed1990

Immunoprecipitation of pyrimidine(6-4)pyrimidone photoproducts and cyclobutane pyrimidine dimers in uv-irradiated DNA.

Biological studies suggest that a significant proportion of the cytotoxicity observed in mammalian cells after uv irradiation may be due to damage other than cyclobutane dimers in DNA. Although pyrimidine-pyrimidone (6-4) photoproducts have been implicated as major contributors to cell lethality, their induction has been measured at considerably less than cyclobutane pyrimidine dimers when measured by chromatographic techniques. Because the yield of (6-4) photoproducts may be reduced by their lability to extreme heat and pH, we have advised an alternative, immunological quantification which does not require DNA hydrolysis. Affinity-purified rabbit antisera were used to precipitate low molecular weight 32P-labeled PM2 DNA irradiated with increasing fluences of uv light. DNA of known molecular weight was used to determine rates of induction for antibody-binding sites associated with (6-4) photoproducts and cyclobutane dimers. These rates were calculated to be 0.6 (6-4) photoproducts and 1.2 cyclobutane dimers/10(8) Da/J/m2. At low uv fluences (6-4) photoproducts were induced at one-half the rate of cyclobutane dimers, whereas at higher fluences (6-4) photoproducts predominated.

Animals↗

PubMed1992

Conformational variations of the cis-syn cyclobutane-type photodimer in DNA and RNA.

The recent NMR study of a cis-syn photodimer B-DNA 10mer-duplex (Taylor et al., Biochemistry 29, 8858 (1990)) showed the cyclobutane (CB) ring with a puckered-twist in a right-handed sense (CB+). This is opposite to that of the crystal structure of cis-syn d-TpT(cyano-ethyl)(d-T[p]T-CE) which has a left-handed puckered-twist (CB-)(Hruska et al., Biopolymers 25, 1399 (1986)). 2D-NOESY experiments were performed on cis-syn d-T[p]T and cis-syn U[p]U at 25 and 35 degrees C, respectively, to investigate the puckering mode of the cyclobutane ring of isolated cis-syn photodimers of the DNA and RNA types. The DNA photodimers showed interconversion of the puckered-twist of the cyclobutane ring between CB- and CB+ and interconversion of the glycosidic angle between syn and anti in both nucleoside residues. Interestingly, in the RNA photodimer only the CB- puckering mode with syn conformation of the glycosidic angle of the U[p]- was observed. These different dynamical behaviors of the photodimer in DNA and RNA might portend differential conformational effects on their corresponding normal nucleic acid regions. In addition these results indicate differences in the cyclobutane ring conformation of the cis-syn d-T[p]T, not only in solution and crystalline states, but also when the dimer is isolated and in duplex forms.

Cyclobutanes↗

PubMed1991

Evidence for defective repair of cyclobutane pyrimidine dimers with normal repair of other DNA photoproducts in a transcriptionally active gene transfected into Cockayne syndrome cells.

Cockayne syndrome (CS) and xeroderma pigmentosum (XP), autosomal recessive diseases with clinical and cellular hypersensitivity to UV radiation, differ in ability to repair UV DNA photoproducts in their overall genome: normal repair in CS, defective repair in XP. In order to characterize a DNA repair defect in an active gene in CS, we measured the capacity of cells from patients with CS and XP to reactivate 2 major types of UV-induced DNA damage, photoreactivatable (i.e., cyclobutane pyrimidine dimers) and non-photoreactivatable (primarily pyrimidine-(6-4)pyrimidone photoproducts), in the actively transcribing chloramphenicol acetyltransferase (cat) gene of the plasmid expression vector pRSV-cat. Epstein-Barr virus-transformed lymphoblast lines from 4 normal persons and from 3 patients with CS and from two with XP were transiently transfected with the plasmid, and the cat activity in cell extracts was determined. When the cells were transfected with UV-irradiated plasmid, expression was abnormally decreased in both the CS and XP cells. When the cyclobutane pyrimidine dimers in the UV-irradiated plasmid were removed by photoreactivation prior to transfection, cat expression in the CS, but not in the XP, lines reached normal levels. These data imply that both the XP and CS cells are unable to repair normally the cyclobutane pyrimidine dimer photoproducts which block transcription of cat. However, the CS, but not XP, cells can repair normally the other UV-induced photoproducts which block transcription. The ability of CS, but not XP, cells to repair these non-dimer photoproducts indicates that the active gene repair mechanism treats the cyclobutane pyrimidine dimer differently from the non-dimer photoproducts.

Cell Line↗

PubMed1995

Sensitive nonradioactive detection of UV-induced cyclobutane pyrimidine dimers in intact mammalian cells.

In this paper we present a sensitive procedure to determine specifically the induction as well as the removal of cyclobutane pyrimidine dimers in intact mammalian cells without radioactive labeling of the DNA. This technique allows the detection of DNA damage by UV doses as low as 0.1 J/m2. The method consists of gentle lysis of cell monolayers, high-salt treatment and incubation with the cyclobutane pyrimidine dimer-specific repair enzyme T4 endonuclease V, followed by alkaline unwinding, hydroxyapatite chromatography and fluorimetric DNA analysis. The number of T4 endonuclease V-sensitive sites correlates well with the amount of UV-induced cyclobutane pyrimidine dimers reported in the literature, indicating that these cyclobutane pyrimidine dimers are recognized quantitatively by the system. The assay is easily transferable to the detection of other types of DNA adducts by applying different damage-specific repair enzymes, providing a sensitive method to investigate the induction and the repair of DNA lesions without the use of radioactive labeling.

Alkalies↗

PubMed1994

Repair of 6-4 photoproducts and cyclobutane pyrimidine dimers in rad mutants of Saccharomyces cerevisiae.

Repair rates of both pyrimidine-pyrimidone (6-4) photoproducts and cyclobutane pyrimidine dimers have been measured in the UV-sensitive mutants of Saccharomyces cerevisiae: rad1 to rad12 and rad14 to rad24. A dot blot immunoassay for UV photoproducts was used which measures lesions in the genome as a whole and which distinguishes 6-4 photoproducts from cyclobutane dimers. The principal findings are: (1) Wild-type yeast cells, like normal mammalian cells, repair 6-4 photoproducts more rapidly than cyclobutane dimers. (2) All mutants that are defective in repair are defective in repair of both lesions. (3) The most sensitive alleles of rad1, rad2, rad3, rad4 and rad10 show no repair of either lesion. (4) Leaky alleles of rad1, rad3 and rad14 show a very marked difference in repair rates of the two lesions, rather like the human XPA revertant cell line XP129 and the Chinese hamster mutants UV61 and V-H1. (5) No mutant repairs cyclobutane dimers more rapidly than 6-4 photoproducts.

DNA Damage↗

PubMed2005

Ab initio study of cyclobutane: molecular structure, ring-puckering potential, and origin of the inversion barrier.

The structure and ring-puckering properties of cyclobutane and its perdeuterated isotopomer are studied using high-level ab initio methods and complete basis set extrapolations. Calculations reveal significant coupling between the ring-puckering (theta) and CH(2)-rocking (alpha) motions, with equilibrium angles (theta(eq) = 29.59 degrees and alpha(eq) = 5.67 degrees) that are within the range of experimentally determined values. Our best estimate of the inversion barrier is 482 cm(-1), in excellent agreement with recent experimental determinations. Ring-inversion transition frequencies are evaluated from the eigenstates of the intrinsic reaction coordinate potentials for cyclobutane and cyclobutane-d(8). Natural bond orbital analysis shows that sigma(CC) --> sigma(CH)* and sigma(CH) --> sigma(CH)* hyperconjugative interactions are strengthened as cyclobutane puckers, thereby suggesting that inversion barriers in four-membered ring systems are a consequence of electronic delocalization rather than torsional strain.

Journal Article↗

PubMed1993

Ultraviolet-induced mutations in Cockayne syndrome cells are primarily caused by cyclobutane dimer photoproducts while repair of other photoproducts is normal.

We compared the contribution to mutagenesis in Cockayne syndrome (CS) cells of the major class of UV photoproducts, the cyclobutane pyrimidine dimer, to that of other DNA photoproducts by using the mutagenesis shuttle vector pZ189. Lymphoblastoid cell lines from the DNA repair-deficient disorders CS and xeroderma pigmentosum (XP) and a normal line were transfected with UV-treated pZ189. Cyclobutane dimers were selectively removed before transfection by photoreactivation (PR), leaving nondimer photoproducts intact. After UV exposure and replication in CS and XP cells, plasmid survival was abnormally reduced and mutation frequency was abnormally elevated. After PR, plasmid survival increased and mutation frequency in CS cells decreased to normal levels but remained abnormal in XP cells. Sequence analysis of > 200 mutant plasmids showed that with CS cells a major mutational hot spot was caused by unrepaired cyclobutane dimers. These data indicate that with both CS and XP cyclobutane dimers are major photoproducts generating reduced plasmid survival and increased mutation frequency. However, unlike XP, CS cells are proficient in repair of nondimer photoproducts. Since XP but not CS patients have a high frequency of UV-induced skin cancers, our data suggest that prevention of UV-induce skin cancers is associated with proficient repair of nondimer photoproducts.

Base Sequence↗

PubMed1989

DNA damage and repair in normal, xeroderma pigmentosum and XP revertant cells analyzed by gel electrophoresis: excision of cyclobutane dimers from the whole genome is not necessary for cell survival.

Human fibroblasts were embedded in microscopic-sized agarose beads and lysed in situ to produce chromosome-sized DNA trapped inside the beads. Conventional alkaline agarose gel electrophoresis of trapped DNA from cells damaged by X-rays before embedding gave mol. wts similar to those obtained with alkaline sucrose gradients. When cells were irradiated with UV light before embedding in agarose and incubated with UV endonuclease to cleave cyclobutane pyrimidine dimer sites, UV damage was detectable by gel electrophoresis over a range of 2.6-52 J/m2 as a linear function of dose, and repair was detectable within 6 h of irradiation. Two independently derived UV-resistant xeroderma pigmentosum (XP) revertants did not remove cyclobutane dimers up to 48 h after irradiation. Incubation of normal and XP revertant cells with cytosine arabinoside after UV irradiation resulted in similar numbers of single-strand breaks; these breaks represent repair of non-dimer photoproducts. Evidently, excision of cyclobutane pyrimidine dimers from the whole genome is not necessary for survival of human cells after UV irradiation; rather, repair of non-dimer photoproducts such as photoproducts in the genome as a whole or cyclobutane dimers in a small number of genes may be more biologically important.

Cell Line↗

PubMed1998

Repair of cyclobutane pyrimidine dimers in unstimulated human mononuclear cells is deficient at very low fluences of ultraviolet B and is not enhanced by addition of deoxyribonucleosides.

Unstimulated human T lymphocytes are exquisitely sensitive to UVB irradiation. This hypersensitivity appears to relate to low deoxyribonucleotide pool sizes. They have also been reported to be defective in global excision of cyclobutane pyrimidine dimers, but such experiments may have been carried out at supralethal doses, where unrepaired excision breaks persist indefinitely. We use a T4 endonuclease Comet assay to show that removal of cyclobutane pyrimidine dimers is defective in the unstimulated mononuclear cell fraction (mainly T lymphocytes) even at sublethal fluences from an FS20 broad spectrum UVB lamp. Moreover, removal is not enhanced by addition of deoxyribonucleosides to the medium. Cells which are failing to remove cyclobutane pyrimidine dimers readily form fresh incision breaks in response to a second UVB fluence, indicating that they retain repair capacity and suggesting that removal of types of damage other than cyclobutane pyrimidine dimers is effective.

Adult↗