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PubMed1999

Effects of a soy milk supplement on plasma cholesterol levels and oxidative DNA damage in men--a pilot study.

BACKGROUND: Phytoestrogens are a major component of Asian diets and may be protective against certain hormone-dependent cancers (breast and prostate) and coronary heart disease. They may also have antioxidant function in scavenging potentially harmful free radicals and thus decreasing oxidative attack on DNA. AIMS OF THE STUDY: A pilot study to determine the effects of a phytoestrogen supplement, in the form of soy milk, on plasma LDL and HDL cholesterol levels and DNA damage in men. METHODS: Ten healthy men participated in the study and were assigned to one of three groups consuming 1 litre of either soy milk, rice dream (vegetable protein control) or semi-skimmed cow's milk (animal protein control) each day for 4 weeks. RESULTS: The soy supplement caused significant increases in plasma genistein and daidzein concentrations despite considerable inter-individual variation (P < 0.001). Supplementation with soy resulted in a decrease in oxidative damage to DNA bases detected using the comet assay compared with controls (P < 0.05). However, there was no significant effect of the soy supplement on plasma cholesterol or triglyceride levels in comparison with control groups. CONCLUSIONS: A 4 week soy milk supplementation in healthy volunteers does not alter serum cholesterol levels but can have a protective effect against oxidative DNA damage in lymphocytes.

Adult↗
PubMed2003

Analysis of 8-hydroxydeoxyguanosine 5'-monophosphate (8-OH-dGMP) as a reliable marker of cellular oxidative DNA damage after gamma-irradiation.

In order to improve 8-hydroxyguanine (8-OH-Gua) detection in DNA, we digested isolated DNA with nuclease P1 and analyzed for 8-hydroxydeoxyguanosine 5'-monophosphate (8-OH-dGMP) using a high-performance liquid chromatography system equipped with an electrochemical detector (HPLC-ECD). The amount of 8-OH-Gua in the DNA was expressed as the ratio of 8-OH-dGMP to deoxycytidine monophosphate (dCMP). Using this analysis, the background level of 8-OH-Gua in DNA from human lung carcinoma cells (A549) was several-fold lower than that obtained by a previous method. A549 cells were exposed to 20-60 Gy of gamma-radiation and an increase in 8-OH-Gua concentration was observed with increasing gamma-ray dose (0.3 residues per 10(7) dCMP per Gy). Moreover, by an immunohistochemical procedure using a commercial FITC-kit, 8-OH-Gua was clearly detected in A549 cells and the fluorescence intensity of cells with oxidative DNA damage increased with the doses of gamma-irradiation. Using an endonuclease nicking assay, we also found that gamma-rays decreased 8-OH-Gua repair activity. The results indicate that 8-OH-dGMP is a useful and sensitive marker for estimating oxidative damage in DNA.

Biomarkers↗
PubMed1996

Oxidative DNA damage through long-range electron transfer.

The possibility has been considered for almost forty years that the DNA double helix, which contains a pi-stacked array of heterocyclic base pairs, could be a suitable medium for the migration of charge over long molecular distances. This notion of high charge mobility is a critical consideration with respect to DNA damage. We have previously found that the DNA double helix can serve as a molecular bridge for photo-induced electron transfer between metallointercalators, with fast rates (> or = 10(10)s-1) and with quenching over a long distance (>40 A). Here we use a metallointercalator to introduce a photoexcited hole into the DNA pi-stack at a specific site in order to evaluate oxidative damage to DNA from a distance. Oligomeric DNA duplexes were prepared with a rhodium intercalator covalently attached to one end and separated spatially from 5'-GG-3' doublet sites of oxidation. Rhodium-induced photo-oxidation occurs specifically at the 5'-G in the 5'-GG-3' doublets and is observed up to 37 A away from the site of rhodium intercalation. We find that the yield of oxidative damage depends sensitively upon oxidation potential and pi-stacking, but not on distance. These results demonstrate directly that oxidative damage to DNA may be promoted from a remote site as a result of hole migration through the DNA pi-stack.

Base Sequence↗
PubMed1990

Oxidative damage to DNA during aging: 8-hydroxy-2'-deoxyguanosine in rat organ DNA and urine.

Oxidative damage to DNA is shown to be extensive and could be a major cause of the physiological changes associated with aging and the degenerative diseases related to aging such as cancer. The oxidized nucleoside, 8-hydroxy-2'-deoxyguanosine (oh8dG), one of the approximately 20 known oxidative DNA damage products, has been measured in DNA isolated from various organs of Fischer 344 rats of different ages. oh8dG was present in the DNA isolated from all the organs studied: liver, brain, kidney, intestine, and testes. Steady-state levels of oh8dG ranged from 8 to 73 residues per 10(6) deoxyguanosine residues or 0.2-2.0 x 10(5) residues per cell. Levels of oh8dG in DNA increased with age in liver, kidney, and intestine but remained unchanged in brain and testes. The urinary excretion of oh8dG, which presumably reflects its repair from DNA by nuclease activity, decreased with age from 481 to 165 pmol per kg of body weight per day for urine obtained from 2-month- and 25-month-old rats, respectively. 8-Hydroxyguanine, the proposed repair product of a glycosylase activity, was also assayed in the urine. We estimate approximately 9 x 10(4) oxidative hits to DNA per cell per day in the rat. The results suggest that the age-dependent accumulation of oh8dG residues observed in DNA from liver, kidney, and intestine is principally due to the slow loss of DNA nuclease activity; however, an increase in the rate of oxidative DNA damage cannot be ruled out.

8-Hydroxy-2'-Deoxyguanosine↗
PubMed2001

Polyphosphate accumulation and oxidative DNA damage in superoxide dismutase-deficient Escherichia coli.

Inorganic polyphosphate is a ubiquitous, linear polymer of phosphate residues linked by high-energy phosphoanhydride bonds. In response to starvation, polyP levels are increased up to 100-fold. It has been proposed that chelation of transition metals by polyP might reduce their toxicity, and that polyP accumulation is vital for survival in stationary phase. SOD-deficient E. coli is unable to survive in stationary phase. We found that deletion of the cytoplasmic SODs does not impair the cell's capability of synthesizing polyP. However, transient accumulation of polyphosphate correlated with increased resistance to H(2)O(2) and protection of DNA against oxidative damage. The reason for this protective effect of polyP is the induction of HPII catalase and DNA repair enzymes as members of the rpoS regulon. PolyP did not directly protect DNA against oxidative damage in vitro and acted as a pro-oxidant by stimulating the production of hydroxyl radical in the Fenton reaction. It is thus suggested that accumulation of poly P and rpoS induction cannot compensate for the lack of cytosolic SODs for survival in stationary phase.

Cyanides↗
PubMed1997

Determination of 8-hydroxy-deoxyguanosine formation in rat organs: assessment of paraquat-evoked oxidative DNA damage.

Paraquat has previously been shown to cause the oxidative damage to DNA in variety of cells and tissues. However, although paraquat-evoked strand breaks has been extensively studied to assess the DNA damage, the effect of paraquat on base modifications, another marker for the oxidative damage, has not yet been investigated. To further characterize paraquat-evoked DNA damage, the effect of paraquat on 8-hydroxy-deoxyguanosine (8-OH-dG) formation in various rat organs was examined. Paraquat markedly increased 8-OH-dG contents in various organs, particularly in brain, lung and heart, and this increase reached the maximum levels at 5 days after the drug administration. In contrast, the formation of 8-hydroxy-guanosine (8-OH-G), a marker for the oxidative damage to RNA, was not significantly affected by paraquat. These results indicate that paraquat causes base modifications as well as strand breaks as a consequence of the oxidative damage to DNA.

8-Hydroxy-2'-Deoxyguanosine↗
PubMed1999

Free radical-mediated oxidative DNA damage in the mechanism of thalidomide teratogenicity.

The sedative drug thalidomide ([+]-alpha-phthalimidoglutarimide), once abandoned for causing birth defects in humans, has found new therapeutic license in leprosy and other diseases, with renewed teratological consequences. Although the mechanism of teratogenesis and determinants of risk remain unclear, related teratogenic xenobiotics are bioactivated by embryonic prostaglandin H synthase (PHS) to a free-radical intermediates that produce reactive oxygen species (ROS), which cause oxidative damage to DNA and other cellular macromolecules. Similarly, thalidomide is bioactivated by horseradish peroxidase, and oxidizes DNA and glutathione, indicating free radical-mediated oxidative stress. Furthermore, thalidomide teratogenicity in rabbits is reduced by the PHS inhibitor acetylsalicylic acid, indicating PHS-catalyzed bioactivation. Here, we show in rabbits that thalidomide initiates embryonic DNA oxidation and teratogenicity, both of which are abolished by pre-treatment with the free radical spin trapping agent alpha-phenyl-N-t-butylnitrone (PBN). In contrast, in mice, a species resistant to thalidomide teratogenicity, thalidomide does not enhance DNA oxidation, even at a dose 300% higher than that used in rabbits, providing insight into an embryonic determinant of species-dependent susceptibility. In addition to their therapeutic implications, these results constitute direct evidence that the teratogenicity of thalidomide may involve free radical-mediated oxidative damage to embryonic cellular macromolecules.

Animals↗
PubMed1999

Analysis of oxidative DNA damage and HPRT mutant frequencies in cancer patients before and after radiotherapy.

Various markers of radiation-induced DNA damage including DNA oxidation were investigated in peripheral lymphocytes of 23 cancer patients prior to and one week after receiving radiotherapy with a cumulative dose of 54-70 Gy. Exposure to ionizing radiation nonsignificantly increased the ratio 2'deoxy-7-dihydro-8-oxoguanosine/2'deoxyguanosine (8-oxodG/dG) from 1.73 x 10(-5) to 3.33 x 10(-5). Frequencies of micronuclei significantly (p = 0.0003) increased from 6.4 to 38.9 per 1000 cells. The frequency of hypoxanthine-guanine-phosphoribosyltransferase (HPRT) mutant lymphocytes measured as 6-thioguanine resistant variant cells by 5-bromodeoxyuridine labeling, was elevated eight-fold, from 4.7 x 10(-6) to 36.2 x 10(-6) (p = 0.008) after termination of the radiotherapy, thus showing a clear response to the radiation treatment. No correlation between levels of oxidative DNA damage and frequencies of HPRT mutant lymphocytes or micronuclei could be established.

8-Hydroxy-2'-Deoxyguanosine↗
PubMed1999

Oxidative DNA damage in the aging mouse brain.

The brain exhibits regional vulnerabilities to many insults, and age itself has differential effects on neuronal populations as exemplified by the age-dependent loss of dopaminergic neurons in the nigrostriatal system. We hypothesized that oxidative damage to DNA was more likely to occur in the nigrostriatal system which undergoes significant neurochemical and functional changes with age. To test this hypothesis, oxidative damage to DNA, indicated by levels of 8-hydroxy2'-deoxyguanosine (oxo8dG), was measured in pons-medulla (PM), midbrain (MB), caudate-putamen (CP), hippocampus (HP), cerebellum (CB), and cerebral cortex (CX) at 3, 18, and 34 months of age in C57/b1 mice. Steady-state levels of oxo8dG increased significantly with age in MB, CP, and CB, but not in PM, HP, or CX. Manganese superoxide dismutase (MnSOD) activity decreased with age in MB, CP, and HP, but not in PM, CB, or CX. Regional activities of Cu/Zn superoxide dismutase (Cu/Zn SOD) and glutathione peroxidase (Glut Px) did not change significantly with age. Concomitant with the regional alterations in DNA damage, there was a significant age-dependent decline in locomotor activity, motor coordination, and striatal dopamine content especially during the interval between 18 and 34 months. In conclusion, oxyradical-associated damage to DNA did not accumulate uniformly across brain regions with age and was highest in brain regions that subserve spontaneous locomotor activity and motor coordination.

Age Factors↗
PubMed1993

Properties and biological functions of the NTH and FPG proteins of Escherichia coli: two DNA glycosylases that repair oxidative damage in DNA.

Oxidative damage to DNA is one of the most important causes of spontaneous mutations and may play a role in aging and related diseases, such as cancer, in humans. Oxidative damage results from the attack of biomolecules by free radicals and reactive oxygen species formed as byproducts of normal cell metabolism or during oxidative stress. To counteract the lethal and mutagenic effects of oxidative lesions in DNA, cells have developed defence strategies including DNA repair systems. In Escherichia coli, the repair of oxidized bases in DNA is mostly mediated by the base excision repair pathway. The first step in this DNA repair pathway is catalysed either by the NTH protein which excises oxidized pyrimidines or by the FPG protein which excises oxidized purines. The nucleotide excision repair pathway mediated by the UvrABC complex may also play a role when the DNA glycosylases are inactive or saturated. This review summarizes the structural and catalytic properties of the NTH and FPG proteins of Escherichia coli and presents evidence to indicate that these two enzymes constitute an important component of the cellular defence against oxidative stress in prokaryotes and eukaryotes.

Amino Acid Sequence↗
PubMed2006

[Establishment of DNA oxidative damage model in colorectal crypt cells by hydrogen peroxide].

OBJECTIVE: To induce DNA oxidative damage in colorectal crypt cells by hydrogen peroxide in vitro. METHODS: Hydrogen peroxide was diluted into 100, 50, 10, 5 and 1 micromol/L with RPMI 1640. Colorectal crypt cells were treated with peroxide for 10 min, 30 min, 1 h, 1.5 h, 12 h and 24 h respectively. The survival of colorectal crypt cell was measured by MTT method, and the DNA oxidative damage special product, 8-OhdG was detected with immunohistochemical staining. Liner regression was used to measure the time trend of survival rate with SPSS 10.0 software. RESULT: Survival rate of colorectal crypt cell was 60% and 80% after 10 min of hydrogen peroxide treatment. The longer treatment of hydrogen peroxide, the lower survival rate; the survival rate was reduced to 30% in 24 h. After 10 or 30 min treatment of 100 or 50 micromol/L hydrogen peroxide, the survival rates of colorectal crypt cells were reduced by 20% compared with those of 10, 5 and 1 micromol/L hydrogen peroxide. However, while cells were treated with different concentrations of hydrogen peroxide for 1.0 h or above, there were no differences in cell survival rates. The time trend test results demonstrated that the survival rates of colorectal crypt cells treated with 10, 5 and 1 micromol/L hydrogen peroxide were significantly decreased with the time length of treatment. Colorectal crypt cells treated with different concentrations of hydrogen peroxide for 15 minutes were positively stained brown in cytoplasm and nuclear by immunohistochemistry with 8-OhdG monoclonal antibody. CONCLUSION: Hydrogen peroxide could induce DNA oxidative damage in colorectal crypt cells. And treated with 1 - 10 micromol/L hydrogen peroxide for 10 - 30 min, DNA oxidative damage is apt to be induced in colorectal crypt cell.

Carbazoles↗
PubMed2006

New evidence of premature oxidative DNA damage: mitochondrial DNA deletion in gingival tissue of patients with periodontitis.

BACKGROUND: Overproduction of reactive oxygen species (ROS) causes increased oxidative stress in gingival tissue. It has been generally accepted that increased oxidative stress might contribute to additional damage of lipids, proteins, and DNA molecules. The mitochondrial DNA (mtDNA) mutation is a superb biomarker of oxidative damage. The aim of the present study was to investigate the mtDNA deletions in the gingival tissue of patients with periodontitis and to explain the correlations between mtDNA deletion in gingival tissue and clinical parameters of periodontitis and age. METHODS: Gingival tissue and blood samples were collected from 30 patients with chronic periodontitis (CP group) and 30 healthy control subjects (H group). To determine the clinical condition of each subject, the plaque index, gingival index, clinical attachment level, and probing depth were measured. Using the polymerase chain reaction (PCR) method, we examined the 7.4- and 5-kbp mtDNA deletions in tissue and blood samples. Three different pairs of PCR primers were used in this study. RESULTS: In this study, we did not detect any deletions in blood DNA samples in either the CP or H group. Also, the 7.4-kbp mtDNA deletion was not detected in gingival tissues of subjects. However, the 5-kbp mtDNA deletion was detected in 24 of the 30 subjects (80%) in the CP group and was not detected in the H group (0%). Significant correlations were found between the occurrence of the 5-kbp mtDNA deletion and all clinical parameters (P <0.01). A similar correlation was found between the occurrence of the 5-kbp mtDNA deletion and age (P <0.05). CONCLUSIONS: The overproduction of ROS by activated polymorphonuclear leukocytes in chronic inflammation may lead to premature oxidative damage of the mtDNA. In this study, the occurrence of the 5-kbp mtDNA deletion in 24 periodontitis subjects may be evidence of premature oxidative DNA damage.

Adult↗
PubMed1990

In vivo oxidative DNA damage: measurement of 8-hydroxy-2'-deoxyguanosine in DNA and urine by high-performance liquid chromatography with electrochemical detection.

HPLC with electrochemical detection is a highly sensitive and selective method for detecting the oxidatively modified DNA residue oh8dG. By this method, the detection of oh8dG from DNA and urine offers a powerful approach for assessing in vivo oxidative damage. Application of this technique to the detection of oh8dG from DNA permits the quantitation of the steady-state levels of this oxidatively modified deoxynucleoside and overcomes the detection problems associated with the extremely low levels present in DNA. In addition, the selectivity gained by this detection method eliminates the problem of separating the signal for oh8dG from normal deoxynucleosides. The quantitation of oh8dG in urine complements the measurement of oh8dG in DNA by estimating cumulative oxidative DNA damage in the body. In addition, the urinary assay provides a noninvasive means of measuring this type of damage in laboratory animals and human populations. Thus, an individual animal or human subject may be monitored over time, possibly under various prooxidant conditions, using oh8dG as a sensitive marker for oxidative DNA damage. This analytical approach may allow one to estimate the exposure of an individual to prooxidant conditions associated with lifestyle, genetic predisposition, degenerative diseases, and environmental toxins.

8-Hydroxy-2'-Deoxyguanosine↗
PubMed2006

Low levels of clustered oxidative DNA damage induced at low and high LET irradiation in mammalian cells.

DNA double-strand breaks (DSBs) and locally multiply damaged sites (LMDS) induced by ionizing radiation (IR) are considered to be very genotoxic in mammalian cells. LMDS consist of two or more clustered DNA lesions including oxidative damage locally formed within one or two helical turns by single radiation tracks following local energy deposition. They are thought to be frequently induced by IR but not by normal oxidative metabolism. In mammalian cells, LMDS are detected after specific enzymatic treatments transforming these lesions into additional DSBs that can be revealed by pulsed-field gel electrophoresis (PFGE). Here, we studied radiation-induced DSBs and LMDS in Chinese hamster ovary cells (CHO-K1). After addition of the iron chelator deferoxamine (DFO) or the antioxidant glutathione (GSH) to the cell lysis solution, we observed reduced spontaneous DNA fragmentation and a clear dose-dependent increase of radiation-induced DSBs. LMDS induction, however, was close to background levels, independently of dose, dose rate, temperature and radiation quality (low and high LET). Under these experimental conditions, artefactual oxidative DNA damage during cell lysis could not anymore be confounded with LMDS. We thus show that radiation-induced LMDS composed of oxidized purines or pyrimidines are much less frequent than hitherto reported, and suggest that they may be of minor importance in the radiation response than DSBs. We speculate that complex DSBs with oxidized ends may constitute the main part of radiation-induced clustered lesions. However, this needs further studies.

Animals↗
PubMed2005

Helicobacter pylori infection is associated with oxidatively damaged DNA in human leukocytes and decreased level of urinary 8-oxo-7,8-dihydroguanine.

Helicobacter pylori infection is responsible for inflammation, increased production of reactive oxygen species and oxidatively damaged DNA in the gastric mucosa. There is also evidence which suggests that H.pylori infection may lead to the development of several extragastroduodenal pathologies with reactive oxygen species involvement. In order to assess whether the infection may impose oxidatively damaged DNA not only in the target organ (stomach) but in other organs as well we decided, for the first time, to analyse the two kinds of oxidatively damaged DNA biomarkers: urinary excretion of 8-oxo-7,8-dihydro-2'-deoxyguanosine (8-oxodG) and 8-oxo-7,8-dihydroguanine (8-oxoGua) as well as the level of oxidatively damaged DNA in leukocytes. Using high performance liquid chromatography prepurification/gas chromatography with isotope dilution mass detection methodology, we examined the amount of oxidatively damaged DNA products excreted into urine and the amount of 8-oxodG in the DNA of leukocytes' (with the the HPLC/EC technique) in three groups of children: (i) control group, (ii) H.pylori infected children and (iii) children with gastritis where H.pylori infection was excluded. The levels of 8-oxodG in DNA isolated from leukocytes of H.pylori infected patients and in the group with gastritis without H.pylori infection were significantly higher than in DNA isolated from the control group. The mean level of 8-oxoGua in urine samples of children infected with H.pylori was significantly lower than in the urine of the group with gastritis without H.pylori infection. The data suggest that inflammation itself, not just H.pylori infection, is responsible for the observed rise of 8-oxodG level in leukocytes. However, the observed decrease in the level of modified base in urine seems to be specific for H.pylori infection and possibly linked with nitric oxide mediated inhibition of a key base excision repair enzyme (human 8-oxo-7, 8-dihydroguanine glycosylase) responsible for the repair of 8-oxo-7,8-dihydroguanine.

Adolescent↗
PubMed2003

The discovery of a new family of mammalian enzymes for repair of oxidatively damaged DNA, and its physiological implications.

Oxidatively damaged bases in the genome are likely to be responsible for mutations leading to sporadic carcinogenesis. Two structurally similar DNA glycosylases, NTH1 and OGG1, which are able to excise most of these damaged bases, were identified previously in mammalian cells. A distinct family, consisting of two human DNA glycosylases orthologous to enzymes in Escherichia coli, has recently been characterized; they have overlapping substrate ranges with NTH1 and OGG1. The presence of multiple enzymes with potential back-up functions underscores the importance of removing both endogenously and exogenously generated oxidatively damaged bases from the genome, and may explain why no cancer or other disease phenotype has so far been linked to the deficiency of a single DNA glycosylase.

Animals↗
PubMed1990

Conditions influencing yield and analysis of 8-hydroxy-2'-deoxyguanosine in oxidatively damaged DNA.

We have conducted studies to obtain practical knowledge regarding the stability, digestion, and analytical determination of the content of 8-hydroxy-2-deoxy-guanosine (8-OHdG) in oxidatively damaged DNA. Utilizing H2O2 plus uv light to form oxidatively damaged DNA, we found that storage of the DNA at -20 degrees C at alkaline pH caused a significant loss of 8-OHdG, whereas storage at -20 degrees C at neutral or acidic pH prevented loss of 8-OHdG. The 8-OHdG within DNA is stable at 100 degrees C for at least 15 min. Formation of 8-OHdG within DNA using uv light and H2O2 as a hydroxyl free radical-generating system yields the highest amounts when low levels of phosphate buffer are used; but the use of Tris or citrate buffers causes a lower yield of 8-OHdG because these buffers act as scavengers for the hydroxyl free radicals. Independent assessment of hydroxyl free radical flux by the use of salicylate trapping allows assessment of competitive radical reactions. Ethanol washing of plastic microfuge tubes prior to DNA enzymatic digestion improved the yield of 8-OHdG and reduced the variability between samples. Digestion of the oxidatively damaged DNA by the use of a method involving DNase I, endonuclease, phosphodiesterase, and alkaline phosphatase produced the highest yield of 8-OHdG.

8-Hydroxy-2'-Deoxyguanosine↗
PubMed1996

Assessment of DNA oxidative damage by quantification of thymidine glycol residues using gas chromatography/electron capture negative ionization mass spectrometry.

A technique to assess DNA oxidative damage by quantification of thymidine glycol residues is described. 2-Methylglycerate was released from thymidine glycol in DNA by alkaline cleavage/borodeuteride reduction, then derivatized to form a combined pentafluorobenzyl-tertbutyldimethylsilyl (PFB-TBDMS) derivative and analyzed by gas chromatography/electron capture negative ionization mass spectrometry. [2H4]Thymine glycol was used as an internal standard. The derivatization chemistry was assessed by using [14C-methyl]glycerate. Successful esterification was achieved with 75-80% yield using tetrabutylammonium sulfate-assisted anhydrous pentafluorobenzylation. The PFB-TBDMS derivative exhibits excellent chromatographic and detection properties with a detection limit of 41 amol injected on column. Freshly dissolved calf thymus DNA was used to test the method performance. The background level of thymidine glycol detected in this DNA was 11.7 +/- 0.3 x 10(-6) mol thymidine glycol per 1 mol thymidine. The thymidine glycol background in undamaged DNA establishes a lower limit of oxidative damage below which biological oxidation events would not be measured by this method. The method was linear for 4-20 micrograms DNA added per tube. The minimum measurable amount of thymidine glycol in DNA sample was 36 fmol. An increased level of thymidine glycol was measured in salmon sperm DNA which had autoxidized during storage in a refrigerated aqueous solution, 71.2 +/- 14.3 x 10(-6) mol thymidine glycol per 1 mol thymidine.

Animals↗