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PubMed1994

Increased 8-hydroxydeoxyguanosine in kidney and liver of rats continuously exposed to copper.

Copper is a ubiquitous metal in the environment, it is a component of dental casting gold alloys and dental amalgams, and it is a main component in some intrauterine contraceptive devices (IUDs). Since copper materials implanted in the human body corrode and release ions into the surrounding tissue, the potential toxicity caused by contact of this metal with bodily fluids needs to be evaluated. We implanted male Wistar rats with osmotic mini pumps that continuously administered saline, CuCl2, or a copper chelate, cupric nitrilotriacetate (Cu-NTA), at a rate of 4 mg copper/kg body wt/day. This experimental design maintained serum copper concentrations at a level 30-70% (CuCl2) or 100-120% (Cu-NTA) higher than in untreated controls. At different times postimplantation, we measured the levels of 8-hydroxydeoxyguanosine (8-OHdG) in DNA of kidney, liver, and tissue surrounding the pump implant, since production of 8-OHdG has been associated with mutagenesis and carcinogenesis. Hepatic and renal levels of 8-OHdG in CuCl2- or Cu-NTA-treated animals were significantly higher than in control animals. In contrast, histopathologic changes in kidneys and livers of rats exposed to CuCl2 and Cu-NTA were limited to mild changes involving hepatic focal necrosis and slightly increased mitotic activity in the renal proximal tubules. These observations suggest that levels of 8-OHdG could be an early marker of copper toxicity. It is unlikely that the high levels of copper at which we observed DNA modification will be encountered after occupational or environmental exposure. A different situation could be found around medical devices that include copper, particularly IUDs, where the amount of copper administered in our experiments could be released in the uterus of women after a few months of continued IUD use.

8-Hydroxy-2'-Deoxyguanosine↗
PubMed2001

AID is required to initiate Nbs1/gamma-H2AX focus formation and mutations at sites of class switching.

Class switch recombination (CSR) is a region-specific DNA recombination reaction that replaces one immunoglobulin heavy-chain constant region (Ch) gene with another. This enables a single variable (V) region gene to be used in conjunction with different downstream Ch genes, each having a unique biological activity. The molecular mechanisms that mediate CSR have not been defined, but activation-induced cytidine deaminase (AID), a putative RNA-editing enzyme, is required for this reaction. Here we report that the Nijmegen breakage syndrome protein (Nbs1) and phosphorylated H2A histone family member X (gamma-H2AX, also known as gamma-H2afx), which facilitate DNA double-strand break (DSB) repair, form nuclear foci at the Ch region in the G1 phase of the cell cycle in cells undergoing CSR, and that switching is impaired in H2AX-/- mice. Localization of Nbs1 and gamma-H2AX to the Igh locus during CSR is dependent on AID. In addition, AID is required for induction of switch region (S mu)-specific DNA lesions that precede CSR. These results place AID function upstream of the DNA modifications that initiate CSR.

Animals↗
PubMed2004

Molecular characterization of clinical Streptococcus pneumoniae isolates with reduced susceptibility to fluoroquinolones emerging in Italy.

Fifteen Streptococcus pneumoniae clinical isolates with reduced fluoroquinolone susceptibility (defined as a ciprofloxacin MIC of > or = 4 microg/ml), all collected in Italy in 2000-2003, were typed and subjected to extensive molecular characterization to define the contribution of drug target alterations and efflux mechanisms to their resistance. Serotyping and pulsed-field gel electrophoresis analysis indicated substantial genetic unrelatedness among the 15 isolates, suggesting that the new resistance traits arise in multiple indigenous strains rather than through clonal dissemination. Sequencing of the quinolone resistance-determining regions of gyrA, gyrB, parC, and parE demonstrated that point mutations producing single amino acid changes were more frequent in topoisomerase IV (parC mutations in 14 isolates and parE mutations in 13) than in DNA gyrase subunits (gyrA mutations in 7 isolates and no gyrB mutations observed). No isolate displayed a quinolone efflux system susceptible to carbonyl cyanide m-chlorophenylhydrazone; conversely, four-fold or greater MIC reductions in the presence of reserpine were observed in all 15 isolates with ethidium bromide, in 13 with ulifloxacin, in 9 with ciprofloxacin, in 5 with norfloxacin, and in none with five other fluoroquinolones. The effect of efflux pump activity on the level and profile of fluoroquinolone resistance in our strains was minor compared with that of target site modifications. DNA mutations and/or efflux systems other than those established so far might contribute to the fluoroquinolone resistance expressed by our strains. Susceptibility profiles to nonquinolone class antibiotics and resistance-associated phenotypic and genotypic characteristics were also determined and correlated with fluoroquinolone resistance. A unique penicillin-binding protein profile was observed in all five penicillin-resistant isolates, whereas the same PBP profile as S. pneumoniae R6 was exhibited by all six penicillin-susceptible isolates. This is the first attempt to molecularly characterize clinical isolates of S. pneumoniae with reduced susceptibility to fluoroquinolones emerging in Italy.

Anti-Bacterial Agents↗
PubMed1985

Factors influencing benzo[a]pyrene metabolism in human mammary epithelial cells in culture.

We have examined the human mammary epithelial cell (HMEC) culture system developed in our laboratory for factors that might influence the metabolism of chemical carcinogens, specifically, the impact of interindividual variation and the effect of different culture conditions. Benzo[a]pyrene metabolism and DNA adduct formation in HMEC from 13 normal reduction mammoplasty specimens, from five nontumorous mastectomy tissues and from eight primary carcinomas were investigated. The interindividual variation in formation of water and organosoluble metabolites was similar in all of the three categories of HMEC. A similar range of variation was found for DNA adduct formation among HMEC from reduction mammoplasty specimens. However, when the individual results of DNA adduct formation in the three categories were examined, HMEC from some specimens from non-tumorous mastectomy tissue and primary carcinomas had significantly increased DNA modification. We also measured the effects of BaP concentration, different culture media, the length of time in culture, the culture density, and the frequency of feeding on the conversion of tritiated BaP to various water and organosoluble metabolites. The BaP metabolite pattern by HMEC was generally stable in the face of these variables. However, suboptimal feeding regimens and lengthy passaging in culture reduced the capacity of the cells to metabolize BaP. The yield of BaP conjugates was reduced 10-fold with lengthy passaging in culture whereas the organosoluble metabolite yield was halved and DNA adduct formation was not affected. Increasing the concentration of BaP decreased the yield of water soluble metabolites relative to that of organosoluble, indicating differences in the capacity of the enzyme systems involved. The HMEC culture system offers several advantages for studies into the biochemical and molecular basis of chemical carcinogenesis in human epithelial cells: the large numbers of cells required can be easily generated; cells at all stages can be frozen for future experiments with no loss in activity; and a high capacity for carcinogen activation is retained during long-term culture.

Benzo(a)pyrene↗
PubMed1994

Chemical structure- and time-dependent effects of polycyclic aromatic hydrocarbon-type inducers on rat liver cytochrome P450, DNA adducts, and I-compounds.

It is well documented that cytochrome P450IA1 (CYP1A1) plays an important role in carcinogen activation. CYP1A1/1A2 induction may serve as a biomarker of exposure to environmental toxins. In order to explore a specific role of CYP1A1 in metabolism of I-compounds (age-dependent indigenous DNA modifications), 2-month-old female Sprague-Dawley rats were treated ip with corn oil (2 ml/kg) or with one of several CYP1A1 inducers, i.e., dibenz[a,c]anthracene (DBA) (93 mumol/kg), benzo[a]pyrene (BP) (93 mumol/kg), naphthacene (NAP) (93 mumol/kg), or beta-naphthoflavone (BNF) (140 mumol/kg), once daily for 4 days. Levels of total cytochrome P450 and activities of CYP1A1-associated enzymes, i.e., ethoxycoumarin O-deethylase (ECD) and ethoxyresorufin O-deethylase (EROD), were determined in liver microsomes at 1, 8, or 15 days after the last treatment. DNA adducts and I-compounds were analyzed by nuclease P1-enhanced 32P-postlabeling. DNA synthesis rate was determined by measuring [3H]methylthymidine incorporation into DNA. Each inducer significantly elevated the total P450 level at 1 day. The enzyme levels in BP-, NAP-, and BNF-treated animals gradually returned to control by 8 and 15 days, but elevated levels persisted in DBA-treated rats. Similar trends were observed for ECD and EROD activities. DBA and BP, but not NAP and BNF, gave rise to several measurable DNA adducts, which persisted throughout the period of study. All P450 inducers, irrespective of adduct formation, strongly depleted both nonpolar and polar I-compounds, the effects being most pronounced at 1 and 8 days. These results imply a specific role for CYP1A1 in the regulation of I-compound metabolism, in addition to PAH activation.

Animals↗
PubMed1987

N-methylation reduces the DNA-binding activity of 7H-dibenzo[c,g]carbazole approximately 300-fold in mouse liver but only approximately 2-fold in skin: possible correlation with carcinogenic activity.

N-methyl-dibenzo[c,g]carbazole (MeDBC) lacks the potent hepatocarcinogenic activity in mice characteristic for 7H-dibenzo[c,g]carbazole (DBC), while both compounds are local carcinogens, leading to papilloma and carcinoma formation in skin after topical application. Because DNA binding is considered an essential step in the initiation of chemical carcinogenesis, the DNA adduction by MeDBC was compared with that by DBC in mouse liver and skin via a 32P-postlabeling technique. Both compounds elicited chromatographically similar adducts in liver; however, the extent of total DNA binding of DBC was 343- and 265-fold greater than that of MeDBC 24 h after topical and i.p. administration, respectively, of a 37 mumol/kg dose. In skin, the adduct pattern elicited by either compound after topical application was different from that seen in liver, and three of four adducts derived from MeDBC were chromatographically distinct from those produced by DBC. Quantitative analysis revealed that total adduction in skin by DBC was 2.3-fold higher than by MeDBC. When the adduct levels were compared between liver and skin, topically applied MeDBC bound preferentially to skin versus liver DNA by a factor of 10, while the opposite was true for DBC. These data are in agreement with the carcinogenicity reported for DBC and MeDBC and support the hypothesis that the extent of covalent DNA modification by these compounds is associated with their biological activity. We conclude that an unsubstituted nitrogen is essential for the genotoxic activity of DBC in liver but not skin. The results also demonstrate the potential of the 32P-postlabeling assay in predicting the organotropism of closely related carcinogens.

Administration, Topical↗
PubMed1979

DNA repair as regulatory factor in the organotropy of alkylating carcinogens.

Monofunctional alkylating agents which react predominantly at nitrogen atoms in DNA bases (e.g. alkyl methanesulphonates, dialkylsulfates) are generally weak carcinogens whereas compounds which lead extensively to oxygen alkylation (e.g. alkylnitrosoureas, dialkylnitrosamines, dialkyl-aryltriazenes) often exhibit a strong carcinogenic activity. O6-Alkylation of guanine is a promutagenic DNA modification possibly involved in the initiation of malignant transformation. O6-Alkylguanine can be enzymically excised and in the rat the induction of neural, renal and colonic tumors by alkylnitrosoureas, 3,3-dimethyll-phenyltriazene, dimethylnitrosamine and 1,2-dimethylhydrazine correlates with an excision repair deficiency in the target tissue. However, species and strain differences in the response to these carcinogens are not paralleled by differences in the excision repair capacity for O6-alkylguanine. Preliminary data suggest that in rat liver there is an inducible enzyme for the removal of O6-alkylguanine from DNA.

Alkylation↗
PubMed1993

Enhancement of age-related increases in DNA I-compound levels by calorie restriction: comparison of male B-N and F-344 rats.

Caloric restriction (CR), known to extend median and maximum life spans, improve resistance to carcinogenesis, and significantly retard age-associated degenerative diseases in rodents, was previously reported to modulate levels of indigenous, age-dependent DNA modifications, called I-compounds, in male Brown-Norway (B-N) rats. Since profiles of these adduct-like derivatives are species-, strain-, sex-, and tissue-specific, we explored this apparent CR/I-compound relationship in a comparative study between male B-N and male Fischer 344 (F-344) rats, the latter having a shorter life expectancy and high incidence of renal disease. Control animals were fed NIH-31 diet ad libitum (AL), while the caloric intake of CR animals was limited to 60% of AL, starting at 3.5 months. Liver and kidney DNA from 1, 8, 12, 16, 24 (AL, CR), and 30 (CR only) month old rats was analyzed by 32P-postlabeling. Corresponding tissues from the two strains yielded similar DNA profiles. Total liver I-compound levels displayed 2.3-4.6-fold age-dependent increases from 1 to 24 months, and kidney values at 24 months were 5.2-8 times higher than those at 1 month. In both strains, I-compound levels of CR animals were higher, up to 2-fold, than in age-matched AL rats. Regression analyses indicated linear relationships between most CR relative adduct labeling values (both total and individual fractions) and age, whereas many AL values exhibited this type of link with log age. These findings confirm that a correlation exists between CR and I-compound levels, and, given the above physiological benefits of CR, indicate that I-compounds represent biomarkers of aging with potential utility in intervention studies.

Aging↗
PubMed2005

Microcompetition and the origin of cancer.

Abnormal gene expression is a common observation in cancer cells. Although genetic alterations via somatic mutations or DNA modifications are considered to be the cause of cancer, they do not explain the observed abnormal gene expression of many wild-type genes in cancer. Now, a new theory, called "Microcompetition", identifies a non-genetic-alteration event as the cause of the observed abnormal gene expression, and therefore, the cause of cancer and other chronic diseases.

Cell Transformation, Neoplastic↗
PubMed1980

[Assay of brain and liver DNA, determination of body growth and of some blood parameters in rats subjected to protein malnutrition during fetal and post-natal development].

The Authors studied the effects of proteinic malnutrition when it occurred at various periods in the life of rats: the last 10 days of fetal life; nursing (the first 3 weeks of life); after weaning (up to 42 day). The results show that:--the growth in weight of the animals was severely restrained when protein deficiency occurred in post-natal life;--in any case, the blood levels of hematocrit, hemoglobin and proteins were significantly lowered;--organ functions and development were greatly compromised if malnutrition occurred during the period of their cell division. In fact, a brain damage, estimated by protein and DNA modifications, is the result of protein deficiency in pre-natal and, particularly, in nursing period. The hepatic damage, instead, becomes more evident in post-natal life and specially after weaning since the cell division in the liver continues for a much longer period of time.

Aging↗
PubMed1998

Use of repair endonucleases for characterization of DNA damage induced by N-heterocyclic aromatic hydrocarbons.

Several repair endonucleases were used to characterize and quantify various types of DNA damage induced by 7H-dibenzo[c,g]carbazole (DBC) and its methyl derivative, N-methyldibenzo[c,g]carbazole (MeDBC). Differences in the DNA damage profile induced by these two derivatives were found to be related to their chemical structure and dependent on the way of their metabolic activation. Different ways of activation gave rise to different numbers of single strand breaks and DNA modifications or, at least, to different ratios of common modifications. DBC induced the highest level of breaks in human hepatal cell line Hep G2, while MeDBC induced most of the breaks in V79 cell line with stable expression of human cytochrome P4501A1. Our results support the idea of two different pathways of biotransformation of DBC and MeDBC.

Benzo(a)pyrene↗
PubMed1990

The effect of insertion of the maize transposable element mutator is dependent on genetic background.

A secondary mutant, derived from an allele of maize alcohol dehydrogenase 1 (Adh1) carrying a Mutator transposable element (Mu1) in its first intron, was reported to exhibit a threefold decrease in ADH enzymatic activity and steady-state RNA levels compared to the original mutant. The original mutant, Adh1-S3034 (abbreviated S3034), was previously characterized at the molecular level. The derivative, abbreviated S3034b, has now been cloned; at the DNA sequence level the insertion and surrounding Adh1 sequences are indistinguishable from S3034. Furthermore, in our lines there is no difference in relative ADH activities between products of the two putative alleles. A comparison of gene expression in heterozygotes obtained by crossing to different tester lines reveals a correlation between the measured decrease in levels of ADH polypeptide produced by the mutant allele and the background in which it is measured; this effect is distinct from any background-related variation in the expression of the progenitor allele. It does not appear to be attributable to alternative patterns of DNA modification. It appears to reflect a background-associated difference in the level of normal Adh1-RNA produced. Thus the previously reported distinction between S3034 and S3034b may be due to differences in the extent to which the mutant allele and a given genetic background interact to produce functional Adh1-RNA.

Alcohol Dehydrogenase↗
PubMed2005

Gain of allelic gene expression for IGF-II occurs frequently in Barrett's esophagus.

The IGF-II gene normally exhibits genomic imprinting, a DNA modification that allows the expression of only one of the two inherited alleles. With loss of imprinting, there is a gain of allelic gene expression (GOAGE) due to IGF-II being expressed by both alleles. GOAGE for IGF-II has been demonstrated in a number of malignancies and in normal epithelia surrounding malignancies, but not in epithelia without associated neoplasia. We hypothesized that nonneoplastic Barrett's epithelium might have GOAGE for IGF-II that could facilitate its progression to neoplasia. Endoscopic biopsies were obtained from metaplastic esophageal, normal gastric, and normal duodenal epithelia from 43 patients with Barrett's esophagus. Genomic DNA were analyzed using PCR followed by ApaI restriction enzyme digestion or allele-specific PCR to identify an ApaI polymorphism of IGF-II. cDNA from patients with the ApaI polymorphism were analyzed for IGF-II GOAGE using exon connection PCR, followed by a secondary nested PCR and ApaI restriction enzyme digestion. We found that 13 (30%) of 43 samples of Barrett's metaplasia contained the ApaI polymorphism and were thus informative for IGF-II, and sufficient material was available for GOAGE analysis in 9 of those 13 cases. GOAGE for IGF-II was demonstrated in five (56%) of those nine cases. All patients with GOAGE in Barrett's metaplasia also demonstrated GOAGE in the gastric and duodenal epithelia. In contrast, patients without GOAGE in Barrett's metaplasia also had no GOAGE in their gastric and duodenal epithelia. We conclude that in patients with Barrett's esophagus, GOAGE for IGF-II is found frequently in the metaplastic esophageal epithelium as well as in normal gastric and duodenal epithelia.

Alleles↗
PubMed1993

I-compounds--endogenous DNA markers of nutritional status, ageing, tumour promotion and carcinogenesis.

Certain bulky DNA modifications increase with age in laboratory animals without known exposure to carcinogens and are known as indigenous or I-compounds. Most of the spots detected on TLC maps by the nuclease P1-enhanced bisphosphate version or the monophosphate version of the 32P-postlabelling assay fit this definition of I-compounds. Chromatographic profiles and levels of these nucleotides greatly depend on animal species, strain, tissue and gender, but are also influenced by the diet and by chemical exposures. Thus, both genetic and environmental factors contribute to the formation of I-compounds. It appears that they are derived from endogenous DNA-reactive compounds generated during normal nutrient metabolism and that regulatory mechanisms exist which control their levels in tissue DNA.

Aging↗
PubMed1991

Hydrogen peroxide formation by cells treated with a tumor promoter.

To determine whether oxidants capable of DNA modification are produced by cells treated with tumor promoters, we adapted a fluorometric method to our needs. HeLa cells were preincubated with 2',7'-dichlorofluorescin diacetate (DCFdAc), treated with various agents, sonicated, centrifuged and fluorescence of the oxidized product (DCF) was determined in supernatants. When cells were exposed to H2O2 in the presence of azide (catalase inhibitor) or o-phenanthroline (a lipophilic Fe chelator), an increase in fluorescence was observed. These results show that some Fe ions were interacting with the H2O2 which entered the cells, thus decreasing its levels available for oxidation of the substrate and potentially increasing formation of .OH, known DNA-damaging species. Glutathione (GSH), which is present in cells in substantial amounts, was found to reduce DCF whereas azide counteracted GSH-mediated reduction. Treatment of HeLa cells with 12-0-tetradecanoyl-phorbol-13-acetate (TPA) in the presence of DCFdAc and azide resulted in dose- and time-dependent formation of DCF. Even when cells were sonicated prior to incubation with TPA, DCF was formed at levels proportional to the number of cells as well as dose of TPA. Flow cytometry of TPA-treated cells confirmed these findings. These results demonstrate that tumor promoters can cause oxidative activation of HeLa cells, which produce active oxygen species, most likely H2O2, that ultimately contribute to the formation of oxidized bases such as 5-hydroxymethyl uracil in cellular DNA. They also show that this fluorometric method can be utilized for determination of cellular H2O2 formation at nM concentrations.

Azides↗
PubMed1984

DNA methylation in the fungi.

A systematic study on the incidence and patterns of cytosine methylation in the fungi has been carried out by restriction and nearest-neighbor analysis of DNAs isolated from undifferentiated cells of several fungal species. With respect to DNA modification, the fungi appear to be a heterogeneous group, with a 5-methylcytosine content ranging from undetectable levels (less than or equal to 0.1% of cytosine residues methylated in 18 out of 20 species tested) to low but detectable levels (e.g. congruent to 0.2 and congruent to 0.5% of the total cytosines methylated in Sporotrichum dimorphosporum and Phycomyces blakesleeanus, respectively). In the species where it has been detected, 5-methylcytosine is located mostly at CpG doublets, and the methylated sites are clustered in long tracts (10-30 kilobase pairs) separated from essentially unmethylated regions. This methylated compartment, which comprises a small fraction (1-11%) of the total DNA, contains at least a specific set of repetitive sequences. These results contrast with the higher 5-methylcytosine content found in the fungus Physarum polycephalum and in vertebrates and higher plants.

5-Methylcytosine↗
PubMed1987

Nitropyrenes are inducers of polyoma viral DNA synthesis.

The biological activity of a series of nitropyrenes was assayed by measuring their ability to induce the asynchronous replication of viral DNA in rat fibroblasts transformed by a ts-a mutant of polyoma virus. Concentrations of 10-30 micrograms/ml of 1-nitropyrene (1-NP) induced viral replication, and this effect was enhanced by addition of rat-liver S9 microsomal fraction (300 micrograms/ml) to the culture medium. The response was less than that obtained with 0.1 micrograms/ml of the activated metabolite of benzo[a]pyrene (BP), BP trans-7,8-dihydrodiol-9,10 epoxide (anti) (BPDE). A series of di-, tri-, and tetra-nitropyrenes were also found to induce polyoma DNA replication, in the absence of exogenous microsomal activation, displaying strongly positive effects at 0.5-2.0 microgram/ml. Dose-response curves with 1,6-dinitropyrene (1,6-DNP) from 0.01 to 0.5 microgram/ml indicated that this compound was approximately equipotent with BPDE for induction of polyoma DNA synthesis. Studies of drug metabolism, DNA binding and DNA adduct formation indicate that 1,6-DNP is metabolized in this cell line, binds to DNA, and forms stable adducts. The level of DNA modification seen with 1,6-DNP is higher than that observed under comparable conditions with an equivalent dose of BPDE. These findings provide additional evidence that the nitropyrene class of compounds can exert biological effects in mammalian cells, and that the dinitropyrenes are more potent than 1-NP.

7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide↗
PubMed2006

Quantification of viral inactivation by photochemical treatment with amotosalen and UV A light, using a novel polymerase chain reaction inhibition method with preamplification.

BACKGROUND: In evaluating a photochemical treatment process for inactivating parvovirus B19, there lacked simple culture methods to measure infectivity. The recently developed enzyme-linked immunospot (ELISpot) infectivity assay uses late-stage erythropoietic progenitor cells and is labor intensive and time consuming. We evaluated a novel, efficient polymerase chain reaction (PCR) inhibition assay and examined correlations with reductions in infectivity. METHODS: Contaminated plasma was treated with 150 micromol/L amotosalen and 3 J/cm(2) ultraviolet A light and then tested for DNA modification using conventional PCR inhibition and a novel preamplification approach. The novel assay subjected the samples to preamplification cycles using long-template PCR, followed by quantitative PCR (QPCR) inhibition detection. Both approaches were tested for correlations with reductions in viral infectivity by comparing ELISpot assay results of identical samples. RESULTS: The B19 preamplification inhibition assay showed detection ranges of 2-2.5 log and demonstrated quantitative correlation with up to a 5.8-log reduction in viral infectivity in ELISpot results. Conventional PCR detected a >5 log reduction in amplification, correlated with a 4.4-log reduction in viral infectivity. A range of 4-log inhibition of hepatitis B virus DNA amplification was also achieved. CONCLUSIONS: The results demonstrated that a novel preamplification QPCR assay is a useful tool for predicting reductions in infectivity after photochemical treatment. This assay was extended to show utility in circumstances where practical in vitro assays are unavailable for the determination of the efficacy of pathogen inactivation.

DNA, Viral↗