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PubMed1981

The combined action of X-irradiation, drug and hyperthermia on the DNA in mammalian cells in vitro.

The effects of the alkylating cytostatic drug PTC on the production of radiation-induced single-strand breaks in DNA, and on the repair in L cells incubated at 37 degrees or 42 degrees C were studied. The same amount of SSB is obtained when the cells are treated simultaneously with PTC and hyperthermia as when irradiated with 2 500 rad, but different rate in the rejoining was observed. There is no potentiation of SSB formation by pretreatment of cells with 10 microgram PTC/ml for 2 hours at 42 degrees C before irradiation, but in these cells less effective repair occurs. The effect of PTC on the rejoining of SSB induced with 2 500 rad depends on the drug's concentration and post-incubation time.

Alkylating Agents↗
PubMed1994

Purification and biochemical characterization of Escherichia coli RecA proteins mutated in the putative DNA binding site.

Escherichia coli RecA protein plays a central role both in DNA repair and in recombination. We report biochemical properties of three new RecA proteins mutated at positions 199 (RecA694), 207 (RecA659), and 211 (RecA611) in the putative DNA binding site. RecA694 had a wild-type phenotype, whereas RecA611 and RecA659 were deficient in promoting both the self-cleavage of LexA repressor and the DNA-strand exchange reaction. In order to determine the origin of this inhibition, we examined the capacity of wild-type and mutant proteins to bind to single-stranded DNA (with and without single-stranded binding protein, SSB), double-stranded DNA, and ATP. DNA strand exchange defects were correlated with the inability of mutant proteins to displace SSB from DNA. For the recA659 mutation this inhibition was reversed by equimolar wild-type protein. In contrast, mixtures of either wild-type/RecA659 or wild-type/RecA611 proteins remained deficient in LexA cleavage, suggesting that the dominant negative phenotype of the mutant proteins may be a consequence of the formation heterologous RecA complexes. Various mutations in the putative DNA binding site of RecA protein altered ATP binding, ATPase activity, displacement of SSB from single-stranded DNA, and protein-protein interactions. These results are consistent with the hypothesis that DNA binding to this site of RecA relays allosteric effects to several functional domains throughout the protein.

Adenosine Triphosphatases↗
PubMed1994

Do low doses of radiation induce a response modulating induction or repair of DNA single-strand breaks?

Many recent reports have indicated interesting structure in the low-dose region of survival curves for mammalian cells (e.g., variations in the effects of oxygen, high-order modulation of the dose-response function, induction of repair, activation of protein-modifying enzymes, influences of cytokines, etc.). Since we have recently identified and corrected several problems causing variability in the results of the alkaline elution methodology, we felt that it was important to investigate the formation and repair of single-strand breaks (SSBs) in this low-dose region. To date we have asked three questions relevant to the structure features noted above: (1) Is the dose response linear at very low radiation doses? (2) Is repair of SSBs complete? (3) Do low "priming" doses of radiation induce subsequent variations in the sensitivity, or rate or extent of repair? To date, we have found no basis in SSB induction and repair for the interesting substructure noted in the survival responses above. At doses from 0.25 Gy to 4 Gy in air, no significant deviations from a linear dose response were observed, and a "priming" dose of 2 Gy has a minimal effect on subsequent sensitivity of SSB formation. Repair of SSBs appears complete at clinical doses of 2 Gy, but substantial unrepaired SSB damage remains 1 h after doses (11 Gy) corresponding to a surviving fraction of 0.01. No significant change in repair of SSBs at 4 h after a 2-Gy priming dose has yet been determined.

Animals↗
PubMedDate not supplied

Collateral sensitivity to thaliblastine and/or hyperthermia exhibited by a rat ovarian tumor cell line selected for resistance to cisplatin.

Drug resistance severely limits the effectiveness of clinical cancer chemotherapy. Employment of drugs other than the selected compounds with different mechanisms of action may provide a potential way to improve the therapeutic effects. Thaliblastine (TBL), a natural compound, showed a 2-fold higher cytotoxicity in a cisplatin (DDP) resistant rat ovarian tumor cell line (0-342/DDP) than in its parental sensitive line (0-342), as determined by an antiproliferation assay with 24 h continuous exposure. This phenomenon was also observed following 2 h pulse exposure if combined with heat treatment (40 degrees C). Further escalation of the temperature to 43 degrees C alone brought about 74.7 +/- 17.0% growth inhibition in the sensitive and 97.2 +/- 1.8% in the resistant line. Under this condition, the ID50 of TBL was again only half as much in 0-342/DDP cells as in the parental cells (12 vs 24 micrograms/ml) when compared to the hyperthermic treatment alone. In a colony formation assay with 2 h pulse exposure, the hypersensitivity of the resistant cells to DDP and/or heat was further confirmed. Alkaline elution showed that 24 h continuous treatment with TBL induced DNA single-strand breaks (SSB) in a dose-dependent manner in 0-342/DDP cells, whereas there was almost no DNA-SSB production by TBL in the sensitive line, possibly in part accounting for the hypersensitivity of the DDP resistant cells to TBL. The heat treatment (40 degrees C for 2 h) induced SSB in both lines, which was further enhanced by combination with TBL. This damage was repaired in part in 0-342 but almost completely in 0-342/DDP line after cells grew in drug-free medium for 48 h following the exposure, indicating that resistant cells can more efficiently repair DNA damage by either TBL or hyperthermia. Altogether, these results suggest that TBL may have potential to be used clinically as an alternative in the treatment of cisplatin-resistant malignancies with hyperthermia.

Animals↗
PubMedDate not supplied

DNA breakage, cytotoxicity, drug accumulation and retention in two human ovarian tumor cell lines AZ224 and AZ364 treated with adriamycin, modulated by verapamil.

We investigated the cytotoxicity of adriamycin in two human ovarian tumor cell lines, AZ224 and AZ364, by the MTT-test and we analysed the formation of DNA single-strand (SSB) and double-strand breaks (DSB) by means of the alkaline and neutral elution technique. The AZ364 cell line was 15 times more resistant to ADR (ID50 = 10.0 micrograms/ml) than the AZ224 cell line (ID50 = 0.66 microgram/ml) after 1hr of drug exposure. Immediately after exposure, we observed a biphasic dose response for SSB in the AZ224 cells over a concentration range of 0.1 to 32.0 micrograms/ml, while practically no DSB were found. Upon drug removal and incubation in drug-free medium, full repair of SSB was observed for an ADR concentration of 1 microgram/ml. On the contrary, the DSB became significantly increased for all tested concentrations and persisted as observed after 3hr and 7hr in drug-free medium. The resistant cell line AZ 364 showed consistently less DNA breakage than the AZ 224 cell line. This inherent difference in sensitivity to ADR could, however, not be explained on the basis of the cellular pharmacokinetics of the drug. Verapamil induced a 3 to 4 fold potentiation of the ADR cytotoxicity in both cell lines after continuous exposure and was associated with an increase in DNA-breakage. The results of our study confirm that there is a lack of correlation between cytotoxicity of ADR and DNA strand breakage immediately after 1 hr of drug exposure. Instead, we emphasize the importance of the formation, extent and persistence of protein-associated DSB upon drug removal to the cytotoxic action of ADR in vitro.

DNA Damage↗
PubMed1993

Yield of strand breaks as a function of scavenger concentration and LET for SV40 irradiated with 4He ions.

We have measured by gel electrophoresis the yields of single- and double-strand breaks (SSBs and DSBs) induced in aqueous solutions of SV40 DNA and the SV40 minichromosome by 137Cs gamma rays (mean LET 0.3 keV micron-1) and 4He ions (mean LETs 85, 102, and 152 keV microns-1). DNA SSBs are caused mainly by the hydroxyl radicals under these conditions and are reduced in yield as either the hydroxyl radical scavenger concentration or the LET is increased (over the range studied). The G(SSB) for 4He ion irradiation is less by a factor of up to 10 than the G(SSB) for gamma irradiation, depending upon the scavenger concentration. The difference in the yields of SSBs agrees well with the difference in the yields of hydroxyl radicals for the radiations in question. In contrast, the yields of DSBs are similar for gamma and 4He ion irradiation over much of the range of scavenging capacity studied. However, at the highest scavenger concentrations the yields of DSBs are greater for 4He ion irradiation. In addition, the yields of DSBs remain almost constant with increasing LET (over the range studied). Therefore the relative yield of DSBs per SSB increases with increasing LET, supporting the hypothesis that increasing LET leads to an increased clustering of damage in DNA.

DNA↗
PubMed1993

Infantile neuroaxonal dystrophy--immunohistochemical and ultrastructural studies on the central and peripheral nervous systems in infantile neuroaxonal dystrophy.

We performed pathological studies on the central and peripheral nervous systems of cases with infantile neuroaxonal dystrophy (INAD). Numerous spheroid bodies in the central and peripheral nervous systems, were seen and divided into large spheroid bodies (LSB) and small spheroid bodies (SSB) photo-microscopically. LSB had a relation to some specific neurons with weak expression of neuron specific enolase, neurofilament and chromogranin using PAP method. SSB showed a relation to the axon without immunohistochemical expression of neuron specific enolase, neurofilament, glial fibrillary acidic protein, myelin basic protein, chromogranin, S 100 protein or antitrypsin. LSB were prominent in the posterior column, gracile nucleus, cuneate nucleus, and the tegmentum of the midbrain and the pons associated with neuronal loss and gliosis. SSB were observed in the thalamus, basal ganglia and the cerebral cortex. The cerebellum was sclerotic with few microtubule-like structures disposed in a dense network in association with degenerated mitochondria. Similar changes were observed in the sural nerves, autonomic nerve endings in the skin, and the nerve plexus of the digestive tract. Although INAD is a generalized neurodegenerative disease, it is suggested that the primary disorder might occur in the neurons and axons of the sensory tracts.

Axons↗
PubMedDate not supplied

Effects of thaliblastine on cytotoxicity and DNA damage in drug-sensitive and -resistant rat ovarian tumor cells treated with cisplatin.

Combination effects of cisplatin (DDP) and thaliblastine (TBL) in DDP-sensitive (0-342) and -resistant (0-342/DDP) rat ovarian tumor cells were investigated. TBL alone, at either 40 or 80 micrograms/ml, exerted higher cytotoxicity in the DDP-resistant 0-342/DDP cells than in the parental sensitive 0-342 cells in growth inhibition assay (% inhibitions: 12.5 and 42.8 in 0-342 cells vs. 37.5 and 66.1 in 0-342/DDP cells, at 40 and 80 micrograms/ml of TBL, respectively). TBL at 40 micrograms/ml showed an additive effect with DDP in the sensitive cells, while a synergistic cytotoxicity was observed in the resistant subline when the two drugs were used in combination, as exhibited by either % inhibition or cell viability. At 80 micrograms/ml of TBL, however, the combination effects were less than additive (infraadditive) in both lines, but still this treatment was more cytotoxic in 0-342/DDP cells. Alkaline elution assay showed that DDP induced higher DNA interstrand crosslings (ISCL) in 0-342 cells, while TBL produced DNA single strand breaks (SSB) in a dose-dependent manner in the resistant line but not in the sensitive cells. Combination of these two compounds resulted in a dramatic increase of DNA-SSB in 0-342/DDP cells. It is tentatively concluded that TBL might have some potential in combination with DDP to conquer the resistance in clinical use, which may result from its selective SSB-inducing activity in the resistant cells.

Animals↗
PubMed1996

Induction of DNA breaks in cardiac myoblast cells by norepinephrine.

We measured DNA single strand breaks (SSB) in cardiac myoblast cells in response to norepinephrine (NE) stimulation. Rat cardiac myoblast cells (H9c2) were stimulated with concentrations of 100 microMs to 1 mM NE for 2, 3, 4, and 12 hours after prior incubation with control solution, bunazosin, propranolol, verapamil, or captopril for 30 min. The DNA damage was measured by fluorometric alkaline elution. The strand scission factor, an index of the severity of SSB, increased slightly after stimulation with 200 microMs NE for 12 hours and with 1 mM NE for 4 hours. This increase was prevented by catalase or superoxide dismutase, which prevent production or accumulation of active oxygen radicals, during the stimulation, but not by pretreatment with a alpha-receptor antagonist, a beta-adrenergic receptor antagonist, a Ca2+ antagonist, or an angiotensin converting enzyme inhibitor. Thus, DNA SSB were induced by NE in cardiac myoblast cells. Certain active oxygen species may contribute to the DNA damage induced by NE.

Adrenergic alpha-Agonists↗
PubMed1996

Interaction of Escherichia coli RecA protein with LexA repressor. I. LexA repressor cleavage is competitive with binding of a secondary DNA molecule.

Essential to the two distinct cellular events of genetic recombination and SOS induction in Escherichia coli, RecA protein promotes the homologous pairing and exchange of DNA strands and the proteolytic cleavage of the LexA repressor, respectively. Since both of these activities require single-stranded DNA (ssDNA) and ATP, the inter-relationship between these reactions was investigated and found to display many parallels. The extent of active complex formed between RecA protein and M13 ssDNA, as measured by both ATP hydrolysis and LexA proteolysis, is stimulated in a similar manner by either a reduction in magnesium ion concentration or the presence of single-stranded DNA binding (SSB) protein. However, unexpectedly, SSB protein inhibits both LexA proteolysis and ATP hydrolysis (in assays containing repressor) at concentrations of RecA protein that are substoichiometric to the ssDNA, arguing that LexA repressor affects the competition between RecA and SSB proteins for limited ssDNA binding sites. Additionally, attenuation of LexA repressor cleavage in the presence of double-stranded DNA or by an excess of ssDNA suggests that interaction of the RecA nucleoprotein filament with either LexA repressor or a secondary DNA molecule is mutually exclusive. The significance of these results is discussed in the context of both the regulation of inducible responses to DNA damage, and the competitive relationship between the processes of SOS induction and genetic recombination.

Adenosine Triphosphate↗
PubMed1996

Interaction of Escherichia coli RecA protein with LexA repressor. II. Inhibition of DNA strand exchange by the uncleavable LexA S119A repressor argues that recombination and SOS induction are competitive processes.

The Escherichia coli RecA protein is involved in SOS induction, DNA repair, and homologous recombination. In vitro, RecA protein serves as a co-protease to cleave LexA repressor, the repressor of the SOS regulon; in addition, RecA protein promotes homologous pairing and DNA strand exchange, steps important to homologous recombination and DNA repair. To determine if these two functions of RecA protein are competing or parallel, the effect of uncleavable LexA S119A repressor on RecA protein-dependent activities was examined. LexA S119A repressor inhibits both the single-stranded DNA (ssDNA)-dependent ATP hydrolysis and DNA strand exchange activities of RecA protein. As for wild-type LexA repressor (Rehrauer, W. M., Lavery, P. E., Palmer, E. L., Singh, R. N., and Kowalczykowski, S. C. (1996) J. Biol. Chem. 271, 23865-23873), inhibition of ATP hydrolysis is dependent upon the presence of E. coli single-stranded DNA binding (SSB) protein, arguing that LexA repressor affects the competition between RecA protein and SSB protein for ssDNA binding sites. In contrast, inhibition of DNA strand exchange activity is SSB protein-independent, suggesting that LexA S119A repressor blocks a site required for DNA strand exchange. These results imply that there is a common site on the RecA protein filament for secondary DNA and LexA repressor binding and raise the possibility that the recombination and co-protease activities of the RecA protein filament are competitive.

Adenosine Triphosphatases↗
PubMed1977

[A method for the preparation and purification of the two blue main components of sudan black B (author's transl)].

Two dimensional thin layer chromatography of four commercial samples of Sudan Black B reveals two blue main components (SSB I and II) and at least 38 further fractions. The quantitative composition of one sample was estimated. SSB-I and SSB-II were isolated and purified by column chromatography supplying amounts for histochemical use. Histochemical experiments are described.

Chromatography, Thin Layer↗
PubMed1997

DNA damage from oxidants: influence of lesion complexity and chromatin organization.

DNA damage by reactive oxygen species results in a spectrum of DNA lesions including single-strand breaks (ssb) and double-strand breaks (dsb). However, most damage is not lethal, and the location and nature of the DNA damage, in addition to total number of breaks, are likely to be critical in determining ultimate survival. Generally associated only with ionizing radiation, multiply damaged sites (i.e., complex lesions and clusters of complex lesions in DNA) are more likely to be lethal because they are less easily repaired. We examined five drugs known to cause DNA adducts, strand breaks, and reactive oxygen species for their ability to produce complex lesions: 4-nitroquinoline-1-oxide (4NQO), H2O2, doxorubicin, Tirapazamine, and etoposide. As indicators of lesion complexity we compared 1) the ratio of ssb to dsb, 2) the rate of rejoining of single-strand breaks, 3) the relative lethality of the breaks (number of breaks per mean lethal dose), and 4) the ability to produce complex lesions. Tirapazamine, etoposide, and doxorubicin gave dsb/ssb ratios similar to that for X-rays, whereas 4NQO and H2O2 showed dsb/ssb ratios of 200 and 3250, respectively. The number of dsb per LD50 varied from 2.5 to 500 for different drugs. There was no apparent relation between ssb rejoining half-time (3.5-85 min) and relative lethality or lesion complexity. A modified (nonionic detergent) filter elution method confirmed that tirapazamine, like ionizing radiation, produced multiple dsb within single chromatin domains. These data indicate that complex lesions can be produced by a number of different chemicals and suggest that the damage that results in killing by these drugs may be related to production of multiply damaged sites in DNA.

Animals↗
PubMed1996

Genotoxic effects in workers exposed to low levels of benzene from gasoline.

To study genotoxic effects of exposure to low levels of benzene, single-strand breaks (SSB) in DNA of leukocytes and urinary levels of the oxidative DNA adduct 8-hydroxydeoxyguanosine (8OHdG) were determined in 33 men occupationally exposed to benzene from gasoline and in 33 controls. The average exposure to benzene over a shift was determined by personal air sampling in the breathing zone. The 8-hr time-weighted average exposure to benzene was 0.13 ppm (mean value, range 0.003-0.6 ppm). Exposed workers had a significant increase of SSB (p = 0.04) over the shift compared with controls. Storage time of the samples seemed to affect the results. An analysis of samples with the same storage time showed a nonsignificant increase among the workers compared with controls. Urinary 8OHdG increased over the shift among the exposed workers but not among the controls. The highest values among the exposed workers were seen in late evening, with a slight decrease the next morning. Multiple linear analysis adjusting for smoking habits showed a significant association between the exposure level of benzene during the shift and the increase of 8OHdG in the urine over the shift among exposed workers (p = 0.02). These findings indicate a genotoxic effect in humans of benzene at relatively low exposure levels, that is, about 0.1 ppm (0.3 mg/m3).

Adult↗
PubMed1999

Time- and concentration-dependent production of superoxide anion, nitric oxide, DNA damage and cellular death by ricin in the J774A.1 macrophage cells.

The time- and concentration-dependent effects of ricin on some biomarkers of cellular toxicity, including production of superoxide anion (O2-), nitric oxide (NO), and DNA single strand breaks (SSB), as well as cellular death, have been examined in the J774A.1 macrophage cell cultures. Various concentrations of ricin have been added to various cell cultures, and the cells were incubated for 12, 24, 36, and 48 hours. Following 12 hour incubation, ricin did not cause significant increases in any of those biomarkers. However, time- and concentration-dependent increases were observed in the induction of all the biomarkers after incubation for 24-48 hours. Approximately twofold increases in the production of O2- were observed after incubation with 1 and 10 ng/mL of ricin for 24 and 36-48 hours, respectively. The concentrations of ricin that caused approximately twofold increases in the rate of DNA-SSB are 10 and 1-10 ng/mL after 24 and 36-48 hours incubation, respectively. Approximately twofold increases in NO production were only observed after incubation of the cultures with 1-10 ng/mL of ricin for 36-48 hours. Fifty percent reductions in cellular viability were also observed with ricin concentrations of 10-100, 10, and 1-10 ng/mL, after incubation for 24, 36, and 48 hours, respectively.

Cell Death↗
PubMed1999

A critical evaluation of enzyme immunoassays for detection of antinuclear autoantibodies of defined specificities. I. Precision, sensitivity, and specificity.

OBJECTIVE: To determine the performance characteristics of enzyme-based immunoassay (EIA) kits for the detection of antinuclear and other autoantibodies of defined specificities. METHODS: Nine manufacturers of EIA kits to detect antibodies of defined specificities participated in a study in which they received coded sera from the Centers for Disease Control and Prevention. These coded sera contained different dilutions of antibody of one specificity mixed with sera containing antibodies of other specificities. The manufacturers were asked to use their standard technology to determine antibody content and send the data to a committee of the International Union of Immunological Societies for analysis. The data were analyzed for sensitivity and specificity in the detection of anti-double-stranded DNA (anti-dsDNA), anti-single-stranded DNA, antihistone, anti-Sm, anti-U1 RNP, anti-SSA/Ro, anti-SSB/La, anti-Scl-70 (DNA topoisomerase I), anticentromere, and anti-Jo-1 antibodies. In addition, replicate samples were included in the coded sera to evaluate the precision of each EIA method. RESULTS: Lack of sensitivity and specificity was most evident in the anti-dsDNA and anti-Sm kits, although 2 kits for anti-dsDNA achieved acceptable sensitivity and specificity. Generally, anti-SSA/Ro, anti-SSB/La, anti-Scl-70, anticentromere, and anti-Jo-1 kits performed well. Many false-positive results were obtained with a multiple myeloma serum containing cryoprecipitates, but multiple myeloma sera without cryoprecipitates presented no problem in the EIA system. Precision, based on evaluation of replicate samples, varied from very good to poor. CONCLUSION: No single manufacturer was clearly superior to others in terms of their products' overall sensitivity, specificity, and precision. Areas that needed improvement were in kits for the detection of antibodies to dsDNA and to Sm antigen. Some EIA kits achieved good sensitivity and specificity. Individual manufacturers were informed of the performance of their respective kits so they could take measures to correct perceived deficiencies and thus improve the reliability of a group of important diagnostic assays used in the evaluation of systemic rheumatic diseases.

Antibodies, Antinuclear↗
PubMedDate not supplied

Intramolecular interference effects in dynamic light scattering: rigid double spirals and superhelical DNAs.

A theory is developed for dynamic light scattering (DLS) from rigid double spirals by treating an invisible rigid cylinder with two helical scattering stripes on opposite sides of its cylindrical surface. The exact initial, or first cumulant, diffusion coefficient Dapp (K) is obtained in terms of the translational diffusion coefficients (D parallel and D perpendicular) parallel and perpendicular to the symmetry axis, the rotational diffusion coefficients (DR parallel and DR perpendicular) around the symmetry and transverse axes, the length (L) and radius (b) of the cylindrical surface bearing the stripes, and the pitch (p). Interference effects, namely geometrical antiresonances, between strands, produce deep minima in the static structure factor S (K) and corresponding prominent peaks in Dapp (K). These peaks in Dapp (K) depend sensitively on the rotational dynamics around the symmetry axis, and nearly vanish when DR parallel = 0. Some results for single spirals are also presented. A simpler model in which scattering points are attached at opposite ends of an otherwise invisible thin rigid rod is also treated, and shown to exhibit modest minima in S (K) and corresponding maxima in Dapp (K). Confining this rod to a plane containing K enhances the amplitudes of the oscillations in S (K) and Dapp (K), as expected. Rigid double spirals are employed as crude models for interwound supercoiled DNAs in order to assess the possible occurrence of interference effects. Although native supercoiled DNAs exhibit a cylinder diameter that is much too small to exhibit geometrical antiresonances in the presently accessible range of K2, nearly relaxed supercoiled DNAs are predicted to exhibit their first maximum in Dapp (K) just inside this range. Previously reported data for the effect of Escherichia coli single-strand binding (ssb) protein on the DLS of supercoiled pBR322 DNA cannot be mimicked by a gradual homogeneous reduction of superhelix density with increasing ssb, but instead can be mimicked by inhomogeneous all-or-none binding in which uncomplexed native DNAs and nearly relaxed saturated ssb/DNA complexes coexist in varying proportions. Experimental Dapp (K) and S (K) data for a sample of relaxed pUC8 dimers display, respectively, a broad maximum and a corresponding minimum, in qualitative agreement with rough theoretical predictions.

DNA Topoisomerases, Type I↗
PubMed1991

Single-strand breaks, chromosome aberrations, sister-chromatid exchanges, and micronuclei in blood lymphocytes of workers exposed to styrene during the production of reinforced plastics.

Chromosome aberrations (CA), micronuclei (MN, cytokinesis-block [CB] method), and sister-chromatid exchanges (SCE) were analysed in blood lymphocytes of 17 workers and 17 control subjects. The mean urinary mandelic acid level (average 9.4 mmol/l) and styrene glycol in blood (average 2.5 mumol/l) implied exposure to about 300 mg/m3 of styrene in the plant. The number of CA was significantly higher in non-smoking workers compared with nonsmoking controls. A significant correlation was observed between duration of exposure and individual CA level of all workers. No significant effects were observed in MN or SCE. Single-strand breaks (SSB) in DNA of isolated lymphocytes were studied in nine of the workers and eight of the controls by the DNA-unwinding technique. The results showed an increase in SSB among the exposed workers. The present findings support earlier reports on the increase of structural CA in blood lymphocytes of workers in the reinforced plastic industry, and also show that SSBs are elevated in such workers.

Chromosome Aberrations↗