Biomedical subjects

M Ding

Publications and source records attributed to M Ding.

At least 73 records · Page 4Linked to original sources

PubMed2000

Premature structural changes at replication origins in a yeast minichromosome maintenance (MCM) mutant.

The Cdc7p protein kinase in the budding yeast Saccharomyces cerevisiae is thought to help trigger DNA replication by modifying one or more of the factors that assemble at replication origins (ARSs). To investigate events catalyzed by Cdc7p, we compared the structure of replication origins in cells containing conditional mutations in Cdc7p and Cdc8p, a thymidylate kinase that is required for DNA synthesis. High resolution genomic footprinting indicated that the presumptive lagging strand template in ARS1 became highly sensitive to KMnO(4) modification after the CDC7 execution point. These results suggested that Cdc7p triggers DNA unwinding. The transition from late G(1) phase to the CDC7 execution point and from the CDC7 to the CDC8 execution points was accompanied by small but ARS-dependent changes in DNA topology. These results suggested that DNA unwinding before the CDC8 execution point either is highly localized or that the torsional stress associated with initial DNA unwinding is minimized by compensatory protein-DNA structural changes. The ARS DNA structural attributes evident in cells blocked at the CDC8 execution point were also evident in alpha-factor-blocked, G(1) phase cells containing the CDC7 bypass mutant mcm5/cdc46-bob1. This result strongly suggests that the structural changes during the transition from the CDC7 to CDC8 execution points depend on the Cdc7p protein kinase and involve alteration of the minichromosome maintenance protein complex.

Base Sequence↗

PubMed2000

Cell cycle-dependent phosphorylation of centrosomes: localization of phosphopeptide specific antibodies to the centrosome.

The microtubule nucleation capacity of the centrosome increases dramatically as cells progress from interphase into mitosis. The increase in nucleation capacity of the centrosome correlates with the cell cycle-dependent localization of the mitotic protein monoclonal-2 (MPM-2) phosphoepitope-specific antibody to the mitotic centrosome. Therefore, the phosphorylation state of centrosomal components may regulate the microtubule nucleation capacity of this organelle during mitosis. Neither the identity of the MPM-2 kinase(s) nor all of the MPM-2-reactive phosphoproteins associated with the centrosome have been fully elucidated. Only recently have the characteristics of the MPM-2 epitope site been defined, and we used this information to prepare polyclonal antibodies against synthetic phosphopeptides containing potential MPM-2 epitopes derived from the sequences of two MPM-2-reactive proteins, topoisomerase II, and microtubule associated protein 1B (MAP1B). We demonstrate that these phosphopeptide-specific antibodies also localize to the centrosome in a cell cycle-dependent fashion. Thus, polyclonal antibodies have been generated against defined phosphopeptides that reiterate many of the immunofluorescence staining properties exhibited by the MPM-2 antibody. These new phosphopeptide-specific antibodies will provide additional probes to examine the phosphorylation of centrosomal components and the functional consequences of their phosphorylation during mitosis.

Amino Acid Sequence↗

PubMed2000

Analysis of tetramethylpyrazine in Ephedrae herba by gas chromatography-mass spectrometry and high-performance liquid chromatography.

A simple and reliable HPLC method was developed for the determination of 2,3,5,6-tetramethylpyrazine (TMP) in Ephedrae herba. Further identification of TMP was achieved using GC-MS. The mobile phase used was methanol-water-35% acetic acid (35:65:0.5, v/v/v) at a flow-rate of 0.8 ml/min. The detection wavelength was set at 290 nm. The linear range of the peak area calibration curve of TMP was 2.64-264 mg/l (r=0.9987) and the recovery for TMP in Ephedrae herba extracts was 101.1-106.9%. The relative standard deviations of retention time and peak area were 0.18 and 1.5% (n=6), respectively. The detection limit of TMP was 0.03 mg/l. The contents of TMP in Ephedrae herba could easily be determined within 10 min.

Calibration↗

PubMed2000

Short-window spectral analysis of cortical event-related potentials by adaptive multivariate autoregressive modeling: data preprocessing, model validation, and variability assessment.

In this article we consider the application of parametric spectral analysis to multichannel event-related potentials (ERPs) during cognitive experiments. We show that with proper data preprocessing, Adaptive MultiVariate AutoRegressive (AMVAR) modeling is an effective technique for dealing with nonstationary ERP time series. We propose a bootstrap procedure to assess the variability in the estimated spectral quantities. Finally, we apply AMVAR spectral analysis to a visuomotor integration task, revealing rapidly changing cortical dynamics during different stages of task processing.

Animals↗

PubMed2000

Quantitative immunochemistry on neuronal loss, reactive gliosis and BBB damage in cortex/striatum and hippocampus/amygdala after systemic kainic acid administration.

Cell specific markers were quantified in the hippocampus, the amygdala/pyriform cortex, the frontal cerebral cortex and the striatum of the rat brain after systemic administration of kainic acid. Neuron specific enolase (NSE) reflects loss of neurons, glial fibrillary acidic protein (GFAP) reflects reactive gliosis, and brain levels of serum proteins measures blood-brain-barrier permeability. While the concentration of NSE remained unaffected in the frontal cerebral cortex and the striatum, their GFAP content increased during the first three days. In the hippocampus and amygdala, NSE levels decreased significantly. GFAP levels in the hippocampus were unaffected after one day and decreased in the amygdala/pyriform cortex. After that, GFAP increased strikingly until day 9 or, in the case of amygdala/pyriform cortex, even longer. This biphasic time course for GFAP was accompanied by a decrease of S-100 during days 1-9 followed by a significant increase at day 27 above the initial level. The regional differences in GFAP and S-100 could result from the degree of neuronal degeneration, the astrocytic receptor set-up and/or effects on the blood-brain barrier.

Amygdala↗

PubMed2000

Parallel plate model for trabecular bone exhibits volume fraction-dependent bias.

Unbiased stereological methods were used in conjunction with microcomputed tomographic (micro-CT) scans of human and animal bone to investigate errors created when the parallel plate model was used to calculate morphometric parameters. Bone samples were obtained from the human proximal tibia, canine distal femur, rat tail, and pig spine and scanned in a micro-CT scanner. Trabecular thickness, trabecular spacing, and trabecular number were calculated using the parallel plate model. Direct thickness, and spacing and connectivity density were calculated using unbiased three-dimensional methods. Both thickness and spacing calculated using the plate model were well correlated to the direct three-dimensional measures (r(2) = 0. 77-0.92). The correlation between trabecular number and connectivity density varied greatly (r(2) = 0.41-0.94). Whereas trabecular thickness was consistently underestimated using the plate model, trabecular spacing was underestimated at low volume fractions and overestimated at high volume fractions. Use of the plate model resulted in a volume-dependent bias in measures of thickness and spacing (p < 0.001). This was a result of the fact that samples of low volume fraction were much more "rod-like" than those of the higher volume fraction. Our findings indicate that the plate model provides biased results, especially when populations with different volume fractions are compared. Therefore, we recommend direct thickness measures when three-dimensional data sets are available.

Adolescent↗

PubMed2000

Quantification of age-related changes in the structure model type and trabecular thickness of human tibial cancellous bone.

Structure model type and trabecular thickness are important characteristics in describing cancellous bone architecture. It has been qualitatively observed that a radical change of trabeculae from plate-like to rod-like occurs in aging, bone remodeling, and osteoporosis. Thickness of trabeculae has traditionally been measured using model-based histomorphometric methods on two-dimensional (2-D) sections. However, no quantitative study has been published based on three-dimensional (3-D) methods on the age-related changes in structure model type and trabecular thickness for human peripheral (tibial) cancellous bone. In this study, 160 human proximal tibial cancellous bone specimens from 40 normal donors, aged 16 to 85 years, were collected. These specimens were micro-computed tomography (micro-CT) scanned, then the micro-CT images were segmented using optimal thresholds. From accurate 3-D data sets, structure model type and trabecular thickness were quantified by means of novel 3-D methods. Structure model type was assessed by calculating the structure model index (SMI). The SMI was quantified based on a differential analysis of the triangulated bone surface of a structure. This technique allows quantification of structure model type, such as plate, rod objects, or mixture of plates or rods. Trabecular thickness is calculated directly from 3-D images, which is especially important for an a priori unknown or changing structure. Furthermore, 2-D trabecular thickness was also calculated based on the plate model. Our results showed that structure model type changed towards more rod-like in the elderly, and that trabecular thickness declined significantly with age. These changes become significant after 80 years of age for human tibial cancellous bone, whereas both properties seem to remain relatively unchanged between 20 and 80 years. Although a fairly close relationship was seen between 3-D trabecular thickness and 2-D trabecular thickness, real 3-D trabecular thickness was significantly underestimated using 2-D method.

Adolescent↗

PubMed2000

Activation of AP-1 through the MAP kinase pathway: a potential mechanism of the carcinogenic effect of arenediazonium ions.

Arenediazonium ions such as those found in the common mushroom Agaricus bisporus have been convincingly demonstrated to be tumorigenic. The specific mechanism of their tumorigenicity remains unclear. It has been shown that arenediazonium ions can be metabolized to aryl radicals, and that reaction of these aryl radicals with DNA produces aryl adducts. These metabolic processes also produce the reactive oxygen species superoxide and hydroxyl radicals which have been implicated in AP-1 activation. To further investigate the mechanism of tumorigenesis by arenediazonium ions, we studied the effect of a representative arenediazonium ion on AP-1 activation and phosphorylation of the signal transduction proteins ERK1, ERK2, JNK, and p38 kinase, both in vitro and in vivo. We also identified the specific radicals produced by spin trapping and ESR analysis. Here, it was found that p-methylbenzenediazonium ion (2a) induced a 16-fold increase in the extent of AP-1 activation at micromolar concentrations, and that this increase coincided with phosphorylation of the signaling kinases ERK1 and -2 and p38 kinase, but not JNK, in JB6 mouse epithelial cells. In vivo studies using AP-1 luciferase reporter-bearing transgenic mice supported the increase in the extent of AP-1 activation in 2a-treated mice over controls, and showed that this effect was different in different tissue types. The antioxidant N-acetylcysteine (NAC), a general antioxidant, showed an inhibitory effect on 2a-mediated AP-1 induction, while aspirin, a hydroxyl radical scavenger, had no effect. Spin trapping studies showed that while NAC suppressed radical formation from 2a, aspirin did not alter radical production from 2a. It appears that 3a, a carbon-centered radical formed from 2a, is responsible for AP-1-induced activation, and therefore, radical species that are not oxygen-centered are also capable of inducing AP-1. These results represent a step toward understanding the mechanism of tumorigenicity of arenediazonium ions.

Acetylcysteine↗

PubMed2000

Antioxidant properties of (-)-epicatechin-3-gallate and its inhibition of Cr(VI)-induced DNA damage and Cr(IV)- or TPA-stimulated NF-kappaB activation.

Electron spin resonance (ESR) spin trapping was utilized to investigate the scavenging effects on hydroxyl radicals (*OH) and superoxide radicals (O2*-) by (-)-epigallocatechin-3-gallate (EGCG), one of the major anticancer compounds in tea. The spin trap used was 5,5-dimethyl-pyrroline N-oxide (DMPO). The Fenton reaction (Fe2+ + H2O2-->Fe3+ + *OH + OH-) was used as a source of *OH radicals. EGCG efficiently scavenges *OH radicals with reaction rate of 4.62 x 10(11) M(-1)sec(-1), which is an order of magnitude higher than several well recognized antioxidants, such as ascorbate, glutathione and cysteine. It also scavenges O2*- radicals as demonstrated by using xanthine and xanthine oxidase system as a source of O2*- radicals. Through its antioxidant properties, EGCG exhibited a protective effect against DNA damage induced by Cr(VI). EGCG also inhibited activation of nuclear transcription factor NF-kappaB induced by Cr(IV) and 12-o-tetradecanoylphorbol-13-acetate (TPA). The present studies provide a mechanistic basis for the reported anticarcinogenic properties of EGCG and related tea products.

Antioxidants↗

PubMed2000

Pilocytic astrocytomas do not show most of the genetic changes commonly seen in diffuse astrocytomas.

AIMS: While it is well known that pilocytic astrocytomas are clinically distinct from diffuse astrocytomas, few comprehensive studies have focused on their genetic differences. The aim of this study was to examine pilocytic astrocytomas for genetic alterations that are commonly seen in diffuse astrocytomas. METHODS AND RESULTS: By using molecular genetic and immunohistochemical techniques, we evaluated p16, p53, CDK4 and PTEN genes in 29 pilocytic astrocytomas. Mutation screening of p53 and PTEN was performed by single strand conformation polymorphism analysis followed by direct sequencing. Loss of heterozygosity (LOH) of p53, p16 and 10q23-25 loci was performed with microsatellite markers and genomic microsatellite instability (MSI) was also screened. Protein expression of p16, p53, CDK4 and PTEN was examined by immunohistochemistry. Five tumours were found to have single genetic alterations, which included a p53 mutation, a PTEN mutation, MSI at a single microsatellite marker of the p16 locus, and one single LOH at each p16 and 10q23 loci. Protein expressions of p16, CDK4 and PTEN were detected in 73%, 61% and 38% of tumours, respectively. Significantly and in sharp contrast to diffuse astrocytomas, no pilocytic astrocytoma in our series stained for p53 protein. CONCLUSION: Pilocytic astrocytomas have neither MSI phenotype nor recurrent alterations of the p53 and p116 genes. However, altered expression of PTEN may be important in the genesis of pilocytic astrocytomas. We conclude that pilocytic astrocytomas are genetically distinct from diffuse astrocytomas. Lack of p53 mutation/immunostaining may serve as a diagnostic adjunct for differentiating pilocytic astrocytomas from diffuse astrocytomas in small neurosurgical biopsies.

Adolescent↗

PubMed2000

Age variations in the properties of human tibial trabecular bone and cartilage.

Initiated and motivated by clinical and scientific problems such as age-related bone fracture, prosthetic loosening, bone remodeling, and degenerative bone diseases, much significant research on the properties of trabecular bone has been carried out over the last two decades. This work has mainly focused on the central vertebral trabecular bone, while little is known about age-related changes in the properties of human peripheral (tibial) trabecular bone. Knowledge of the properties of peripheral (tibial) trabecular bone is of major importance for the understanding of degenerative diseases such as osteoarthrosis and osteoporosis, and for the design, fixation and durability of total joint prosthesis. The specific aims of the present studies were: 1) to investigate normal age-related variations in the mechanical, physical/compositional, and structural properties of human tibial trabecular bone; and 2) to investigate the age-related and osteoarthrosis-related changes in the mechanical properties of the human tibial cartilage-bone complex; and 3) to evaluate mutual associations among various properties. Normal specimens from human autopsy proximal tibiae were used for investigation of age variations in the properties of trabecular bone and the cartilage-bone complex, and osteoarthrotic specimens were used for the investigation of changes in the mechanical properties of the cartilage-bone complex induced by this disease process. The mechanical properties and physical/compositional properties of trabecular bone were quantified by means of standard techniques, and trabecular bone structure was quantified by means of unbiased three-dimensional methods. The present study demonstrated that the mechanical properties, such as Young's modulus, ultimate stress, ultimate strain and failure energy, and the densities, such as apparent, apparent ash and collagen densities of human tibial trabecular bone have significant relationships with age. Tissue density and mineral concentration remain constant throughout life. Trabecular bone is tougher in the younger age, i.e. fracture requires more energy. Collagen density was the single best predictor of failure energy, and collagen concentration was the only predictor of ultimate strain. The decrease in mechanical properties of trabecular bone mainly is a consequence of the loss of trabecular bone substance. This study showed that the degree of anisotropy (preferential orientation of trabeculae), mean marrow space volume, and bone surface-to-volume ratio increased significantly with age. Bone volume fraction, mean trabecular volume, and bone surface density decreased significantly with age. Connectivity did not have a general relationship with age, yet a trend exists. Age-related changes in the microstructural properties had the same trends for both medial and lateral condyles of the tibia. The observed increase of anisotropy may be interpreted as the consequence of structural adaptation secondary to age-induced bone loss. The aging trabeculae align more strongly to the primary direction, which is parallel to the longitudinal loading axis of the tibia. The mechanical properties of the normal cartilage and bone vary with age and respond simultaneously to mechanical loading. Both cartilage and bone in early-stage OA are mechanically inferior to normal, and OA cartilage and bone have lost their unit function to mechanical loading.

Adolescent↗

PubMed2000

Integrated approach to the assessment of long range correlation in time series data

To assess whether a given time series can be modeled by a stochastic process possessing long range correlation, one usually applies one of two types of analysis methods: the spectral method and the random walk analysis. The first objective of this work is to show that each one of these methods used alone can be susceptible to producing false results. We thus advocate an integrated approach which requires the use of both methods in a consistent fashion. We provide the theoretical foundation of this approach and illustrate the main ideas using examples. The second objective relates to the observation of long range anticorrelation (Hurst exponent H < 1/2) in real world time series data. The very peculiar nature of such processes is emphasized in light of the stringent condition under which such processes can occur. Using examples, we discuss the possible factors that could contribute to the false claim of long range anticorrelations, and demonstrate the particular importance of the integrated approach in this case.

Journal Article↗

PubMed2000

Anomalous diffusion and the first passage time problem

We study the distribution of the first passage time (FPT) in Levy type anomalous diffusion. Using the recently formulated fractional Fokker-Planck equation we obtain three results. (1) We derive an explicit expression for the FPT distribution in terms of Fox or H functions when the diffusion has zero drift. (2) For the nonzero drift case we obtain an analytical expression for the Laplace transform of the FPT distribution. (3) We express the FPT distribution in terms of a power series for the case of two absorbing barriers. The known results for ordinary diffusion (Brownian motion) are obtained as special cases of our more general results.

Journal Article↗

PubMed2000

The role of hydroxyl radical as a messenger in Cr(VI)-induced p53 activation.

The present study investigates whether reactive oxygen species (ROS) are involved in p53 activation, and if they are, which species is responsible for the activation. Our hypothesis is that hydroxyl radical (.OH) functions as a messenger for the activation of this tumor suppressor protein. Human lung epithelial cells (A549) were used to test this hypothesis. Cr(VI) was employed as the source of ROS due to its ability to generate a whole spectrum of ROS inside the cell. Cr(VI) is able to activate p53 by increasing the protein levels and enhancing both the DNA binding activity and transactivation ability of the protein. Increased cellular levels of superoxide radicals (O(2)(-).), hydrogen peroxide (H(2)O(2)), and.OH radicals were detected on the addition of Cr(VI) to the cells. Superoxide dismutase, by enhancing the production of H(2)O(2) from O(2)(-). radicals, increased p53 activity. Catalase, an H(2)O(2) scavenger, eliminated.OH radical generation and inhibited p53 activation. Sodium formate and aspirin,.OH radical scavengers, also suppressed p53 activation. Deferoxamine, a metal chelator, inhibited p53 activation by chelating Cr(V) to make it incapable of generating radicals from H(2)O(2). NADPH, which accelerated the one-electron reduction of Cr(VI) to Cr(V) and increased.OH radical generation, dramatically enhanced p53 activation. Thus.OH radical generated from Cr(VI) reduction in A549 cells is responsible for Cr(VI)-induced p53 activation.

Carcinogens, Environmental↗

PubMed2000

A missense mutation G2320R in the thyroglobulin gene causes non-goitrous congenital primary hypothyroidism in the WIC-rdw rat.

A convincing line of evidence is being developed that the congenital nongoitrous hypothyroidism and dwarfism observed in the WIC-rdw rat may indeed be caused by a primary defect in thyroid hormonogenesis. In support of this hypothesis, several recent reports have shown the presence of elevated molecular chaperone levels in the WIC-rdw thyrocytes, the endoplasmic reticulum of which was markedly dilated, suggesting a defect in intracellular protein transport. Here the studies were undertaken to identify the precise molecular defect in the WIC-rdw rat. First, the genetic linkage analysis revealed that the rdw locus was on rat chromosome 7 and was identical to the thyroglobulin (Tg) gene locus. Moreover, the Tg protein level was reduced in the WIC-rdw thyroid despite a similar level of the Tg gene transcripts that were indistinguishable in their size from the normal. Next, the complete sequencing of the rdw and the normal rat Tg cDNAs revealed a single nucleotide change, G6958C, resulting in a G2320R missense mutation in a highly conserved region of the Tg molecule. Finally, transient expression of the intact Tg cDNA containing the rdw mutation in the COS-7 cells showed no detectable Tg in the secreted media, indicating a severe defect in the export of the mutant Tg. Together, our observations suggest that a missense mutation, G2320R, in the Tg gene is responsible for the rdw mutation in the WIC-rdw rat.

Animals↗

PubMed2000

Toxoplasma gondii catalase: are there peroxisomes in toxoplasma?

The intracellular protozoan parasite Toxoplasma gondii, like all members of the phylum Apicomplexa, is known to possess many organelles: in addition to mitochondria and the compartments of the secretory pathway, there is a reduced chloroplast (the apicoplast) and the phylum-specific components of the apical complex: dense granules, micronemes and rhoptries. Conspicuously missing so far are microbodies, organelles that can be found in nearly all eukaryotic organisms. Microbodies show a large variation with regard to their size, number and contents, depending on the organism and cell type. One marker enzyme of this single membrane-bound organelle is catalase, which is responsible for the degradation of hydrogen peroxide to water and oxygen. The EST project in T. gondii revealed the existence of two overlapping clones which showed similarity with catalase, and these were used to clone the corresponding gene. The predicted sequence of T. gondii catalase has -AKM at the C terminus, which falls within the consensus of the PTS1 peroxisomal targeting signal. Southern blot analysis confirmed the presence of a single copy gene. Northern and western blot analyses showed that the catalase gene is transcribed and translated. Immunofluorescence assays using an antibody raised against a catalase peptide identified a distinct structure towards the apical end, but other catalase-specific antibodies failed to confirm this localisation. Cell fractionations indicated that the majority of the enzyme was in the cytosol. The fusion of the C-terminal twelve amino acids, including AKM, or the canonical peroxisomal targeting signal, -SKL, to GFP resulted in predominantly cytosolic localization in T. gondii. There was therefore no evidence for membrane-bound peroxisomes in Toxoplasma.

Amino Acids↗

PubMed2000

On the role of hydroxyl radical and the effect of tetrandrine on nuclear factor--kappaB activation by phorbol 12-myristate 13-acetate.

Nuclear factor kappaB (NF-kappaB) is considered to be an important target for therapeutic intervention because of its role in the regulation of proinflammatory and profibrotic mediators. The present study examined the role of hydroxyl (*OH) radical and the effect of tetrandrine, an alkaloid extracted from the Chinese medicinal herb Stephania tetrandra, on NF-kappaB activation by a tumor promoter, phorbol 12-myristate 13-acetate (PMA) in human lymphoid T cells (ie, Jurkat cells). Exogenous superoxide dismutase (SOD) enhanced the NF-kappaB activation by PMA, while catalase blocked it. Formate, a scavenger of *OH radical, also was inhibitory, as was deferoxamine, a metal chelator. These data suggest an important role of *OH radical in PMA-induced NF-kappaB activation. Incubation of the cells with tetrandrine prior to the stimulation of the cells was found to inhibit PMA-induced NF-kappaB activation. Tetrandrine activity was so potent that 50 microM of tetrandrine was sufficient to inhibit activation of NF-kappaB completely. Electron spin resonance (ESR) spin trapping was used to investigate the antioxidant action of tetrandrine using 5,5-dimethyl-1-pyrroline N-oxide (DMPO) as a spin trap. Tetrandrine is an antioxidant for both *OH and superoxide (O2-)radicals. The reaction rate constant of tetrandrine with *OH is 1.4 x 10(10) M(-1)sec(-1), which is comparable with several well established antioxidants, such as ascorbate, glutathione, and cysteine. The Fenton reaction (Fe(II) + H2O2-->Fe(III) + *OH + OH-) and xanthine/xanthine oxidase were used as sources of *OH and O2- radicals. The free radical scavenging activity of tetrandrine is responsible for its inhibition of PMA-induced NF-kappaB activation.

Alkaloids↗

PubMed2000

Antioxidant properties of pyrrolidine dithiocarbamate and its protection against Cr(VI)-induced DNA strand breakage.

Pyrrolidine dithiocarbamate (PDTC) is considered an antioxidant and is frequently used to study the role of free radical reactions in various biological processes and against free radical-induced cellular injuries. However, its antioxidant properties are not characterized. In this study, electron spin resonance (ESR) was used to investigate the antioxidant potential of PDTC with hydroxyl radical (*OH) and superoxide anion radicals (O2*-). The Fenton reaction [Fe(II) + H2O2 --> Fe(II) + *OH + OH-)] and xanthine and xanthine oxidase were used as sources of *OH and O2*- radicals, respectively. The results show that PDTC effectively scavenges *OH radicals with a reaction rate constant of approximately 2.73 x 10(10) M(-1) s(-1), which is comparable to other efficient *OH radical scavengers, such as ascorbate and glutathione. PDTC is also able to scavenge O2*- radicals. Through its antioxidant properties, PDTC protects against Cr(VI)-induced DNA strand breakage.

Antioxidants↗