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Hong Zhang

Publications and source records attributed to Hong Zhang.

At least 73 records · Page 4Linked to original sources
PubMed2006

Signature patterns revealed by microarray analyses of mice infected with influenza virus A and Streptococcus pneumoniae.

We used cDNA microarrays to identify differentially expressed genes in mice in response to infections with influenza virus A/PR/8/34 (H1N1) and Streptococcus pneumoniae. Expression microarray analysis showed up-regulation and down-regulation of many genes involved in the defense, inflammatory response and intracellular signaling pathways including chemokine, apoptosis, MAPK, Notch, Jak-STAT, T-cell receptor and complement and coagulation cascades. We have revealed signature patterns of gene expression in mice infected with two different classes of pathogens: influenza virus A and S. pneumoniae. Quantitative real-time RT-PCR results confirmed microarray results for most of the genes tested. These studies document clear differences in gene expression profiles between mice infected with influenza virus A and S. pneumoniae. Identification of genes that are differentially expressed after respiratory infections can provide insights into the mechanisms by which the host interacts with different pathogens, useful information about stage of diseases and selection of suitable targets for early diagnosis and treatments. The advantage of this novel approach is that the detection of pathogens is based on the differences in host gene expression profiles in response to different pathogens instead of detecting pathogens directly.

Animals↗
PubMed2006

Alpha-amino-beta-carboxymuconic-epsilon-semialdehyde decarboxylase (ACMSD) is a new member of the amidohydrolase superfamily.

The enzymatic activity of Pseudomonas fluorescens alpha-amino-beta-carboxymuconic-epsilon-semialdehyde decarboxylase (ACMSD) is critically dependent on a transition metal ion [Li, T., Walker, A. L., Iwaki, H., Hasegawa, Y., and Liu, A. (2005) J. Am. Chem. Soc. 127, 12282-12290]. Sequence analysis in this study further suggests that ACMSD belongs to the amidohydrolase superfamily, whose structurally characterized members comprise a catalytically essential metal cofactor. To identify ACMSD's metal ligands and assess their functions in catalysis, a site-directed mutagenesis analysis was conducted. Alteration of His-9, His-177, and Asp-294 resulted in a dramatic loss of enzyme activity, substantial reduction of the metal-binding ability, and an altered metallocenter electronic structure. Thus, these residues are confirmed to be the endogenous metal ligands. His-11 is implicated in metal binding because of the strictly conserved HxH motif with His-9. Mutations at the 228 site yielded nearly inactive enzyme variants H228A and H228E. The two His-228 mutant proteins, however, exhibited full metal-binding ability and a metal center similar to that of the wild-type enzyme as shown by EPR spectroscopy. Kinetic analysis on the mutants indicates that His-228 is a critical catalytic residue along with the metal cofactor. Since the identified metal ligands and His-228 are present in all known ACMSD sequences, it is likely that ACMSD proteins from other organisms contain the same cofactor and share similar catalytic mechanisms. ACMSD is therefore the first characterized member in the amidohydrolase superfamily that represents a C-C breaking activity.

Amidohydrolases↗
PubMed2006

A novel chemical-defined medium with bFGF and N2B27 supplements supports undifferentiated growth in human embryonic stem cells.

Traditionally, undifferentiated human embryonic stem cells (hESCs) are maintained on mouse embryonic fibroblast (MEF) cells or on matrigel with an MEF-conditioned medium (CM), which hampers the clinical applications of hESCs due to the contamination by animal pathogens. Here we report a novel chemical-defined medium using DMEM/F12 supplemented with N2, B27, and basic fibroblast growth factor (bFGF) [termed NBF]. This medium can support prolonged self-renewal of hESCs. hESCs cultured in NBF maintain an undifferentiated state and normal karyotype, are able to form embryoid bodies in vitro, and differentiate into three germ layers and extraembryonic cells. Furthermore, we find that hESCs cultured in NBF possess a low apoptosis rate and a high proliferation rate compared with those cultured in MEF-CM. Our findings provide a novel, simplified chemical-defined culture medium suitable for further therapeutic applications and developmental studies of hESCs.

Apoptosis↗
PubMed2006

Phosphorylation of STAT3 serine-727 by cyclin-dependent kinase 1 is critical for nocodazole-induced mitotic arrest.

Signal transducer and activator of transcription 3 (STAT3) mediates cellular responses to diverse cytokines and growth factors by modulating the expression of specific target genes. While phosphorylation of STAT3 at Tyr-705 has been demonstrated to be a prerequisite for STAT3 dimerization, nuclear translocation, and activation of gene transcription, the role of Ser-727 in regulation of STAT3 activity is controversial. Kinetworks KPSS-1.1 phospho-site screening of nocodazole-treated HeLa cells revealed that STAT3 Ser-727 phosphorylation was enhanced during mitosis, and this correlated with a reduction of Tyr-705 phosphorylation. Overexpression of STAT3 mutants in which these phosphorylation sites were separately abolished revealed that phosphorylation at these sites appeared to be mutually antagonistic. The nocodazole-induced STAT3 Ser-727 phosphorylation was reduced by selective inhibition of CDK1 phosphotransferase activity, and CDK1 could directly phosphorylate GST-STAT3 Ser-727 in vitro and co-immunoprecipitate with STAT3 in vivo. Blocking Ser-727 phosphorylation enhanced STAT3 DNA-binding activity toward its target gene promoters, implying a negative effect of Ser-727 phosphorylation on its transcriptional activity. Interference of Ser-727 phosphorylation resulted in an exit from mitotic arrest induced by nocodazole treatment and a cell cycle arrest at the G1 phase, as indicated by the accumulation of 2N cell population and enhanced expression of G1 cell cycle regulators including p21(CIP1/WAF1), p27(Kip1), and cyclin E. Taken together, our observations point to a novel role of STAT3 Ser-727 phosphorylation in control of the onset and maintenance of the M phase during the cell cycle through downregulation of CDK inhibitors.

CDC2 Protein Kinase↗
PubMed2006

A biochemical rationale for the anticancer effects of Hsp90 inhibitors: slow, tight binding inhibition by geldanamycin and its analogues.

Heat shock protein (Hsp)90 is emerging as an important therapeutic target for the treatment of cancer. Two analogues of the Hsp90 inhibitor geldanamycin are currently in clinical trials. Geldanamycin (GA) and its analogues have been reported to bind purified Hsp90 with low micromolar potency, in stark contrast to their low nanomolar antiproliferative activity in cell culture and their potent antitumor activity in animal models. Several models have been proposed to account for the approximately 100-fold-greater potency in cell culture, including that GA analogues bind with greater affinity to a five-protein Hsp90 complex than to Hsp90 alone. We have determined that GA and the fluorescent analogue BODIPY-GA (BDGA) both demonstrate slow, tight binding to purified Hsp90. BDGA, used to characterize the kinetics of ligand-Hsp90 interactions, was found to bind Hsp90alpha with k(off) = 2.5 x 10(-3) min(-1), t(1/2) = 4.6 h, and Ki* = 10 nM. It was found that BDGA binds to a functional multiprotein Hsp90 complex with kinetics and affinity identical to that of Hsp90 alone. Also, BDGA binds to Hsp90 from multiple cell lysates in a time-dependent manner with similar kinetics. Therefore, our results indicate that the high potency of GA in cell culture and in vivo can be accounted for by its time-dependent, tight binding to Hsp90 alone. In the broader context, these studies highlight the essentiality of detailed biochemical characterization of drug-target interactions for the effective translation of in vitro pharmacology to cellular and in vivo efficacy.

Animals↗
PubMed2006

Antisense oligonucleotide inhibition of tumor necrosis factor receptor 1 protects the liver from radiation-induced apoptosis.

PURPOSE: Liver damage by radiation limits its efficacy in cancer treatment. As radiation can generate apoptotic signals, we wished to examine the potential to protect the liver by inhibiting apoptosis through two key mediators, FAS and tumor necrosis factor receptor 1 (TNFR1). EXPERIMENTAL DESIGN: Radiation-induced liver damage was assessed by serum aspartate aminotransferase and alanine aminotransferase, hepatocyte micronucleus formation, and apoptosis assays (terminal nucleotidyl transferase-mediated nick end labeling and caspase-3 cleavage) in mice. Protection was evaluated by pretreating mice with antisense oligonucleotides (ASO) for FAS or TNFR1 prior to radiation. TNF-alpha production in liver and in Kupffer cells were determined by ELISA. RESULTS: Radiation increased liver FAS and TNFR1 transcription in a dose- and time-dependent manner (maximized at 25 Gy and 8 hours postirradiation). Pretreatment with ASOs for FAS and TNFR1 resulted in the inhibition of liver FAS and TNFR1 by 78% and 59%, respectively. Inductions of serum aspartate aminotransferase and alanine aminotransferase were observed at 2 hours after radiation and could be reduced by pretreating mice with ASO for TNFR1 but not FAS or control oligonucleotide. Radiation-induced liver apoptosis (terminal nucleotidyl transferase-mediated nick end labeling staining and caspase-3 activation on Western blot) and hepatocyte micronucleus formation were reduced by pretreatment with ASO for TNFR1. In addition, radiation stimulated TNF-alpha production both in irradiated liver and in cultured Kupffer cells by >50% and 100%, respectively. CONCLUSION: This study suggests that ionizing radiation activates apoptotic signaling through TNFR1 in the liver, and thus provides a rationale for anti-TNFR1 apoptotic treatment to prevent radiation-induced liver injury.

Animals↗
PubMed2006

Comparison of clonogenic assay with premature chromosome condensation assay in prediction of human cell radiosensitivity.

AIM: To determine whether the number of non-rejoining G2-chromatid breaks can predict the radiosensitivity of human cell lines. METHODS: Cell lines of human ovary carcinoma cells (HO8910), human hepatoma cells (HepG2) and liver cells (L02) were irradiated with a range of doses and assessed both of cell survival and non-rejoining G2-chromatid breaks at 24 h after irradiation. Cell survival was documented by a colony assay. Non-rejoining G2-chromatid breaks were measured by counting the number of non-rejoining G2 chromatid breaks at 24 h after irradiation, detected by the prematurely chromosome condensed (PCC) technique. RESULTS: A linear-quadratic survival curve was observed in three cell lines, and HepG2 was the most sensitive to gamma-radiation. A dose-dependent linear increase was observed in radiation-induced non-rejoining G2-PCC breaks measured at 24 h after irradiation in all cell lines, and HepG2 was the most susceptible to induction of non-rejoining G2-PCC breaks. A close correlation was found between the clonogenic radiosensitivity and the radiation-induced non-rejoining G2-PCC breaks (r = 0.923). Furthermore, survival-aberration correlations for two or more than two doses lever were also significant. CONCLUSION: The number of non-rejoining G2 PCC breaks holds considerable promise for predicting the radiosensitivity of normal and tumor cells when two or more than two doses lever is tested.

Cell Line, Tumor↗
PubMed2006

HOCl Ro-vibrational bound-state calculations for nonzero total angular momentum.

The Lanczos homogeneous filter diagonalization method has been employed to compute the HOCl ro-vibrational states for a range of total angular momenta (J = 0, 1, 5, 10, 11, 20, 30) on a newly developed ab initio potential energy surface by Nanbu et al. (J. Theor. Comput. Chem. 2002, 1, 263). For such computationally challenging calculations, a parallel computing strategy has been incorporated into our method to perform the matrix-vector multiplications. For the computed low bound states, a spectroscopic assignment has been made and the widely used approximate adiabatic rotation method has been tested for the broad range of total angular momenta for this deep-well system. Comparison of experimental results with exact quantum mechanical calculations for the selected far-infrared transitions involving the range of total angular momenta has been made possible for the first time.

Computer Simulation↗
PubMed2006

Spectroscopic studies of the interaction between quercetin and G-quadruplex DNA.

Quercetin is a kind of flavonoid which has been proved to exhibit anti-tumor activity. The interaction modes of quercetins with monomeric and dimeric G-quadruplexes were studied by absorption, fluorescence, CD, and (1)H NMR spectroscopies. The ligands were found to be stacked with terminal tetrads of monomeric G-quadruplexes by intercalation and bound to dimeric G-quadruplexes by groove binding.

Binding Sites↗
PubMed2006

Serum concentrations of MMP-1, MMP-2, and TIMP-1 in Chinese women: age-related changes, and the relationships with bone biochemical markers, bone mineral density.

BACKGROUND: Osteoblast-derived matrix metalloproteinse-1 (MMP-1), MMP-2 and tissue inhibitor of metalloproteinase-1 (TIMP-1) play a role in bone metabolism by degrading bone matrix. METHODS: We measured MMP-1, MMMP-2, TIMP-1 and associated results with age and bone metabolism in 591 Chinese women aged 20-80 y. RESULTS: Serum MMP-1, MMP-2, and TIMP-1 concentrations exhibited positive correlation with age. Serum concentrations of MMP-1 were higher in 40-69 y old women. The concentrations of MMP-2 were significantly increased in the 50-69 y olds. Serum TIMP-1 concentrations were significantly lower in women aged 30-59 y, and then these were followed by an increase at >60 y olds. We found a significant negative weaker correlation between MMP-2 and BMD. But multiple linear stepwise regression analysis showed that MMP-2 was not a determinant factor for BMD. There were significant positive correlations between MMP-2 and bone alkaline phosphatase (BAP), osteocalcin (OC), and cross-linked N-telopeptides of type I collagen (NTX). CONCLUSIONS: The serum concentrations of MMP-1, MMP-2, and TIMP-1 exhibit age-related changes, and circulating MMP-2 and bone turnover are related.

Adult↗
PubMed2006

Adenosine downregulates DPPIV on HT-29 colon cancer cells by stimulating protein tyrosine phosphatase(s) and reducing ERK1/2 activity via a novel pathway.

The multifunctional cell-surface protein dipeptidyl peptidase IV (DPPIV/CD26) is aberrantly expressed in many cancers and plays a key role in tumorigenesis and metastasis. Its diverse cellular roles include modulation of chemokine activity by cleaving dipeptides from the chemokine NH(2)-terminus, perturbation of extracellular nucleoside metabolism by binding the ecto-enzyme adenosine deaminase, and interaction with the extracellular matrix by binding proteins such as collagen and fibronectin. We have recently shown that DPPIV can be downregulated from the cell surface of HT-29 colorectal carcinoma cells by adenosine, which is a metabolite that becomes concentrated in the extracellular fluid of hypoxic solid tumors. Most of the known responses to adenosine are mediated through four different subtypes of G protein-coupled adenosine receptors: A(1), A(2A), A(2B), and A(3). We report here that adenosine downregulation of DPPIV from the surface of HT-29 cells occurs independently of these classic receptor subtypes, and is mediated by a novel cell-surface mechanism that induces an increase in protein tyrosine phosphatase activity. The increase in protein tyrosine phosphatase activity leads to a decrease in the tyrosine phosphorylation of ERK1/2 MAP kinase that in turn links to the decline in DPPIV mRNA and protein. The downregulation of DPPIV occurs independently of changes in the activities of protein kinases A or C, phosphatidylinositol 3-kinase, other serine/threonine phosphatases, or the p38 or JNK MAP kinases. This novel action of adenosine has implications for our ability to manipulate adenosine-dependent events within the solid tumor microenvironment.

Adenosine↗
PubMed2006

Ultrafast charge separation in a photoreactive rhenium-appended porphyrin assembly monitored by picosecond transient infrared spectroscopy.

Rhenium(bipyridine)(tricarbonyl)(picoline) units have been linked covalently to tetraphenylmetalloporphyrins of magnesium and zinc via an amide bond between the bipyridine and one phenyl substituent of the porphyrin. The resulting complexes, abbreviated as [Re(CO)(3)(Pic)Bpy-MgTPP][OTf] and [Re(CO)(3)(Pic)Bpy-ZnTPP][OTf], exhibit no signs of electronic interaction between the Re(CO)(3)(bpy) units and the metalloporphyrin units in their ground states. However, emission spectroscopy reveals solvent-dependent quenching of porphyrin emission on irradiation into the long-wavelength absorption bands localized on the porphyrin. The characteristics of the excited states have been probed by picosecond time-resolved absorption (TRVIS) spectroscopy and time-resolved infrared (TRIR) spectroscopy in nitrile solvents. The presence of the charge-separated state involving electron transfer from MgTPP or ZnTPP to Re(bpy) is signaled in the TRIR spectra by a low-frequency shift in the nu(CO) bands of the Re(CO)(3) moiety similar to that observed by spectroelectrochemical reduction. Long-wavelength excitation of [Re(CO)(3)(Pic)Bpy-MTPP][OTf] results in characteristic TRVIS spectra of the S(1) state of the porphyrin that decay with a time constant of 17 ps (M = Mg) or 24 ps (M = Zn). The IR bands of the CS state appear on a time scale of less than 1 ps (Mg) or ca. 5 ps (Zn) and decay giving way to a vibrationally excited (i.e., hot) ground state via back electron transfer. The IR bands of the precursors recover with a time constant of 35 ps (Mg) or 55 ps (Zn). The short lifetimes of the charge-transfer states carry implications for the mechanism of reaction in the presence of triethylamine.

Journal Article↗
PubMed2006

Histological and magnetic resonance imaging assessment of cortical layering and thickness in autism spectrum disorders.

BACKGROUND: Qualitative reports of the cerebral cortex in a small number of autism spectrum disorder (ASD) cases have suggested an increase in thickness and disruptions in migration and lamination patterns. METHODS: We examined postmortem ASD individuals and age-matched controls using magnetic resonance imaging (MRI) to evaluate total cortical thickness, and histological samples to evaluate the pattern of cortical layering. RESULTS: Overall, thickness measures from ASD subjects were equivalent to control cases. Individual regions showed marginal but nonsignificant thickness differences in the temporal lobes. Cortical thickness values in ASD subjects decreased significantly with age. Quantitative examination of proportional layer thickness in histological sections indicated that the pattern of cortical layering was largely undisturbed, while qualitative examination of these same samples revealed evidence of cell clustering and supernumerary cells in layer I and the subplate. These features were not severe and were never found in a majority of cases. CONCLUSIONS: These findings support limited disturbances in cortical cell patterning, but do not indicate a major deficit in the orderly migration of cortical neuroblasts during development, or their subsequent aggregation into the laminar pattern found in typically developing individuals.

Adolescent↗
PubMed2006

Change of dissolved gaseous mercury concentrations in a southern reservoir lake (Tennessee) following seasonal variation of solar radiation.

A 12-month field study was conducted consecutively from June 2003 to May 2004 to quantify temporal variations of dissolved gaseous mercury (DGM) concentrations in Cane Creek Lake, a southern reservoir lake (Cookeville, TN). Diurnal changes of DGM concentrations in two periods (morning increase vs afternoon decrease with an around-noon peak) were observed, and the changes closely followed daily solar radiation variation trends. The diurnal patterns prevailed in the late spring and summer, but became vague in the late fall and winter. The monthly mean DGM concentrations peaked at 40.8 pg L(-1) in July and reached the lowest at 14.2 pg L(-1) in December and 21.9 pg L(-1) in January; this DGM concentration change closely followed the monthly mean solar radiation variation trend. The increase of the lake DGM concentration from January to July and its decrease from July to December mirror the typical daily rhythm of DGM concentration variations in the two periods. This finding supports the following hypothesis: The natural phenomenon of daily oscillation of freshwater DGM concentrations that follows diurnal solar radiation variation would manifest on a seasonal scale. High DGM concentrations were found in the spring and summer and low in the fall and winter (seasonal mean: 34.2, 37.5, 20.0, 24.4 pg L(-1), respectively). This seems to suggest an annual occurrence of two periods of the seasonal DGM level fluctuation (spring and summer high vs fall and winter low DGM levels). Linear relationships of the monthly mean DGM concentrations were found with the monthly mean global solar radiation (R2 = 0.82, P < 0.05) and UVA radiation (R2 = 0.84, P < 0.05). Linear relationships of the seasonal mean DGM concentrations were also found with the seasonal mean global solar radiation (R2 = 0.85, P = 0.08) and UVA radiation (R2 = 0.93, P < 0.05).

Gases↗
PubMed2006

Expression and regulation of AT1 receptor in rat lung microvascular endothelial cell.

BACKGROUND: The renin-angiotensin system is thought to be involved in the development and progression of vascular endothelium inflammation, thereby contributing to vascular endothelium injury. To clarify the role of angiotensin II (Ang II) in rat pulmonary microvascular endothelial cells (RPMVECs), we examined the expression and functional significance of angiotensin II (Ang II) receptors in normal and lipopolysacchride (LPS) treated RPMVECs. METHODS: The expressions of Ang II type 1(AT(1)) and Ang II type 2 (AT(2)) receptors in cultured RPMVECs were identified by the reverse transcription-polymerase chain reaction (RT-PCR) technique, Western blot and (125)I-labeled [Sar(1),Ile(8)] Ang II binding assays. The RPMVECs were treated with LPS (0.1-100 microg/ml) and Ang II (10(-8)-10(-5) M) for 24 h, respectively. Next, RPMVECs were treated with 10 microg/ml LPS or 10(-7) M Ang II for various times (3, 6, 12, and 24 h). The mRNA and protein levels of, AT(1) and AT(2) receptors, were evaluated at 3, 6, 12, and 24 h, respectively. RESULTS: The presence of specific Ang II binding sites in RPMVECs was found by Ang II saturated assays. RT-PCR revealed that only the AT(1) receptor mRNA is presented in RPMVECs. Western blot analysis of the RPMVECs protein extracts showed only one prominent band of the protein at approximately 41 KDa when probed with anti-AT(1) antibody and anti-AT(2) antibody. No AT(2) receptor mRNA and protein was detected. LPS treated cells resulted in an increase in the mRNA and protein levels of AT(1) receptor, whereas, Ang II treated cells showed a decrease in the mRNA and protein levels of AT(1) receptor. CONCLUSIONS: We found that primary cultured RPMVECs expressed only AT(1) receptor, but not AT(2) receptor. LPS up-regulated the transcriptional and post-transcriptional expression of AT(1) receptor in RPMVECS; in contrast, Ang II treatment caused a reduction in the mRNA and protein of AT(1) receptor in a time-dependent manner.

Angiotensin II↗
PubMed2006

Mitochondrial thioredoxin-2 has a key role in determining tumor necrosis factor-alpha-induced reactive oxygen species generation, NF-kappaB activation, and apoptosis.

Tumor necrosis factor-alpha (TNF-alpha) is a cytokine that is involved in numerous pathologies, in part through stimulation of the mitochondrial production of reactive oxygen species (ROS). Previous studies show that in addition to mitochondrial superoxide dismutase- and glutathione-dependent systems, mitochondria also contain thioredoxin-2 (Trx2), an antioxidant protein that can detoxify ROS. The purpose of this study was to determine whether Trx2 protects against oxidative damage triggered by TNF-alpha. After a 30-min treatment in HeLa cells, TNF-alpha (5-40 ng/ml) oxidized Trx2 but not cytoplasmic Trx1. Preferential, significant Trx2 oxidation occurred within 10 min of TNF-alpha treatment. Moreover, overexpression of Trx2, but not Trx1, decreased TNF-alpha-induced ROS generation, suggesting mitochondrial compartmentation of ROS production and subsequent specific detoxification by Trx2, not Trx1. Overexpression of Trx2 or the active-site mutant C93S Trx2 was used to evaluate their downstream effects following TNF-alpha stimulation. Results showed that nuclear translocation of NF-kappaB was inhibited with Trx2 overexpression but not with the dominant negative active-site mutant C93S Trx2. Moreover, when cotransfected with a NF-kappaB-luciferase reporter and then treated with TNF-alpha, NF-kappaB activity was significantly attenuated with Trx2 overexpression but not with C93S Trx2 expression. Trx2 overexpression, but not C93S Trx2, significantly inhibited TNF-alpha-induced apoptosis as measured by terminal dUTP nick-end labeling assay. These findings support the interpretation that mitochondrial-generated ROS is a principal component in TNF-alpha-induced effects and that Trx2 blocks TNF-alpha-induced ROS generation and downstream NF-kappaB activation and apoptosis.

Apoptosis↗
PubMed2006

Chromosomal aberrations induced by (12)C6+ ions and 60Co gamma-rays in mouse immature oocytes.

The ovaries of Kun-Ming strain mice (3 weeks) were irradiated with different doses of (12)C6+ ion or (60)Co gamma-ray. Chromosomal aberrations were analyzed in metaphase II oocytes at 7 weeks after irradiation. The relative biological effectiveness (RBE) of (12)C6+ ion was calculated with respect to 60Co gamma-ray for the induction of chromosomal aberrations. The (12)C6+ ion and 60Co gamma-ray dose-response relationships for chromosomal aberrations were plotted by linear quadratic models. The data showed that there was a dose-related increase in frequency of chromosomal aberrations in all the treated groups compared to controls. The RBE values for (12)C6+ ions relative to 60Co gamma-rays were 2.49, 2.29, 1.57, 1.42 or 1.32 for the doses of 0.5, 1.0, 2.0, 4.0 or 6.0 Gy, respectively. Moreover, a different distribution of the various types of aberrations has been found for (12)C6+ ion and 60Co gamma-ray irradiations. The dose-response relationships for (12)C6+ ion and 60Co gamma-ray exhibited positive correlations. The results from the present study may be helpful for assessing genetic damage following exposure of immature oocytes to ionizing radiation.

Animals↗