China
Africa
Explore chapters and articles related to this topic
In Vitro Techniques to Study the Transport of Radiotracers
Published in Lelio G. Colombetti, Biological Transport of Radiotracers, 2020
Marco Salvatore, Luigi Mansi, Gianni Morrone, Rosa Ferraiuolo, Salvatore Venuta
Our chicken embryo fibroblasts system permits an easy and efficient control of changes in growth rate which can be measured by the incorporation of (3H) thymidine (3H-TdR) and the uptake of (3H)-2-deoxy-glucose, (3H-2dGlc). It has been demonstrated that 2dGlc uptake increases in fast-growing cells.15 Of course the incorporation of TdR in DNA is due to the chromosome duplication which procèdes cell division.
Unified Theory on the Basic Mechanism of Normal Mitotic Control and Oncogenesis*
Published in Richard C. Niemtzow, Transmembrane Potentials and Characteristics of Immune and Tumor Cell, 2020
Although mitosis of cells with tetra- and higher ploidy levels can take place at the expense of a reduction in ploidy without preceding or intervening DNA synthesis, it is a general fact that mitosis of normal diploid somatic cells must be preceded by DNA replication and chromosome duplication (to produce mitotic chromatids).11 In accord with this fact, it has been demonstrated for a large number of somatic cell types in vivo that the vast majority of cells remains arrested in the G1 period, presumably until either natural death occurs or some natural mitotic stimulation takes place (whence DNA synthesis commences and the cell moves on through the complete division process).1, 12 Since DNA synthesis is thus an essential prerequisite for normal mitosis, any mechanism which acts to prevent DNA synthesis can constitute an effective block to mitosis; since the cell remains in the G1 period during such an arrest, the blocking agent or mechanism may appropriately be referred to as a G1 mitotic block. During such a naturally imposed mitotic block in vivo, operation of the specific, overall G1 metabolic regime characteristic of the particular cell type must remain undisturbed by the blockage, and consequently, any natural blockage mechanism must be fully compatible with these metabolic requirements, thus greatly restricting the range of potential G1 blocking mechanisms.
DNA-Binding Proteins and DNA-Synthesizing Enzymes in Eukaryotes
Published in Lubomir S. Hnilica, Chromosomal Nonhistone Proteins, 2018
Mammalian cells contain at least three distinct DNA polymerases, i.e., DNA polymerases α, β, and γ Experimental evidence suggests that DNA polymerase α is responsible for DNA replication and DNA polymerase β seems to be involved in DNA repair. DNA polymerase γ is required in mitochondrial DNA replication. However, the role of nuclear DNA polymerase γ is still unknown. The infidelity of DNA polymerase α in DNA synthesis was demonstrated in malignant cells and cells induced by carcinogens. Chromosome duplication is discontinuous in nature. DNA ligases join the intermediate fragments to high molecular DNA. DNA-binding proteins unwind DNA helix, while others bind to the single-stranded DNA and even stimulate homologous DNA polymerase activities.
Cytogenetic effects of antidiabetic drug metformin
Published in Drug and Chemical Toxicology, 2022
Deniz Yuzbasioglu, Jalank H. Mahmoud, Sevcan Mamur, Fatma Unal
To the best of our knowledge, there have been limited and conflicting studies on the genotoxicity of MET in human lymphocytes. However, the cytotoxic and genotoxic effects of MET and its combinations with other antidiabetic drugs on different cells were previously reported. The results of the present study showed that MET significantly increased the frequency of CAs and CAs/cell in all the concentrations at long-term (48 h) treatment (except 12.5 µg/mL) compared to the negative control in human lymphocytes. However, it did not affect the frequency of CAs at 24 h treatment. MET commonly induced chromatid and chromosome breaks. These aberrations indicated that the chemical may act possibly after the chromosome duplication at the G2 phase of the cell cycle (Biswas et al.2004, Norppa et al.2006, Ginzkey et al.2014). MET also significantly increased the frequency of SCEs/cell at both treatment periods (except 12.5 µg/mL at 24 h) versus the negative control in this study. However, Sant’Anna et al. (2013) demonstrated that MET (12.5, 25, and 50 µM) did not show any significant increase in the frequency of CAs in human lymphocytes. Similarly, in another study, MET (114.4 and 572 µg/ml) did not affect the frequency of CAs in Chinese hamster ovary cells (Amador et al.2012). These discrepancies between results may be generated from the differences in the cell types and concentrations used in these studies.
In vitro genotoxic and cytotoxic effects of some paraben esters on human peripheral lymphocytes
Published in Drug and Chemical Toxicology, 2019
Devrim Güzel Bayülken, Berrin Ayaz Tüylü
The number of CAs were also increased after the treatment of cells with paraben esters at 24 and 48 h, except after butyl paraben and isopropyl paraben treatment for 48 h when compared with the solvent control. PBs induced five types of chromosomal aberration, indicating their clastogenic effects. These were chromatid breaks, chromosome breaks, sister-chromatid union, dicentric chromosomes and ring chromosomes. In this study, chromatid and chromosome breaks have been observed as the most common aberrations. This may result from breaking the phosphodiester backbone of DNA (Rencüzoğulları 2004). Occurrence of CAs, especially breaks, may indicate that possible effects of chemicals after chromosome duplication at the G2 phase of the cell cycle. An increased number of CAs in peripheral blood lymphocytes of healthy individuals represent a marker of susceptibility to cancer (Boffetta et al. 2007). In a study, the propyl paraben and butyl paraben increased the CAs and SCEs in CHO-K1 cells. Also, these chemicals caused DNA migration in the comet assay (Tayama et al.2008). The results of CBMN assay corroborate the CA assay, because micronuclei provide an indirect measurement of the induction of structural CA’s.
Detecting novel mutations and combined Klinefelter syndrome in Usher syndrome cases
Published in Acta Oto-Laryngologica, 2019
Xiaohong Li, Shasha Huang, Yongyi Yuan, Yu Lu, Dejun Zhang, Xiaobin Wang, Huijun Yuan, Weiju Han, Pu Dai
Targeted NGS and Sanger sequencing analysis of the proband identified the mutations c.2168-1G > C and c.99_100insT (p.R34Sfs*41) in the USH2A gene. The former mutation in the proband was inherited from his mother and the latter from his father (Figure 3(C)). Both mutations have been reported to cause USH2 [11,12]. In addition, heterozygous duplication of all targeted genes on the X chromosome was detected in the proband (Figure 3(D)). An X chromosome duplication indicating KS was confirmed by low-coverage WGS analysis of CNV(Figure 3(E)). The proband was diagnosed with USH2 combined with KS.