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Gene Transfer into Human Hematopoietic Stem Cells
Published in Richard K. Burt, Alberto M. Marmont, Stem Cell Therapy for Autoimmune Disease, 2019
Serguei Kisselev, Tatiana Seregina, Richard K. Burt, Charles J. Link
Another area of interest is the introduction of drug resistance genes into HSC to allow protection from some types of chemotherapy. Upon exposure to chemotherapy, drug resistant cells should have an in vivo selective advantage. P-glycoprotein, a cellular transmembrane transporter that protects cells from cytotoxic drugs such as vinca alkaloids, anthracyclines, podophyllins, and paclitaxel, is the product of the multi-drug resistance (MDR1) gene.101 In preclinical models, expression of MDR1 in HSC increases resistance to these cytotoxic agents.102 Transfer of the 06-Methylguanine DNA methyltransferase (MGMT) gene under control of the phosphoglycerate kinase promoter into mouse HSC improves viability of bone marrow cells to 1,3-bis (2-chloroethyl)-1-nitrosourea (BCNU).103 Expression of the mutant 06-benzylguanine (6-BG)-resistance MGMT gene into HSC can effectively protect transduced hematopoietic cells to 6-BG while malignant cells, expressing wild type of MGMT remain highly sensitive to 6-BG.104 The pre-clinical data also demonstrated an unexpected complication. In a murine model, MDR-1 transduced HSC were shown to acquire a growth advantage over the normal bone marrow progenitor cells leading to myeloproliferative disorders.105
The Role of Nanotechnology in the Treatment of Drug Resistance Cancer
Published in Bhaskar Mazumder, Subhabrata Ray, Paulami Pal, Yashwant Pathak, Nanotechnology, 2019
Sandipan Dasgupta, Anup Kumar Das, Paulami Pal, Subhabrata Ray, Bhaskar Mazumder
Anticancer drugs like alkylsulphonates, nitrosourea compounds, cisplatin, and nitrogen mustards cause DNA base damage, where the DNA double strands break apart, forming bulky DNA adducts. But these lesions are being healed by cancer cells through the BER and NER pathways, together with alkyltransferases (ATs), which is another major repair pathway. Antimetabolite drugs like 5-FU and thiopurine interfere with nucleotide metabolism and DNA synthesis, causing replication lesions in cancer cells, but cancer cells have evolved themselves by triggering the BER pathway mechanism.
Physical Constants of Organic Compounds
Published in W. M. Haynes, David R. Lide, Thomas J. Bruno, CRC Handbook of Chemistry and Physics, 2016
W. M. Haynes, David R. Lide, Thomas J. Bruno
Methyl 3-nitrobenzoate Methyl 4-nitrobenzoate 2-Methyl-4-nitro-1H-imidazole N-Methyl-N-nitromethanamine 2-Methyl-1-nitronaphthalene N-Methyl-N'-nitro-N-nitrosoguanidine 3-Methyl-4-nitrophenol 4-Methyl-2-nitrophenol 1-Methyl-2-(4-nitrophenoxy)benzene 2-Methyl-2-nitro-1,3-propanediol 2-Methyl-2-nitro-1-propanol 3-Methyl-4-nitroquinoline-Noxide N-Methyl-N-nitrosoaniline N-Methyl-N-nitrosourea N-Nitroso-N-methylurea 2-Methylphenyl 4-nitrophenyl ether
Neuroprotective effect of peanut against oxidative stress in streptozotocin-induced diabetic rats
Published in Egyptian Journal of Basic and Applied Sciences, 2022
Norhan H. Mohamed, Hassan Elsayad, Yasser M. Elsherbini, Mohamed E. Abdraboh
A paucity of literature has been devoted to understanding deleterious mechanisms involved in diabetes and its complications. Streptozotocin (STZ) is a glucosamine-nitrosourea compound that has been widely used in many studies to induce diabetes in a variety of animals by affecting degeneration and necrosis of pancreatic β-cells [13]. Rodents with STZ-induced diabetes are the most common model that has been developed to decipher the mechanisms involved in diabetes and to study potential prophylactic/therapeutic strategies for ameliorating diabetic complications.
Performance of HepaRG and HepG2 cells in the high-throughput micronucleus assay for in vitro genotoxicity assessment
Published in Journal of Toxicology and Environmental Health, Part A, 2020
Xiaoqing Guo, Ji-Eun Seo, Dayton Petibone, Volodymyr Tryndyak, Un Jung Lee, Tong Zhou, Timothy W. Robison, Nan Mei
The micronucleus (MN) assay is another essential assay used for genotoxicity testing. Unlike the Comet assay which detects single and/or double-strand breakage of DNA at the single-cell level, the MN assay detects two types of genotoxic mechanisms – clastogenicity (chromosome breaks or rearrangements) and aneugenicity (abnormal number of chromosomes) by measuring MN formation in the cytoplasm of interphase cells (Avlasevich et al. 2011; OECD 2016). Performance of HepaRG cells in the MN assay was evaluated in several studies. In 2010, the first published HepaRG MN study reported that cylindrospermopsin, a freshwater cyanotoxin, induced significantly higher cytotoxicity and MN frequencies in differentiated HepaRG cells than it did in undifferentiated HepaRG cells (Bazin et al. 2010). Several Ames-positive or Ames-negative/equivocal in vivo genotoxicants were examined using differentiated HepaRG cells with the cytokinesis-block MN (CBMN) assay (Josse et al. 2012; Le Hegarat et al. 2010; 2014). Following 24-hr treatment, positive responses were noted for four aneugens [colchicine, nocodazole, taxol, and diethylstilbestrol (DES)], a direct-acting clastogen [methyl methanesulfonate (MMS)], two potent gene mutagens [N-ethyl-N-nitrosourea (ENU) and 4-nitroquinoline (4-NQO)], and six indirect-acting clastogens [aflatoxin B1 (AFB1), benzo[a]pyrene (B[a]P), cyclophosphamide (CPA), 7,12-dimethylbenzanthracene (DMBA), 2-acetylaminofluorene (2-AAF), and 2-nitrofluorene (2-NF)]. These findings demonstrated the capability of metabolically competent HepaRG cells to assess and detect genotoxicity of compounds relevant to human exposure, especially for compounds requiring metabolic activation. However, the CBMN assay is usually conducted using microscope-based technology, making sample processing and MN scoring labor-intensive and time-consuming.
Pesticide exposure and genotoxic effects as measured by DNA damage and human monitoring biomarkers
Published in International Journal of Environmental Health Research, 2021
Jones A. Kapeleka, Elingarami Sauli, Patrick A. Ndakidemi
DNA damage can also be measured by 32P-Postlabeling analysis. This is a powerful technique for detecting, identifying and quantifying DNA adducts induced by mutagens or carcinogens, which are covalently formed by the reaction of DNA with chemical carcinogens and mutagens including N-methyl-N-nitrosourea, dimethyl sulfate, formaldehyde (Győrffy et al. 2007; Muller et al. 2014).