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Published in Valerio Voliani, Nanomaterials and Neoplasms, 2021
Eun-Kyung Lim, Taekhoon Kim, Soonmyung Paik, Seungjoo Haam, Yong-Min Huh, Kwangyeol Lee
Drugs such as cisplatin, the antibiotics daunorubicin and DOX, and etoposide disrupt the replication of the DNA and cause formation of nonsense DNA or RNA by inhibiting telomerase activity or eliminating telomeric DNA. Telomerase as the natural enzyme for elongating telomeres enables cancer cells to divide virtually forever. Immortalization of cancer cells is considered to stem from their activity [354, 360]. Therefore, DOX, which is effective in treatments of acute leukemia, malignant lymphoma, and a variety of solid tumors, acts by intercalating between nucleic acid bases. It also inhibits the action of the enzyme topoisomerase II, thereby interfering with DNA and RNA biosynthesis. The four planar rings of the drug intercalate into DNA, whereas the hydroxyl group on the side chain interacts with topoisomerases II, which causes cleavage of DNA to stop the replication process [372, 373]. However, because it induces common toxicities, including cardiotoxicity [38], attempts to reduce its toxicity have been made by introducing novel carrier systems such as PEGylated liposomes [374–380]. Etoposide does not intercalate into DNA but forms a ternary complex with DNA and topoisomerase II enzyme, thereby preventing religation of the DNA strands, inducing errors in DNA synthesis and apoptosis of cancer cells [372–373].
PLGA-Based Nanoparticles for Cancer Therapy
Published in Jince Thomas, Sabu Thomas, Nandakumar Kalarikkal, Jiya Jose, Nanoparticles in Polymer Systems for Biomedical Applications, 2019
Etoposide is an anticancer agent used in the treatment of a variety of malignancies, including malignant lymphomas. It acts by inhibition of topoisomerase-II and activation of oxidation–reduction reactions to create derivatives that bind directly to DNA and cause DNA damage. The successful chemotherapy of tumors depends on continual exposure to anticancer agents for long-lasting periods. Etoposide has a short biological half-life (3.6 h), and although intraperitoneal injection would cause initial high local tumor concentrations, long-lasting exposure of tumor cells may not be probable. It is envisaged that intraperitoneal delivery of etoposide through NPs would be a better approach for effectual treatment of peritoneal tumors. In this perception, etoposide-loaded NPs were prepared applying nanoprecipitation and emulsion-solvent evaporation methods using PLGA in the presence of Pluronic F68 by Reddy et al. The process produced NPs with high entrapment efficiency of around 80% with continuous release of the drug up to 48 h.89
Drug-induced bronchospasm
Published in Philippe Camus, Edward C Rosenow, Drug-induced and Iatrogenic Respiratory Disease, 2010
K Suresh Babu, Jaymin Morjaria
Etoposide and teniposide are antimitotic agents used in the treatment of ovarian germ-cell tumours, small-cell lung carcinoma, testicular tumours, and many other tumours.82 Reactions range from 6 to 41 per cent, and there is a 0.7–14 per cent incidence of anaphylaxis with epipodophyllotoxins.83,84 As these reactions occurred with the first dose, it is unlikely to be immunologically mediated. Probably, like taxanes, they may cause direct mast-cell mediator release. There are no standard prophylaxis regimens, and fewer than 50 per cent who have had a drug-induced reaction are able to tolerate the drug on re-administration.81
The emergence of nanoporous materials in lung cancer therapy
Published in Science and Technology of Advanced Materials, 2022
Deepika Radhakrishnan, Shan Mohanan, Goeun Choi, Jin-Ho Choy, Steffi Tiburcius, Hoang Trung Trinh, Shankar Bolan, Nikki Verrills, Pradeep Tanwar, Ajay Karakoti, Ajayan Vinu
A facile synthesis of CaAl-LDH (calcium aluminium LDH) nanoparticles and a simple anion exchange technique to load drug etoposide into Ca-Al-LDH showed a synergistic effect of both tumour reduction and suppression of CAMKIIα expression with SOD gene activity in the lung cancer cells (Figure 4C). It is known that free etoposide administration has several side effects such as acute toxicity to healthy cells, peripheral neuropathy and strong inflammatory response at the injection site. At the molecular level, CAMKIIα expression and SOD gene activity indicate the inflammation and toxicity levels of the drug response. After 24 hours and 72 hours of incubation of etoposide-LDH nanoparticles in A549 cells, there was a significant growth inhibition of 21.56% (confirmed by apoptosis) in cancer cells along with a reduction of CAMKIIα expression (95.14 pg/ml) and a four-fold reduction in SOD gene activity (Figure 4 DI, II) [215].
Development of a database on key characteristics of human carcinogens
Published in Journal of Toxicology and Environmental Health, Part B, 2019
Mustafa Al-Zoughool, Michael Bird, Jerry Rice, Robert A. Baan, Mélissa Billard, Nicholas Birkett, Daniel Krewski, Jan M Zielinski
Some agents interfere with multiple pathways that involve the induction of DNA damage as well as other types of effects not involving DNA reactivity. Examples of the latter include changes in gene expression, activation of cell-signaling pathways, immunosuppression, and inflammation. Further, DNA damage induced by chemical exposures may occur as a secondary or tertiary effect of the cascade of events mediated through the metabolism of the agent or its reaction with cellular constituents such as receptor binding. It was found that TCDD metabolism results in enhanced production of reactive intermediates that increase oxidative stress and subsequently induce oxidative DNA damage (Knerr and Schrenk 2006). Chronic inflammation from exposure to fibers results in genotoxic damage (Catalán et al. 2017). The chemotherapeutic agent etoposide produces genetic damage without chemically interacting with DNA. The postulated pathway, in this case, involves binding to the topoisomerase IIα enzyme (Alessandra, Zanetta, and Biamonti 2015). The etoposide-topoisomerase IIα complex interferes with DNA re-ligation, thereby enhancing the production of DNA double-strand breaks. In other cases, the prevalent non-genotoxic pathway may eventually lead to a genotoxic event, as is the case in HBV-related hepatocellular carcinoma (HCC) where enhanced cellular proliferation from inflammatory responses to chronic viral infection produces double-strand DNA breaks and facilitate viral integration (Hollingworth and Grand 2015). Similarly, genomic instability associated with chromosomal aberrations and MN formation in response to exposure to heavy metals, including As, cadmium, Be and nickel, may result from interference with DNA repair (Morales et al. 2016).