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Pulmonary hypertension induced by drugs and toxins
Published in Philippe Camus, Edward C Rosenow, Drug-induced and Iatrogenic Respiratory Disease, 2010
Kim Bouillon, Yola Moride, Lucien Abenhaim, Marc Humbert
Mitomycin-C (Fig. 29.4) is used in chemotherapy for malignant tumours combined with other chemotherapy. Anecdotal reports showed that histologically confirmed PVOD occurred in patients treated for metastatic cervical carcinoma,88,89 metastatic gastric adenocarcinoma90 and non-small-cell lung cancer.91,92 It also causes an interstitial lung disease and a vasculitis with the haemolytic–uraemia syndrome.
Surface modification of ureteral stents: development history, classification, function, and future developments
Published in Expert Review of Medical Devices, 2023
Kaiguo Xia, Xudong Shen, Xiaojie Ang, Bingbing Hou, Yang Chen, Kaiping Zhang, Zongyao Hao
Urothelial tumor of the upper urinary tract has a high recurrence rate，and intracavitary instillation of adjuvant chemotherapy could be used to reduce tumor recurrence after nephron-sparing treatment. Soria F et al. [87] loaded mitomycin C into a silk fibroin matrix wrapped around the surface of the degradable stent BraidStent, the study revealed that mitomycin C in the silk fibroin matrix can be released in the urinary environment for 6–12 hours [88]. In an vitro experimental study, it was found that mitomycin C in the silk fibroin matrix still preserves greater cytotoxicity to tumor cells, and these results confirm the feasibility of reducing the recurrence rate in patients with upper tract urothelial carcinomas by increasing the retention time of anti-cancer drugs [89].
Protective effects and DNA repair induction of a coumarin-chalcone hybrid against genotoxicity induced by mutagens
Published in Journal of Toxicology and Environmental Health, Part A, 2022
Jefferson Hollanda Véras, Camila Regina Do Vale, Elisa Flávia Luiz Cardoso Bailão, Murilo Machado Dos Anjos, Clever Gomes Cardoso, Matheus Gabriel de Oliveira, José Realino de Paula, Guilherme Roberto de Oliveira, Carolina Ribeiro E Silva, Lee Chen-Chen
Previously Véras et al. (2020) examined the genotoxic and antigenotoxic activities of the coumarin–chalcone hybrid [7-methoxy-3-(E)-3-(3,4,5-trimethoxyphenyl)acryloyl-2 H-chromen-2-one] (4-MET, Figure 1) in Drosophila melanogaster somatic cells using the somatic mutation and recombination test (SMART). Our results showed that 4-MET was not genotoxic. However, this compound was able to protect D. melanogaster cells against mitomycin C-induced genotoxicity (Véras et al. 2020). Although SMART test results are widely recognized to assess genotoxicity (Alaraby et al. 2016; Demir 2022; Vecchio 2015), the use of multiple tests (in vitro and in vivo) is necessary to comprehensively cover genetic endpoints, as no individual test provides a multitude of information regarding a compound’s performance (OECD 2015).
The expression of Phase II drug-metabolizing enzymes in human B-lymphoblastoid TK6 cells
Published in Journal of Environmental Science and Health, Part C, 2022
Xilin Li, Yuxi Li, Kylie G. Ning, Si Chen, Lei Guo, Jessica A. Bonzo, Nan Mei
The NQO gene family consists of two members, NQO1 and NQO2. Both of them encode cytosolic flavoenzymes that catalyze the reduction of quinone to hydroquinone, which is considered an antioxidation and detoxification process.32 For example, NQO1 deficiency leads to increased genotoxicity (as measured by the micronucleus assay) of benzene in mice.33 However, such a reduction is not always protective in cells. It is well documented that NQO1 catalyzes the bioreductive activation of mitomycin C, generating leucomitomycin C that causes DNA interstrand crosslinking.34 We found the mRNA of NQO1 was highly expressed in TK6 cells – the expression value ranked the 3rd highest among the 84 Phase II enzymes investigated (Table 1). NQO1 protein was also identified in TK6 cells, although the band intensity was weak due to an extremely high level of NQO1 expressed in HepG2 cells (Figure 1A). Notably, the gene expression level of NQO1 in HepG2 cells was significantly higher than that in TK6 cells and PHHs, respectively (Table 1). PHHs had no detectable protein level of NQO1, and the trend was consistent with the gene expression level (Figure 1A). Since many genotoxicants, especially dietary supplements, exert their DNA-damaging effects via oxidative stress, HepG2 cells may be less sensitive in detecting the genotoxicity of these agents due to a relatively high level of NQO1.