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Drug Analysis of Protein Microspheres: From Pharmaceutical Preparation to In Vivo Fate
Published in Neville Willmott, John Daly, Microspheres and Regional Cancer Therapy, 2020
Jeffrey Cummings, David Watson, John F. Smyth
HPLC has proved useful for identifying conversion of mitomycin C into 2,7-diaminomitosene in vitro and likewise for the resolution of DNA adducts in vitro. Detection of chromatographic peaks is normally by ultraviolet visible spectrophotometry because mitomycin C has a strong absorption maximum at 360 nm (molar extinction coefficient 21,800 M−1 cm−1), allowing for both good sensitivity and selectivity in biological matrices. It is important to stress that mitosene products exhibit a hypsochromic shift to 310 nm (molar extinction coefficient 6026 M−l cm−1) with considerable quenching, which is unusual considering the increase in conjugation. Effectively, this means that either dual wavelength detection or preferably DAD should be obligatory.
High-Performance Liquid Chromatography
Published in Adorjan Aszalos, Modern Analysis of Antibiotics, 2020
Joel J. Kirschbaum, Adorjan Aszalos
Mitomycin C, two mitosomes, and twelve mitosene derivatives were characterized using an octadecylsilane analytical column (100 × 8 mm) and guard column (70 × 2.1 mm, 37-μm particles) and gradient elution starting from 100% 0.01 M potassium phosphate buffer, pH 7.0, to 100% methanol in 13 min.
Anticancer therapy and lung injury: molecular mechanisms
Published in Expert Review of Anticancer Therapy, 2018
Li Li, Henry Mok, Pavan Jhaveri, Mark D Bonnen, Andrew G Sikora, N. Tony Eissa, Ritsuko U Komaki, Yohannes T Ghebre
Is an anticancer drug used for over 40 years in the treatment of cancers of the breast and upper gastrointestinal tract. As an antitumor antibiotics, one of its main mechanisms in killing bacteria and cancer cells is the potent DNA cross-linking activity by which mitomycin is chemically transformed to mitosene; a DNA reactive compound [9]. As a result, mitomycin C is involved in inhibition of DNA synthesis, induction of genetic recombination events, and mutagenesis of mammalian DNA. In addition, the drug is involved in the generation of ROS and other species that are highly tissue reactive and capable of causing apoptotic cell death and tissue injury [10]. One of the tissues that suffer collateral damage upon mitomycin C treatment is the lungs. The use of mitomycin C in some cancer patients is associated with higher incidences of interstitial pneumonitis, pulmonary fibrosis and pulmonary veno-occlusive disease (PVOD) [11]. Mechanistically, mitomycin C-induced pulmonary injury might be associated with the downregulation of members of the SMAD signaling pathway and inhibition of the general control nonderepressible 2 protein (GCN2); a protein encoded by the Eukaryotic Translation Initiation Factor 2 α Kinase 4 (EIF2 αK4) [11]. Genetic mutations in the EIF2 αK4 gene are reported to be associated with hereditary PVOD [12].