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Biotransformation of Monoterpenoids by Microorganisms, Insects, and Mammals
Published in K. Hüsnü Can Başer, Gerhard Buchbauer, Handbook of Essential Oils, 2020
Yoshiaki Noma, Yoshinori Asakawa
Racemic linalool (206 and 206′) is cyclized into cis- and trans-linalool oxides by various microorganisms such as Streptomyces albus NRRL B1865, Streptomyces hygroscopicus NRRL B3444, Streptomyces cinnamonensis ATCC 15413, Streptomyces griseus ATCC 10137, and Beauveria sulfurescens ATACC 7159 (David and Veschambre, 1984) (Figure 22.17).
Halogenases with Potential Applications for the Synthesis of Halogenated Pharmaceuticals
Published in Peter Grunwald, Pharmaceutical Biocatalysis, 2019
Georgette Rebollar-Pérez, Cynthia Romero-Guido, Antonino Baez, Eduardo Torres
Rebeccamycin is a member of the indolocarbazole family, this halogenated natural compound, produced by the actinomycete Lechevaliera aerocolonigenes, is an antibiotic and antitumor drug that act on DNA topoisomerase I or II. The complete gene cluster encoding rebeccamycin biosynthesis was cloned and sequenced by Sánchez et al. (2002). The expression of the complete gene cluster in the heterologous host Streptomyces albus J1074 was successful for rebeccamycin biosynthesis producing several fold rebeccamycin levels in S. albus J1074 than in L. aerocolonigenes. Also, the heterologous gene cluster expression allowed the elucidation of rebeccamycin biosynthetic genes. Based on sequence analysis and database comparison, authors proposed that rebO, rebD, rebC and rebP gene products could be involved in indolocarbazole core formation of rebeccamycin. In order of action, RebO could catalyze the oxidative deamination of L-tryptophan to yield indolepyruvic acid, RebD could condensate two l-tryptophan-derived units to yield the first bis-indole intermediate that could be decarboxylated by RebC and then suffer an oxidative closure of a bis-indole intermediate to form the indolocarbazole core. While rebG, rebM, rebH and rebH gene products could be involved in indolocarbazole modification. RebG could form an N-glycosidic bond between a nucleotide-activated D-glucose and the rebeccamycin indolocarbazole core. After glycosylation, RebM could catalyze a methylation at the 4-hydroxy position of a D-glucose moiety. RebH and RebF could form a two-component halogenase system in which RebH chlorinate L-tryptophan to form 7-chlorotryptophan (prior to RebO action) or chlorinate a later intermediate during rebeccamycin biosynthesis, and RebF supplies the reduced diffusible flavin that RebH needs to function (Fig. 16.2). Proposed biosynthetic pathway of rebeccamycin. RebU and RebT could participate in rebeccamycin resistance and/or secretion.From Sánchez et al. (2002) with permission. Copyright (2002) National Academy of Sciences, U.S.A.
Salinomycin induces cell cycle arrest and apoptosis and modulates hepatic cytochrome P450 mRNA expression in HepG2/C3a cells
Published in Toxicology Mechanisms and Methods, 2022
Andressa Megumi Niwa, Simone Cristine Semprebon, Glaucia Fernanda Rocha D’Epiro, Lilian Areal Marques, Thalita Alves Zanetti, Mário Sérgio Mantovani
Salinomycin (SAL, molecular formula: C42H70O11) (Figure 1) is a monocarboxylic polyether ionophore antibiotic isolated from Streptomyces albus (Miyazaki et al. 1974; Antoszczak and Huczyński 2019). SAL exhibits an effective antitumor potential against numerous human cancer cells (Antoszczak and Huczyński 2015) including uveal melanoma (Zhou et al. 2019) and leukemia (Zhao et al. 2018), as well as thyroid (Alqahtani et al. 2020), lung (Hochmair et al. 2020), breast (Niwa et al. 2016), prostate (Zhang et al. 2017), and colorectal (Zhou et al. 2019) cancer, among others. It has been demonstrated that SAL acts by inducing apoptosis (Zhao et al. 2018) and cell cycle arrest (Alqahtani et al. 2020), reducing cancer cell migration (Schenk et al. 2015) and invasion (Liu et al. 2018). SAL has also been demonstrated to possess antiangiogenic properties and reduce tumor growth in xenograft mouse models (Li et al. 2016). An important mechanism of SAL is its potential in inhibiting cancer stem cells and stem-like cells within tumors, which are responsible for metastasis and cancer relapse (Gupta et al. 2009; Zhang et al. 2017; Wang et al. 2019). Moreover, several studies have shown that SAL acts selectively against cancer cells, with lower toxicity to normal cells (Niwa et al. 2016; Zhang et al. 2017).