Baeyer-Villiger monoxygenases (BVMOs) are flavin-dependant oxidative enzymes capable to catalyse the insertion of an oxygen atom between a carbonylic Csp2 and the Csp3 at the alpha position, therefore transforming linear and cyclic ketones into esters and lactones. These enzymes are dependent on nicotinamides (NAD(P)H) for the flavin reduction and subsequent reaction with molecular oxygen to furnish peroxyflavin, the ultimate responsible for the substrate oxidation. BVMOs can be included in cascade reactions, coupled to other redox enzymes such as alcohol dehydrogenases (ADHs) or ene-reductases (EREDs), so that the direct conversion of alcohols or α,β-unsaturated carbonylic compounds to the corresponding esters can be achieved. This way, it is possible to develop smart synthetic strategies with a convenient cofactor recycling, both using whole cells (native or genetically engineered) as well as isolated enzymes, via multi-steps reaction through sequential or parallel methodologies. Some examples will be commented dealing with these biotransformations, highlighting the advantages of the coupling of enzymatic steps.

This review uses the National Cancer Institute (NCI) COMPARE program to establish an extensive list of heterocyclic iminoquinones and quinones with similarities in differential growth inhibition across the 60-cell line panel of the NCI Developmental Therapeutic Program (DTP). Many natural products and synthetic analogues are revealed, as potential NAD(P)H:quinone oxidoreductase 1 (NQO1) substrates through correlations to dipyridoimidazo[5,4-f]benzimidazoleiminoquinone (DPIQ), and as potential thioredoxin reductase (TrxR) inhibitors, through correlations to benzo[1,2,4]triazin-7-ones and pleurotin. The strong correlation to NQO1 infers the enzyme has a major influence on the amount of active compound with benzo[e]perimidines, phenoxazinones, benz[f]pyrido[1,2-a]indole-6,11-quinones, seriniquinones, kalasinamide, indolequinones, and furano[2,3-b]naphthoquinones, hypothesized as prodrugs. Compounds with very strong correlations to known TrxR inhibitors had inverse correlations to the expression of both reductase enzymes, NQO1 and TrxR, including naphtho[2,3-b][1,4]oxazepane-6,11-diones, benzo[a]carbazole-1,4-diones, pyranonaphthoquinones (including kalafungin, nanomycin A, and analogues of griseusin A), and discorhabdin C. Quinoline-5,8-dione scaffolds based on streptonigrin and lavendamycin can correlate to either reductase. Inhibitors of TrxR are not necessarily (imino)quinones, e.g., parthenolides, while oxidizing moieties are essential for correlations to NQO1, as with the mitosenes. Herein, an overview of synthetic methods and biological activity of each family of heterocyclic imino(quinone) is provided.

Smoking has been established as a major risk factor for developing oral squamous cell carcinoma (OSCC), but less attention has been paid to the effects of smokeless tobacco products. Our objective is to identify potential biomarkers to distinguish the biological effects of combustible tobacco products from those of non-combustible using oral cell lines. Normal human gingival epithelial cells (HGEC), non-metastatic (101A) and metastatic (101B) OSCC cell lines were exposed to different tobacco product preparations (TPPs) including cigarette smoke total particulate matter (TPM), whole-smoke conditioned media (WS-CM), smokeless tobacco extract in complete artificial saliva (STE), or nicotine (NIC) alone. We performed microarray-based gene expression profiling and found 3456 probe sets from 101A, 1432 probe sets from 101B, and 2717 probe sets from HGEC to be differentially expressed. Gene Set Enrichment Analysis (GSEA) revealed xenobiotic metabolism and steroid biosynthesis were the top two pathways that were upregulated by combustible but not by non-combustible TPPs. Notably, aldo-keto reductase genes, AKR1C1 and AKR1C2, were the core genes in the top enriched pathways and were statistically upregulated more than 8 fold by combustible TPPs. Our qRT-PCR results statistically support AKR1C1 as a potential biomarker for differentiating the biological effects of combustible from non-combustible tobacco products.

Patterning, stability, and dispersion of the semiconductor quantum dots (scQDs) are the three issues strictly interconnected for successful device manufacturing. Recently several authors adopted direct optical patterning (DOP) as a step forward in photolithography to position the scQDs in a selected area. However, the chemistry behind the stability, dispersion, and patterning has to be carefully integrated to obtain a functional and therefore, commercial device. In this review are described different chemical strategies suitable to stabilize the scQDs both at a single level and as an ensemble with a special focus on the ones compatible with direct optical patterning (DOP). With the same purpose, the scQDs dispersion in a matrix was described in terms of the scQDs surface ligands interactions with the matrix itself. The chemical processes behind the DOP are illustrated and discussed for five different approaches that consider together stability, dispersion, and the patterning itself of the scQDs.