Cellular reactive oxygen species (ROS) status is stabilized by a balance of ROS generation and elimination called redox homeostasis. ROS is increased by activation of endoplasmic reticulum stress, nicotinamide adenine dinucleotide phosphate (NADPH) oxidase family members and adenosine triphosphate (ATP) synthesis of mitochondria. Increased ROS is detoxified by superoxide dismutase, catalase, and peroxiredoxins. ROS has a role as a secondary messenger in signal transduction. Cancer cells induce fluctuations of redox homeostasis by variation of ROS regulated machinery, leading to increased tumorigenesis and chemoresistance. Redox-mediated mechanisms of chemoresistance include endoplasmic reticulum stress-mediated autophagy, increased cell cycle progression, and increased conversion to metastasis or cancer stem-like cells. This review discusses changes of the redox state in tumorigenesis and redox-mediated mechanisms involved in tolerance to chemotherapeutic drugs in cancer.
In
this study, we developed a metal-free and highly chemoselective
method for the reduction of aromatic nitro compounds. This reduction
was performed using tetrahydroxydiboron [B2(OH)4] as the reductant and 4,4′-bipyridine as the organocatalyst
and could be completed within 5 min at room temperature. Under optimal
conditions, nitroarenes with sensitive functional groups, such as
vinyl, ethynyl, carbonyl, and halogen, were converted into the corresponding
anilines with excellent selectivity while avoiding the undesirable
reduction of the sensitive functional groups.
Highly efficient ligand-free Suzuki–Miyaura cross-coupling in aqueous solvent at room temperature was developed using metal oxides with low Pd content via a fluorescence-based high-throughput screening method.
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