Zingerone protects keratinocyte stem cells from UVB-induced damage.

The epidermis, the outermost layer of the skin, is a stratified epithelium that protects the body from the external environment. Keratinocyte stem cells (KSCs) are involved in epidermis homeostasis by maintaining epidermal integrity through a process of constant regeneration. Ultraviolet B (UVB) radiation is a major inducer of cellular damage in the epidermis.

S-Nitrosylation of p47(phox) enhances phosphorylation by casein kinase 2.

Objectives: Leukocyte NADPH oxidase, which is active in neutrophils, is a membrane-bound enzyme that catalyzes the reduction of oxygen to O2(-) by using NADPH as an electron donor. Previously, we reported that casein kinase 2 (CK2), a ubiquitous and highly conserved Ser/Thr kinase, is responsible for p47(phox) phosphorylation and that phosphorylation of p47(phox) by CK2 regulates the deactivation of NADPH oxidase.

Methods: Here, we report that the residue Cys(196) of p47(phox) is a target of S-nitrosylation by S-nitrosothiol and peroxynitrite and that this modification enhanced phosphorylation of p47(phox) by CK2.

Antagonizing Effects of Aspartic Acid against Ultraviolet A-Induced Downregulation of the Stemness of Human Adipose Tissue-Derived Mesenchymal Stem Cells.

Ultraviolet A (UVA) irradiation is responsible for a variety of changes in cell biology. The purpose of this study was to investigate effects of aspartic acid on UVA irradiation-induced damages in the stemness properties of human adipose tissue-derived mesenchymal stem cells (hAMSCs). Furthermore, we elucidated the UVA-antagonizing mechanisms of aspartic acid.

Antagonist effects of veratric acid against UVB-induced cell damages.

Ultraviolet (UV) radiation induces DNA damage, oxidative stress, and inflammatory processes in human epidermis, resulting in inflammation, photoaging, and photocarcinogenesis. Adequate protection of skin against the harmful effect of UV irradiation is essential. In recent years naturally occurring herbal compounds such as phenolic acids, flavonoids, and high molecular weight polyphenols have gained considerable attention as beneficial protective agents.

Antagonizing effects and mechanisms of afzelin against UVB-induced cell damage.

Ultraviolet (UV) radiation induces DNA damage, oxidative stress, and inflammatory processes in human keratinocytes, resulting in skin inflammation, photoaging, and photocarcinogenesis. Adequate protection of skin against the harmful effects of UV irradiation is essential. Therefore, in this study, we investigated the protective effects of afzelin, one of the flavonoids, against UV irradiation in human keratinocytes and epidermal equivalent models.

Ursolic acid sensitizes prostate cancer cells to TRAIL-mediated apoptosis.

Prostate cancer is one of the most commonly occurring malignancies in men, and because existing treatments are not able to manage this neoplasm adequately, novel approaches are needed. Although tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) has strong antitumor activity via the induction of apoptotic cell death in a wide range of tumor cell types and has negligible toxicity to most normal cells, some prostate carcinoma cells are resistant to the apoptotic effects of TRAIL. Therefore, combinatorial approaches with TRAIL and different chemotherapeutic agents have been developed to overcome the resistance of cancer cells to TRAIL.

S-glutathionylation regulates GTP-binding of Rac2.

Phagocyte NADPH oxidase catalyzes the reduction of molecular oxygen to superoxide and is essential for defense against microbes. Rac2 is a low molecular weight GTP-binding protein that has been implicated in the regulation of phagocyte NADPH oxidase. Here we report that Cys(157) of Rac2 is a target of S-glutathionylation and that this modification is reversed by dithiothreitol as well as enzymatically by thioltransferase in the presence of GSH.

Regulation of brefeldin A-induced ER stress and apoptosis by mitochondrial NADP⁺-dependent isocitrate dehydrogenase.

Brefeldin A (BFA), an endoplasmic reticulum (ER)-Golgi transport inhibitor, has been shown to cause accumulation of proteins in the ER, ER stress, and ultimately apoptosis. In this paper, we demonstrate that the knockdown of mitochondrial NADP(+)-dependent isocitrate dehydrogenase (IDPm), a mitochondrial NADPH-generating enzyme, by small interfering RNA (siRNA) enhanced BFA-induced apoptosis. However, attenuated IDPm activity results in the suppression of ER stress response, presumably, via the inhibition of the PI3K/Akt pathway.

Autophagy inhibition enhances ursolic acid-induced apoptosis in PC3 cells.

The phosphoinositol 3-kinase/Akt pathway plays a critical role in oncogenesis and the dysregulation of this pathway through loss of PTEN is a particularly common phenomenon in aggressive prostate cancers. Several recent studies have indicated that ursolic acid (UA), a pentacyclic triterpenoid, and its derivatives inhibit the growth of cancer cells by cell cycle arrest and the stimulation of apoptosis. In the present study, we report a novel autophagic response of UA in PTEN-deficient PC3 prostate cancer cells.

Cytosolic NADP(+)-dependent isocitrate dehydrogenase regulates cadmium-induced apoptosis.

Cadmium ions have a high affinity for thiol groups. Therefore, they may disturb many cellular functions. We recently reported that cytosolic NADP(+)-dependent isocitrate dehydrogenase (IDPc) functions as an antioxidant enzyme to supply NADPH, a major source of reducing equivalents to the cytosol.

Glutathionylation regulates cytosolic NADP+-dependent isocitrate dehydrogenase activity.

Cytosolic NADP+-dependent isocitrate dehydrogenase (IDPc) is susceptible to inactivation by numerous thiol-modifying reagents. This study now reports that Cys269 of IDPc is a target for S-glutathionylation and that this modification is reversed by dithiothreitol as well as enzymatically by cytosolic glutaredoxin in the presence of GSH. Glutathionylated IDPc was significantly less susceptible than native protein to peptide fragmentation by reactive oxygen species and proteolytic digestion.

Silencing of cytosolic NADP(+)-dependent isocitrate dehydrogenase by small interfering RNA enhances the sensitivity of HeLa cells toward staurosporine.

Staurosporine induces the production of reactive oxygen species, which play an important causative role in apoptotic cell death. Recently, it was demonstrated that the control of cellular redox balance and the defense against oxidative damage is one of the primary functions of cytosolic NADP(+)-dependent isocitrate dehydrogenase (IDPc) by supplying NADPH for antioxidant systems. The present report shows that silencing of IDPc expression in HeLa cells greatly enhances apoptosis induced by staurosporine.

Protective effect of Rehmannia glutinosa on the UV-induced apoptosis in U937 cells.

Ultraviolet (UV) radiation has been shown to generate reactive oxygen species (ROS), such as singlet oxygen, superoxide radicals, hydroxyl radicals and hydrogen peroxide in a variety of cells. These ROS have the potential to damage critical cellular components such as DNA, proteins, and lipids and eventually result in physical and chemical damage to tissues that may lead to cell death. The steamed root of Rehmannia glutinosa (Saeng Jihuang, SJH) is reported to have an antioxidant activity.

Hypochlorous acid-induced modulation of cellular redox status in HeLa cells.

Myeloperoxidase catalyzes the formation of hypochlorous acid (HOCI) via reaction of H2O2 with CI(-) ions. Although HOCI plays a major role in the human immune system by killing bacteria and other invading pathogens, excessive generation of this oxidant causes damage to tissues. Exposure of HeLa cells to HOCI decreased viability, inactivated antioxidant enzymes, damaged mitochondria, and modulated cellular redox status.

Inactivation of mitochondrial NADP+-dependent isocitrate dehydrogenase by hypochlorous acid.

Myeoloperoxidase catalyses the formation of hypochlorous acid (HOCl) via reaction of H(2)O(2) with Cl(-) ion. Although HOCl is known to play a major role in the human immune system by killing bacteria and other invading pathogens, excessive generation of this oxidant is known to cause damage to tissue. Recently, it was demonstrated that the control of mitochondrial redox balance and oxidative damage is one of the primary functions of mitochondrial NADP(+)-dependent isocitrate dehydrogenase (IDPm) to supply NADPH for antioxidant systems.

Regulation of heat shock-induced apoptosis by sensitive to apoptosis gene protein.

Heat shock may increase oxidative stress due to increased production of reactive oxygen species and/or the promotion of cellular oxidation events. Sensitive to apoptosis gene (SAG) protein, a novel zinc RING finger protein that protects mammalian cells from apoptosis by redox reagents, is a metal chelator and a potential reactive oxygen species scavenger, but its antioxidant properties have not been completely defined. In this report, we demonstrate that modulation of SAG expression in U937 cells regulates heat shock-induced apoptosis.

Epigallocatechin gallate, a constituent of green tea, regulates high glucose-induced apoptosis.

A high concentration of glucose has been implicated as a causal factor in initiation and progression of diabetic complications, and there is evidence to suggest that hyperglycemia increases the production of free radicals and oxidative stress. Therefore, compounds that scavenge reactive oxygen species may confer regulatory effects on high glucose-induced apoptosis. Epigallocatechin gallate (EGCG), the major polyphenolic of green tea, is reported to have an antioxidant activity.

Silencing of mitochondrial NADP+-dependent isocitrate dehydrogenase by small interfering RNA enhances heat shock-induced apoptosis.

Heat shock may increase oxidative stress due to increased production of reactive oxygen species and/or the promotion of cellular oxidation events. Mitochondrial NADP(+)-dependent isocitrate dehydrogenase (IDPm) produces NADPH, an essential reducing equivalent for the antioxidant system. In this report, we demonstrate that silencing of IDPm expression in HeLa cells greatly enhances apoptosis induced by heat shock.

Mitochondrial NADP+-dependent isocitrate dehydrogenase protects cadmium-induced apoptosis.

Cadmium is known to exhibit high affinity for thiol groups and may therefore severely disturb many cellular functions. We have demonstrated that the control of mitochondrial redox balance and oxidative damage is one of the primary functions of mitochondrial NADP+-dependent isocitrate dehydrogenase (IDPm). When exposed to cadmium, IDPm was susceptible to loss of enzyme activity and structural alterations.

N-t-Butyl hydroxylamine regulates heat shock-induced apoptosis in U937 cells.

Heat shock may increase oxidative stress due to increased production of reactive oxygen species and/or the promotion of cellular oxidation events. Therefore, compounds that scavenge reactive oxygen species may regulate heat shock-induced cell death. Recently, it has been shown that the decomposition product of the spin-trapping agent alpha-phenyl-N-t-butylnitrone, N-t-butyl hydroxylamine (NtBHA), mimics alpha-phenyl-N-t-butylnitrone and is much more potent in delaying reactive oxygen species-associated senescence.