Silver nanoparticles synthesized from Adenium obesum leaf extract induced DNA damage, apoptosis and autophagy via generation of reactive oxygen species

Farah, Mohammad Abul; Ali, Mohammad Ajmal; Chen, Shen‐Ming; Liu, Ying; Al-Hemaid, Fahad M.A.; Abou-Tarboush, Faisal M.; Al-Anazi, Khalid Mashay; Lee, Dong Kun

doi:10.1016/j.colsurfb.2016.01.027

Cited by 147 publications

(81 citation statements)

References 75 publications

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“…To analyze autophagy, cells were reacted with acridine orange (Invitrogen) for 15 min and fluorescence was measured using a fluorescence microscope (BH2-RFL-T3; Olympus, Tokyo, Japan) (Farah et al 2016). Depending on the acidity, autophagic lysosomes appeared as orange/red fluorescent cytoplasmic vesicles, while the nuclei were stained green.…”

Section: Methodsmentioning

confidence: 99%

Particulate matter 2.5 damages skin cells by inducing oxidative stress, subcellular organelle dysfunction, and apoptosis

et al. 2018

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The skin is the largest organ of the human body and the one mostly exposed to outdoor contaminants. To evaluate the biological mechanisms underlying skin damage caused by fine particulate matter (PM2.5), we analyzed the effects of PM2.5 on cultured human keratinocytes and the skin of experimental animals. PM2.5 was applied to human HaCaT keratinocytes at 50 µg/mL for 24 h and to mouse skin at 100 µg/mL for 7 days. The results indicate that PM2.5 induced oxidative stress by generating reactive oxygen species both in vitro and in vivo, which led to DNA damage, lipid peroxidation, and protein carbonylation. As a result, PM2.5 induced endoplasmic reticulum stress, mitochondrial swelling, and autophagy, and caused apoptosis in HaCaT cells and mouse skin tissue. The PM2.5-induced cell damage was attenuated by antioxidant N-acetyl cysteine, confirming that PM2.5 cellular toxicity was due to oxidative stress. These findings contribute to understanding of the pathophysiological mechanisms triggered in the skin by PM2.5, among which oxidative stress may play a major role.

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Section: Methodsmentioning

confidence: 99%

Particulate matter 2.5 damages skin cells by inducing oxidative stress, subcellular organelle dysfunction, and apoptosis

et al. 2018

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“…[32][33][34][35][36][37] ROS are generated in several cellular systems, such as plasma membrane, peroxisomes, cytosol, endoplasmic reticulum, and membranes of mitochondria. 37 The imbalance between ROS generation and antioxidant system triggers oxidative stress, which is related to much pathology, including cancer, diabetes, rheumatoid arthritis, cardiovascular disease, and other diseases.…”

Section: Introductionmentioning

confidence: 99%

Polyethylenimine-functionalized silver nanoparticle-based co-delivery of paclitaxel to induce HepG2 cell apoptosis

Guo

Lin

et al. 2016

IJN

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“…ROS are important signalling molecules that mediate many signal transduction pathways and benefit for cellular survival (Focaccetti et al 2015); however, the overproduction of ROS damage cell by activation of apoptosis or necrosis. Growing evidence reveal that ROS also play an important role in the regulation of autophagy (Farah et al 2016). Consistent with former study, here, we found that ROS are critical for rasfonin-dependent autophagy, necrosis and apoptosis.…”

Section: Discussionmentioning

confidence: 99%

Rasfonin promotes autophagy and apoptosis via upregulation of reactive oxygen species (ROS)/JNK pathway

Sun

Che²,

Jiang

2016

Mycology

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Rasfonin is a fungal secondary metabolite demonstrating with antitumour effects. Reactive oxygen species (ROS) are formed as a natural by-product of the normal metabolism of oxygen and have important roles in cell signalling and homeostasis. Studies reported that many fungal secondary metabolites activated either autophagy or apoptosis through ROS generation. In former study, we revealed that rasfonin induced both autophagy and apoptosis, however, whether it promoted aforementioned processes via upregulation of ROS generation remains explored. In the current work, we demonstrated that rasfonin induced autophagy and apoptosis concomitant with a dramatically ROS production. N-Acetylcysteine (NAC), an often used ROS inhibitor, decreased both autophagic flux and caspase-dependent apoptosis by rasfonin. Flow cytometry analysis revealed NAC was able to reduce rasfonin-dependent apoptosis and necrosis. In methanethiosulfonate (MTS) assay, we observed that NAC significantly blocked rasfonin-induced cell viability loss. In addition, we found that rasfonin increased the phosphorylation of c-Jun NH2-terminal kinase (JNK), which was inhibited by NAC. SP600125, an inhibitor of JNK, reduced rasfonin-dependent autophagic flux and apoptosis. Moreover, we demonstrated that rasfonin inhibited the phosphorylation of both 4E-binding protein 1 (4E-BP1) and S6 kinase 1 (S6K1), two main substrates of mammalian target of rapamycin (mTOR). Collectively, rasfonin activated autophagy and apoptosis through upregulation of ROS/JNK signalling.

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Silver nanoparticles synthesized from Adenium obesum leaf extract induced DNA damage, apoptosis and autophagy via generation of reactive oxygen species

Cited by 147 publications

References 75 publications

Particulate matter 2.5 damages skin cells by inducing oxidative stress, subcellular organelle dysfunction, and apoptosis

Particulate matter 2.5 damages skin cells by inducing oxidative stress, subcellular organelle dysfunction, and apoptosis

Polyethylenimine-functionalized silver nanoparticle-based co-delivery of paclitaxel to induce HepG2 cell apoptosis

Rasfonin promotes autophagy and apoptosis via upregulation of reactive oxygen species (ROS)/JNK pathway

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