Efficiency of CellROX deep red<sup>®</sup>and CellROX orange<sup>®</sup>fluorescent probes in identifying reactive oxygen species in sperm samples from high and low fertility bulls

Celeghini, Eneiva Carla Carvalho; Alves, Maíra Bianchi Rodrigues; Arruda, Rubens Paes de; Rezende, Gabriela Marques de; Florez-Rodriguez, S. A.; Filho, Manoel Francisco de Sá

doi:10.1080/10495398.2019.1654485

Cited by 27 publications

(22 citation statements)

References 24 publications

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“…H 2 O 2 -induced oxidative injury is inhibited by 4-OI in osteoblasts H 2 O 2 stimulation in cultured osteoblasts/osteoblastic cells would induce oxidative stress and cause profound protein damage, lipid peroxidation, and DNA breaks 4,8,30,31 . In human osteoblastic OB-6 cells, H 2 O 2 (400 μM) significantly increased ROS production, evidenced by the increased CellROX intensity 32,33 (Fig. 2a).…”

Section: Nrf2 Cascade Activation By 4-oi In Osteoblastsmentioning

confidence: 95%

Four-octyl itaconate activates Nrf2 cascade to protect osteoblasts from hydrogen peroxide-induced oxidative injury

et al. 2020

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Four-octyl itaconate (4-OI) is the cell-permeable derivative of itaconate that can activate Nrf2 signaling by alkylating Keap1’s cysteine residues. Here, we tested the potential effect of 4-OI on hydrogen peroxide (H2O2)-induced oxidative injury in osteoblasts. In OB-6 cells and primary murine osteoblasts, 4-OI was able to activate Nrf2 signaling cascade and cause Keap1–Nrf2 disassociation, Nrf2 protein stabilization, cytosol accumulation, and nuclear translocation. 4-OI also augmented antioxidant-response element reporter activity and promoted expression of Nrf2-dependent genes (HO1, NQO1, and GCLC). Pretreatment with 4-OI inhibited H2O2-induced reactive oxygen species production, cell death, and apoptosis in osteoblasts. Furthermore, 4-OI inhibited H2O2-induced programmed necrosis by suppressing mitochondrial depolarization, mitochondrial cyclophilin D-ANT1 (adenine nucleotide translocase 1)-p53 association, and cytosol lactate dehydrogenase release in osteoblasts. Ectopic overexpression of immunoresponsive gene 1 (IRG1) increased endogenous itaconate production and activated Nrf2 signaling cascade, thereby inhibiting H2O2-induced oxidative injury and cell death. In OB-6 cells, Nrf2 silencing or CRISPR/Cas9-induced Nrf2 knockout blocked 4-OI-induced osteoblast cytoprotection against H2O2. Conversely, forced Nrf2 activation, by CRISPR/Cas9-induced Keap1 knockout, mimicked 4-OI-induced actions in OB-6 cells. Importantly, 4-OI was ineffective against H2O2 in Keap1-knockout cells. Collectively, 4-OI efficiently activates Nrf2 signaling to inhibit H2O2-induced oxidative injury and death of osteoblasts.

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Section: Nrf2 Cascade Activation By 4-oi In Osteoblastsmentioning

confidence: 95%

Four-octyl itaconate activates Nrf2 cascade to protect osteoblasts from hydrogen peroxide-induced oxidative injury

et al. 2020

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“…4b). Interestingly, A1874-induced significant oxidative injury in colon cancer cells, increasing CellROX fluorescence intensity 43 in pCan1 and pCan2 cells (Fig. 4c).…”

Section: A1874 Induces P53 Protein Stabilization and Oxidative Injurymentioning

confidence: 90%

The therapeutic effect of the BRD4-degrading PROTAC A1874 in human colon cancer cells

Qin

Jin

et al. 2020

Cell Death Dis

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A1874 is a novel BRD4-degrading proteolysis targeting chimera (PROTAC). In primary colon cancer cells and established HCT116 cells, A1874 potently inhibited cell viability, proliferation, cell cycle progression, as well as cell migration and invasion. The BRD4-degrading PROTAC was able to induce caspase and apoptosis activation in colon cancer cells. Furthermore, A1874-induced degradation of BRD4 protein and downregulated BRD-dependent genes (c-Myc, Bcl-2, and cyclin D1) in colon cancer cells. Significantly, A1874-induced anti-colon cancer cell activity was more potent than the known BRD4 inhibitors (JQ1, CPI203, and I-BET151). In BRD4-knockout colon cancer cells A1874 remained cytotoxic, indicating the existence of BRD4-independent mechanisms. In addition to BRD4 degradation, A1874 cytotoxicity in colon cancer cells was also associated with p53 protein stabilization and reactive oxygen species production. Importantly, the antioxidant N-acetyl-cysteine and the p53 inhibitor pifithrin-α attenuated A1874-induced cell death and apoptosis in colon cancer cells. In vivo, A1874 oral administration potently inhibited colon cancer xenograft growth in severe combined immuno-deficient mice. BRD4 degradation and p53 protein elevation, as well as apoptosis induction and oxidative stress were detected in A1874-treated colon cancer tissues. Together, A1874 inhibits colon cancer cell growth through both BRD4-dependent and -independent mechanisms.

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“…We therefore tested whether GDC-0349 altered ROS contents in NSCLC cells. Using a CellROX dye assay 45,46 , we showed that cellular ROS levels were significantly elevated following GDC-0349 treatment in A549 cells and NSCLC-1 cells (Fig. 4g).…”

Section: Gdc-0349 Inhibits Sphk1 Activation and Provokes Oxidative Stmentioning

confidence: 99%

GDC-0349 inhibits non-small cell lung cancer cell growth

Han

Zhao

et al. 2020

Cell Death Dis

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Non-small cell lung cancer (NSCLC) is a leading cause of cancer-related human mortality with a clear need for new therapeutic intervention. GDC-0349 is a potent and selective ATP-competitive mTOR inhibitor. In A549 cells and primary human NSCLC cells, GDC-0349 inhibited cell growth, proliferation, cell cycle progression, migration and invasion, while inducing significant apoptosis activation. Although GDC-0349 blocked Akt-mTORC1/2 activation in NSCLC cells, it also exerted cytotoxicity in Akt1-knockout A549 cells. Furthermore, restoring Akt-mTOR activation by a constitutively-active Akt1 only partially attenuated GDC-0349-induced A549 cell apoptosis, indicating the existence of Akt-mTOR-independent mechanisms. In NSCLC cells GDC-0349 induced sphingosine kinase 1 (SphK1) inhibition, ceramide accumulation, JNK activation and oxidative injury. Conversely, N-acetylcysteine, the JNK inhibitor and sphingosine 1-phosphate alleviated GDC-0349-induced NSCLC cell apoptosis. In vivo, daily oral administration of GDC-0349 potently inhibited NSCLC xenograft growth in mice. Akt-mTOR in-activation, SphK1 inhibition, JNK activation and oxidative stress were detected in NSCLC xenograft tissues with GDC-0349 administration. In summary, GDC-0349 inhibits NSCLC cell growth via Akt-mTOR-dependent and Akt-mTOR-independent mechanisms.

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Efficiency of CellROX deep red^®and CellROX orange^®fluorescent probes in identifying reactive oxygen species in sperm samples from high and low fertility bulls

Cited by 27 publications

References 24 publications

Four-octyl itaconate activates Nrf2 cascade to protect osteoblasts from hydrogen peroxide-induced oxidative injury

Four-octyl itaconate activates Nrf2 cascade to protect osteoblasts from hydrogen peroxide-induced oxidative injury

The therapeutic effect of the BRD4-degrading PROTAC A1874 in human colon cancer cells

GDC-0349 inhibits non-small cell lung cancer cell growth

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Efficiency of CellROX deep red®and CellROX orange®fluorescent probes in identifying reactive oxygen species in sperm samples from high and low fertility bulls

Cited by 27 publications

References 24 publications

Four-octyl itaconate activates Nrf2 cascade to protect osteoblasts from hydrogen peroxide-induced oxidative injury

Four-octyl itaconate activates Nrf2 cascade to protect osteoblasts from hydrogen peroxide-induced oxidative injury

The therapeutic effect of the BRD4-degrading PROTAC A1874 in human colon cancer cells

GDC-0349 inhibits non-small cell lung cancer cell growth

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Product

Resources

About

Efficiency of CellROX deep red^®and CellROX orange^®fluorescent probes in identifying reactive oxygen species in sperm samples from high and low fertility bulls