3,4-Dihydroxybenzaldehyde attenuates pentachlorophenol-induced cytotoxicity, DNA damage and collapse of mitochondrial membrane potential in isolated human blood cells

2020 ◽  
pp. 1-18
Author(s):  
Nikhil Maheshwari ◽  
Riaz Mahmood
Keyword(s):  
Dna Damage ◽  
Membrane Potential ◽  
Mitochondrial Membrane Potential ◽  
Human Blood ◽  
Blood Cells ◽  
Mitochondrial Membrane ◽  
Human Blood Cells

scholarly journals Effects of Berberine on Cell Cycle, DNA, Reactive Oxygen Species, and Apoptosis in L929 Murine Fibroblast Cells

2015 ◽  
Vol 2015 ◽  
pp. 1-13 ◽  
Author(s):  
Manman Gu ◽  
Jing Xu ◽  
Chunyang Han ◽  
Youxi Kang ◽  
Tengfei Liu ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Cell Cycle ◽  
Dna Damage ◽  
Membrane Potential ◽  
Mitochondrial Membrane Potential ◽  
Cell Apoptosis ◽  
Mitochondrial Membrane ◽  
Oxygen Species ◽  
Cycle Arrest ◽  
Murine Fibroblast

Berberine, an isoquinoline alkaloid isolated from several traditional Chinese herbal medicines (TCM), exhibits a strong antimicrobial activity in the treatment of diarrhea. However, it causes human as well as animal toxicity from heavy dosage. The present study was conducted to investigate the cytotoxicity of berberine and its possible trigger mechanisms resulting in cell cycle arrest, DNA damage, ROS (reactive oxygen species) level, mitochondrial membrane potential change, and cell apoptosis in L929 murine fibroblast (L929) cells. The cells were culturedin vitroand treated with different concentrations of berberine for 24 h. The results showed that cell viability was significantly decreased in a subjected dose-dependent state; berberine concentrations were higher than 0.05 mg/mL. Berberine at a concentration above 0.1 mg/mL altered the morphology of L929 cells. Cells at G2/M phase were clear that the level of ROS and cell apoptosis rates increased in 0.1 mg/mL group. Each DNA damage indicator score (DIS) increased in groups where concentration of berberine was above 0.025 mg/mL. The mitochondrial membrane potential counteractive balance mechanics were significantly altered when concentrations of berberine were above 0.005 mg/mL. In all, the present study suggested that berberine at high dosage exhibited cytotoxicity on L929 which was related to resultant: cell cycle arrest; DNA damage; accumulation of intracellular ROS; reduction of mitochondrial membrane potential; and cell apoptosis.

In vitro DNA damage by Casiopeina II-gly in human blood cells

2016 ◽  
Vol 40 (2) ◽  
pp. 164-170 ◽  
Author(s):  
Juan José Rodríguez-Mercado ◽  
Diana Florín-Ramírez ◽  
Lucila Álvarez-Barrera ◽  
Mario Agustín Altamirano-Lozano
Keyword(s):  
Dna Damage ◽  
Human Blood ◽  
Blood Cells ◽  
Human Blood Cells

scholarly journals EPAC1 Inhibition Protects the Heart from Doxorubicin-Induced Toxicity

2021 ◽  
Author(s):  
Marianne Mazevet ◽  
Maxance Ribeiro ◽  
Anissa Belhadef ◽  
Delphine Dayde ◽  
Anna Llach ◽  
...  
Keyword(s):  
Dna Damage ◽  
Cell Death ◽  
Membrane Potential ◽  
Dilated Cardiomyopathy ◽  
Mitochondrial Membrane Potential ◽  
Mitochondrial Membrane ◽  
Dna Intercalation ◽  
Antitumoral Activity ◽  
Ros Generation

Rationale: The widely used chemotherapeutic agent Doxorubicin (Dox) induces cardiotoxicity leading to dilated cardiomyopathy and heart failure. This cardiotoxicity has been related to ROS generation, DNA intercalation, bioenergetic distress and cell death. However, alternative mechanisms are emerging, focusing on signaling pathways. Objective: We investigated the role of Exchange Protein directly Activated by cAMP (EPAC), key factor in cAMP signaling, in Dox-induced cardiotoxicity. Methods and Results: Dox was administrated in vivo (10 +/- 2 mg/kg, i.v.; with analysis at 2, 6 and 15 weeks post injection) in WT and EPAC1 KO C57BL6 mice. Cardiac function was analyzed by echocardiography and intracellular Ca2+ homeostasis by confocal microscopy in isolated ventricular cardiomyocytes. 15 weeks post-injections, Dox-treated WT mice, developed a dilated cardiomyopathy with decreased ejection fraction, increased telediastolic volume and impaired Ca2+ homeostasis, which were totally prevented in the EPAC1 KO mice. The underlying mechanisms were investigated in neonatal and adult rat cardiac myocytes under Dox treatment (1-10 uM). Flow cytometry, Western blot, BRET sensor assay, and RT-qPCR analysis showed that Dox induced DNA damage and cardiomyocyte cell death with apoptotic features rather than necrosis, including Ca2+-CaMKKβ-dependent opening of the Mitochondrial Permeability Transition Pore, dissipation of the Mitochondrial membrane potential, caspase activation, cell size reduction, and DNA fragmentation. Dox also led to an increase in both cAMP concentration and EPAC1 protein level and activity. The pharmacological inhibition of EPAC1 (CE3F4) but not EPAC2 alleviated the whole Dox-induced pattern of alterations including DNA damage, Mitochondrial membrane potential, apoptosis, mitochondrial biogenesis, dynamic, and fission/fusion balance, and respiratory chain activity, suggesting a crucial role of EPAC1 in these processes. Importantly, while preserving cardiomyocyte integrity, EPAC1 inhibition potentiated Dox-induced cell death in several human cancer cell lines. Conclusion: Thus, EPAC1 inhibition could be a valuable therapeutic strategy to limit Dox-induced cardiomyopathy without interfering with its antitumoral activity.

scholarly journals Corrigendum to “Dark coffee consumption protects human blood cells from spontaneous DNA damage” [J. Funct. Foods 55 (2019) 285–295]

2020 ◽  
Vol 71 ◽  
pp. 103989
Author(s):  
Gudrun Pahlke ◽  
Eva Attakpah ◽  
Georg Aichinger ◽  
Katarina Ahlberg ◽  
Christina Maria Hochkogler ◽  
...  
Keyword(s):  
Dna Damage ◽  
Human Blood ◽  
Blood Cells ◽  
Coffee Consumption ◽  
Human Blood Cells

Long non-coding RNA ENST00000414355 as a biomarker of cadmium exposure regulates DNA damage and apoptosis

2021 ◽  
pp. 074823372110481
Author(s):  
Asmaa Mohammad Moawad ◽  
Fatma Mohamed Hassan ◽  
Dina Sabry Abdelfattah ◽  
Hoda Ahmed Mohamed Basyoni
Keyword(s):  
Dna Damage ◽  
Membrane Potential ◽  
Mitochondrial Membrane Potential ◽  
Mitochondrial Membrane ◽  
Statistical Significance ◽  
Venous Blood ◽  
Significant Negative Correlation ◽  
Serine Threonine Kinase ◽  
Non Coding Rna ◽  
Exposed Workers

Human exposure to cadmium (Cd) may induce severe effects in different organs. Recent studies suggest that long non-coding RNAs (lncRNAs) are closely involved in the pathophysiological mechanisms of Cd-related diseases. This study evaluated the use of lncRNA (ENST00000414355) as an expression signature of Cd exposure and assessed its ability to modulate DNA damage and apoptosis by measuring the expression of ATM serine/threonine kinase (ATM) and mitochondrial membrane potential (ΔΨm) in Cd-exposed workers. A total of 139 (74 non-smokers and 65 smokers) participants from a Cd battery manufacturer were included in the study. Venous blood samples were collected to determine the blood Cd level and detect blood ENST00000414355 and its target gene (ATM) using real-time reverse transcription-polymerase chain reaction (qRT-PCR). Mitochondrial membrane potential was used to assess the Cd effect on mitochondrial permeability. Our results indicated a significant positive correlation between blood Cd level and lncRNA-ENST00000414355 and ATM expression and a significant negative correlation between blood Cd level and ΔΨm ( p < 0.0001). Moreover, significant correlations were observed between the expression of lncRNA-ENST00000414355 and ATM expression and ΔΨm ( p < 0.0001). Statistical significance was found in the blood Cd level, lncRNA-ENST00000414355 expression, ATM expression, and ΔΨm ( p < 0.0001) between smokers and non-smokers. This study confirmed the upregulation of the lncRNA-ENST00000414355 expression, DNA damage-checkpoint-related gene (ATM), and decreased ΔΨm in Cd-exposed workers. Thus, lncRNA-ENST00000414355 may serve as a valuable biomarker for the exposure and toxicity of Cd.

Blood Cells With Reduced Mitochondrial Membrane Potential and Cytosolic Cytochrome C Can Survive and Maintain Clonogenicity Given Appropriate Signals to Suppress Apoptosis

Blood ◽  
1998 ◽  
Vol 92 (12) ◽  
pp. 4545-4553 ◽  
Author(s):  
Quan Chen ◽  
Naoshi Takeyama ◽  
Ged Brady ◽  
Alastair J.M. Watson ◽  
Caroline Dive
Keyword(s):  
Membrane Potential ◽  
Cytochrome C ◽  
Mitochondrial Membrane Potential ◽  
Blood Cells ◽  
Mitochondrial Membrane ◽  
Mitochondrial Cytochrome ◽  
Abl Tyrosine Kinase ◽  
Key Events ◽  
Cytosolic Cytochrome ◽  
Mitochondrial Cytochrome C

Reduction of mitochondrial membrane potential (Ψm) and release of cytochrome c from mitochondria appear to be key events during apoptosis. Apoptosis was induced in IC.DP premast cells by the withdrawal of interleukin-3 (IL-3). Ψm decreased by 12 hours and cytochrome c was detected in the cytosol at 18 hours. Despite these changes in the mitochondria after 18 hours of IL-3 deprivation, clonogenicity was unaffected when IL-3 was replenished at 18 hours. Activation of v-Abl tyrosine kinase (v-Abl TK) in IC.DP cells before IL-3 depletion led to increased levels of Bcl-XL, prevented reduction of Ψm and the release of mitochondrial cytochrome c, and suppressed apoptosis. Activation of v-Abl TK 18 hours after withdrawal of IL-3 when ≤10% of the cells had died restored Ψm in the remaining cells. More than 40% of cells thus rescued by v-Abl TK between 18 and 42 hours could subsequently form colonies in the presence of IL-3. These data suggest that reduction in Ψm precedes loss of mitochondrial cytochrome c in IC.DP cells; that v-Abl TK activation, probably via upregulation of Bcl-XL, prevents loss of Ψm and blocks the release of cytochrome c from mitochondria; and that neither of these mitochondrial events is sufficient for commitment to apoptosis.

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