Pb(NO3)2 induces cell apoptosis through triggering of reactive oxygen species accumulation and disruption of mitochondrial function via SIRT3/SOD2 pathways

Lead (Pb) is nonbiodegradable and toxic to the lungs. To investigate the potential mechanisms of Pb‐induced reactive oxygen species (ROS) accumulation and cell death in the lungs, human non‐small lung carcinoma H460 cells were stimulated with Pb(NO3)2 in this study. The results showed that Pb(NO3)2...

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Published inEnvironmental toxicology Vol. 39; no. 3; pp. 1294 - 1302
Main Authors Lin, Hui‐Wen, Lee, Hsiang‐Lin, Shen, Ting‐Jing, Ho, Meng‐Ting, Lee, Yi‐Ju, Wang, Inga, Lin, Ching‐Pin, Chang, Yuan‐Yen
Format Journal Article
LanguageEnglish
Published Hoboken, USA John Wiley & Sons, Inc 01.03.2024
Wiley Subscription Services, Inc
Subjects
Accumulation
Apoptosis
Caspase-3
cell apoptosis
Cell death
Cells
Disulfide reductase
ecotoxicology
Glutathione
glutathione-disulfide reductase
Humans
Hydrogen peroxide
Lead
Lung cancer
Lung carcinoma
lung neoplasms
Lungs
Membrane potential
Mitochondria
Mitochondria - metabolism
mitochondrial
mitochondrial membrane
Mortality
Neoplasms
oxidoreductive activity
Oxygen
Pb(NO3)2
Reactive oxygen species
Reactive Oxygen Species - metabolism
Reductases
ROS
Sirtuin 3 - metabolism
sirtuins
Superoxide dismutase
Superoxide Dismutase - metabolism
toxicity
cell apoptosis
mitochondrial
oxidoreductive activity
Pb(NO3)2
ROS
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Abstract Lead (Pb) is nonbiodegradable and toxic to the lungs. To investigate the potential mechanisms of Pb‐induced reactive oxygen species (ROS) accumulation and cell death in the lungs, human non‐small lung carcinoma H460 cells were stimulated with Pb(NO3)2 in this study. The results showed that Pb(NO3)2 stimulation increased cell death by inducing cell apoptosis which showed a reduced Bcl‐2 expression and an enhanced caspase 3 activation. Pb(NO3)2 also caused the production of H2O2 in H460 cells that triggering the buildup of ROS and mitochondrial membrane potential loss. We found that Pb(NO3)2 modulates oxidoreductive activity through reduced the glutathione‐disulfide reductase and glutathione levels in Pb(NO3)2‐exposed H460 cells. Furthermore, the superoxide dismutase (SOD) upstream molecule sirtuin 3 (SIRT3) was increased with Pb(NO3)2 dose. Collectively, these results demonstrate that Pb(NO3)2 promotes lung cell death through SIRT3/SOD‐mediated ROS accumulation and mitochondrial dysfunction.
AbstractList Lead (Pb) is nonbiodegradable and toxic to the lungs. To investigate the potential mechanisms of Pb‐induced reactive oxygen species (ROS) accumulation and cell death in the lungs, human non‐small lung carcinoma H460 cells were stimulated with Pb(NO3)2 in this study. The results showed that Pb(NO3)2 stimulation increased cell death by inducing cell apoptosis which showed a reduced Bcl‐2 expression and an enhanced caspase 3 activation. Pb(NO3)2 also caused the production of H2O2 in H460 cells that triggering the buildup of ROS and mitochondrial membrane potential loss. We found that Pb(NO3)2 modulates oxidoreductive activity through reduced the glutathione‐disulfide reductase and glutathione levels in Pb(NO3)2‐exposed H460 cells. Furthermore, the superoxide dismutase (SOD) upstream molecule sirtuin 3 (SIRT3) was increased with Pb(NO3)2 dose. Collectively, these results demonstrate that Pb(NO3)2 promotes lung cell death through SIRT3/SOD‐mediated ROS accumulation and mitochondrial dysfunction.
Lead (Pb) is nonbiodegradable and toxic to the lungs. To investigate the potential mechanisms of Pb-induced reactive oxygen species (ROS) accumulation and cell death in the lungs, human non-small lung carcinoma H460 cells were stimulated with Pb(NO3 )2 in this study. The results showed that Pb(NO3 )2 stimulation increased cell death by inducing cell apoptosis which showed a reduced Bcl-2 expression and an enhanced caspase 3 activation. Pb(NO3 )2 also caused the production of H2 O2 in H460 cells that triggering the buildup of ROS and mitochondrial membrane potential loss. We found that Pb(NO3 )2 modulates oxidoreductive activity through reduced the glutathione-disulfide reductase and glutathione levels in Pb(NO3 )2 -exposed H460 cells. Furthermore, the superoxide dismutase (SOD) upstream molecule sirtuin 3 (SIRT3) was increased with Pb(NO3 )2 dose. Collectively, these results demonstrate that Pb(NO3 )2 promotes lung cell death through SIRT3/SOD-mediated ROS accumulation and mitochondrial dysfunction.Lead (Pb) is nonbiodegradable and toxic to the lungs. To investigate the potential mechanisms of Pb-induced reactive oxygen species (ROS) accumulation and cell death in the lungs, human non-small lung carcinoma H460 cells were stimulated with Pb(NO3 )2 in this study. The results showed that Pb(NO3 )2 stimulation increased cell death by inducing cell apoptosis which showed a reduced Bcl-2 expression and an enhanced caspase 3 activation. Pb(NO3 )2 also caused the production of H2 O2 in H460 cells that triggering the buildup of ROS and mitochondrial membrane potential loss. We found that Pb(NO3 )2 modulates oxidoreductive activity through reduced the glutathione-disulfide reductase and glutathione levels in Pb(NO3 )2 -exposed H460 cells. Furthermore, the superoxide dismutase (SOD) upstream molecule sirtuin 3 (SIRT3) was increased with Pb(NO3 )2 dose. Collectively, these results demonstrate that Pb(NO3 )2 promotes lung cell death through SIRT3/SOD-mediated ROS accumulation and mitochondrial dysfunction.
Lead (Pb) is nonbiodegradable and toxic to the lungs. To investigate the potential mechanisms of Pb‐induced reactive oxygen species (ROS) accumulation and cell death in the lungs, human non‐small lung carcinoma H460 cells were stimulated with Pb(NO3)2 in this study. The results showed that Pb(NO3)2 stimulation increased cell death by inducing cell apoptosis which showed a reduced Bcl‐2 expression and an enhanced caspase 3 activation. Pb(NO3)2 also caused the production of H2O2 in H460 cells that triggering the buildup of ROS and mitochondrial membrane potential loss. We found that Pb(NO3)2 modulates oxidoreductive activity through reduced the glutathione‐disulfide reductase and glutathione levels in Pb(NO3)2‐exposed H460 cells. Furthermore, the superoxide dismutase (SOD) upstream molecule sirtuin 3 (SIRT3) was increased with Pb(NO3)2 dose. Collectively, these results demonstrate that Pb(NO3)2 promotes lung cell death through SIRT3/SOD‐mediated ROS accumulation and mitochondrial dysfunction.
Lead (Pb) is nonbiodegradable and toxic to the lungs. To investigate the potential mechanisms of Pb‐induced reactive oxygen species (ROS) accumulation and cell death in the lungs, human non‐small lung carcinoma H460 cells were stimulated with Pb(NO₃)₂ in this study. The results showed that Pb(NO₃)₂ stimulation increased cell death by inducing cell apoptosis which showed a reduced Bcl‐2 expression and an enhanced caspase 3 activation. Pb(NO₃)₂ also caused the production of H₂O₂ in H460 cells that triggering the buildup of ROS and mitochondrial membrane potential loss. We found that Pb(NO₃)₂ modulates oxidoreductive activity through reduced the glutathione‐disulfide reductase and glutathione levels in Pb(NO₃)₂‐exposed H460 cells. Furthermore, the superoxide dismutase (SOD) upstream molecule sirtuin 3 (SIRT3) was increased with Pb(NO₃)₂ dose. Collectively, these results demonstrate that Pb(NO₃)₂ promotes lung cell death through SIRT3/SOD‐mediated ROS accumulation and mitochondrial dysfunction.
Lead (Pb) is nonbiodegradable and toxic to the lungs. To investigate the potential mechanisms of Pb‐induced reactive oxygen species (ROS) accumulation and cell death in the lungs, human non‐small lung carcinoma H460 cells were stimulated with Pb(NO 3 ) 2 in this study. The results showed that Pb(NO 3 ) 2 stimulation increased cell death by inducing cell apoptosis which showed a reduced Bcl‐2 expression and an enhanced caspase 3 activation. Pb(NO 3 ) 2 also caused the production of H 2 O 2 in H460 cells that triggering the buildup of ROS and mitochondrial membrane potential loss. We found that Pb(NO 3 ) 2 modulates oxidoreductive activity through reduced the glutathione‐disulfide reductase and glutathione levels in Pb(NO 3 ) 2 ‐exposed H460 cells. Furthermore, the superoxide dismutase (SOD) upstream molecule sirtuin 3 (SIRT3) was increased with Pb(NO 3 ) 2 dose. Collectively, these results demonstrate that Pb(NO 3 ) 2 promotes lung cell death through SIRT3/SOD‐mediated ROS accumulation and mitochondrial dysfunction.
Lead (Pb) is nonbiodegradable and toxic to the lungs. To investigate the potential mechanisms of Pb-induced reactive oxygen species (ROS) accumulation and cell death in the lungs, human non-small lung carcinoma H460 cells were stimulated with Pb(NO ) in this study. The results showed that Pb(NO ) stimulation increased cell death by inducing cell apoptosis which showed a reduced Bcl-2 expression and an enhanced caspase 3 activation. Pb(NO ) also caused the production of H O in H460 cells that triggering the buildup of ROS and mitochondrial membrane potential loss. We found that Pb(NO ) modulates oxidoreductive activity through reduced the glutathione-disulfide reductase and glutathione levels in Pb(NO ) -exposed H460 cells. Furthermore, the superoxide dismutase (SOD) upstream molecule sirtuin 3 (SIRT3) was increased with Pb(NO ) dose. Collectively, these results demonstrate that Pb(NO ) promotes lung cell death through SIRT3/SOD-mediated ROS accumulation and mitochondrial dysfunction.
Author Lin, Ching‐Pin
Ho, Meng‐Ting
Lin, Hui‐Wen
Lee, Yi‐Ju
Wang, Inga
Chang, Yuan‐Yen
Lee, Hsiang‐Lin
Shen, Ting‐Jing
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  organization: Chung Shan Medical University, and Clinical Laboratory, Chung Shan Medical University Hospital
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Keywords cell apoptosis
mitochondrial
oxidoreductive activity
Pb(NO3)2
ROS
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Snippet Lead (Pb) is nonbiodegradable and toxic to the lungs. To investigate the potential mechanisms of Pb‐induced reactive oxygen species (ROS) accumulation and cell...
Lead (Pb) is nonbiodegradable and toxic to the lungs. To investigate the potential mechanisms of Pb-induced reactive oxygen species (ROS) accumulation and cell...
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SubjectTerms Accumulation
Apoptosis
Caspase-3
cell apoptosis
Cell death
Cells
Disulfide reductase
ecotoxicology
Glutathione
glutathione-disulfide reductase
Humans
Hydrogen peroxide
Lead
Lung cancer
Lung carcinoma
lung neoplasms
Lungs
Membrane potential
Mitochondria
Mitochondria - metabolism
mitochondrial
mitochondrial membrane
Mortality
Neoplasms
oxidoreductive activity
Oxygen
Pb(NO3)2
Reactive oxygen species
Reactive Oxygen Species - metabolism
Reductases
ROS
Sirtuin 3 - metabolism
sirtuins
Superoxide dismutase
Superoxide Dismutase - metabolism
toxicity
Title Pb(NO3)2 induces cell apoptosis through triggering of reactive oxygen species accumulation and disruption of mitochondrial function via SIRT3/SOD2 pathways
URI https://onlinelibrary.wiley.com/doi/abs/10.1002%2Ftox.24019
https://www.ncbi.nlm.nih.gov/pubmed/37948429
https://www.proquest.com/docview/2922699365
https://www.proquest.com/docview/2889243324
https://www.proquest.com/docview/3040353361
Volume 39
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