Search

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. [ABSTRACT FROM AUTHOR]

Kaempferol is a flavonoid with anticancer and anti‐metastasis activity in different cancer‐cell lines. However, the underlying mechanisms by which kaempferol acts on human retinal pigment epithelial (ARPE‐19) cells remain unclear. In this study, we demonstrated that kaempferol inhibited migration and invasion in ARPE‐19 cells at non‐toxic dosages. We discovered that kaempferol obviously reduced the enzyme activity and protein expression of matrix metalloproteinase‐2 by increasing the phosphorylated levels of extracellular signal‐regulated kinases 1/2 (ERK1/2) signaling pathways. Additionally, ERK1/2‐specific inhibitor PD98059 significantly reversed kaempferol's inhibitory effects on migration and expression of MMP‐2 in ARPE‐19 cells. Overall, our results are the first to demonstrate that kaempferol is capable of inhibiting cell migration by targeting ERK1/2 signaling in human retinal pigment epithelial cells. [ABSTRACT FROM AUTHOR]

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., (© 2023 Wiley Periodicals LLC.)