Propyl gallate decreases the proliferation of Calu‐6 and A549 lung cancer cells via affecting reactive oxygen species and glutathione levels

Park, Woo Hyun

doi:10.1002/jat.4231

Cited by 9 publications

(9 citation statements)

References 35 publications

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“…14 Furthermore, increasing studies have identified that oxidative damage caused by PG is an important route of PG performs its cytotoxicity, and PG either increases or decreases ROS level depending on its dose and time of exposure. 57 In our study, exposure to PG increased the level of ROS in oocytes and induced apoptosis, which is consistent with the above data. Given that ROS has been confirmed as a crucial way of multiple environmental toxicants to exert harmful influences in female reproduction, 23,39,[58][59][60] we conjectured that PG induced the elevation of ROS in oocytes is responsible for mitochondria dysfunction, ATP depletion and DNA damage.…”

Section: Discussionsupporting

confidence: 93%

“…Published data suggested that the anti‐oxidative and cytoprotective properties of PG could change to pro‐oxidative, cytotoxic and genotoxic properties in the presence of Cu(II) 14 . Furthermore, increasing studies have identified that oxidative damage caused by PG is an important route of PG performs its cytotoxicity, and PG either increases or decreases ROS level depending on its dose and time of exposure 57 . In our study, exposure to PG increased the level of ROS in oocytes and induced apoptosis, which is consistent with the above data.…”

Section: Discussionmentioning

confidence: 99%

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High‐dose synthetic phenolic antioxidant propyl gallate impairs mouse oocyte meiotic maturation through inducing mitochondrial dysfunction and DNA damage

Yang

Wang

Zhang

et al. 2023

Environmental Toxicology

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Propyl gallate (PG) is one of the most widely used antioxidants in food products, cosmetics and pharmaceutical industries. Increased research has suggested that exposure to PG influences reproductive health in humans and animals. However, until now, it has not yet been confirmed whether PG would impact oocyte quality. In this study, the hazardous effects of PG on oocyte meiotic maturation were investigated in mice. The findings showed that PG exposure compromises oocyte meiosis by inducing mitochondrial stress which activates apoptosis to trigger oocyte demise.Moreover, DNA damage was significantly induced in PG-treated oocytes, which might be another cause of oocyte developmental arrest and degeneration. Besides, the level of histone methylation (H3K27me2 and H3K27me3) in oocyte was also significantly increased by PG exposure. Furthermore, PG-induced oxidative stress was validated by the increased level of reactive oxygen species (ROS), which might be the underlying reason for these abnormities. In conclusion, the foregoing findings suggested that PG exposure impaired oocyte meiotic maturation by yielding mitochondrial stress to activate apoptosis, inducing DNA damage and oxidative stress, and altering histone methylation level.

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Section: Discussionsupporting

confidence: 93%

Section: Discussionmentioning

confidence: 99%

High‐dose synthetic phenolic antioxidant propyl gallate impairs mouse oocyte meiotic maturation through inducing mitochondrial dysfunction and DNA damage

Yang

Wang

Zhang

et al. 2023

Environmental Toxicology

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“…PG is a synthetic agent that has anti-growth effects in many cell types, including endothelial cells [27,28], leukemia cells [29], breast cancer [30], hepatocellular carcinoma cells [31], and cervical cancer cells [6,32]. Recently, our group has found that PG treatment inhibits the growth of lung cancer cells, especially A549 epithelial adenocarcinoma cells via apoptosis or GSH depletion [33,34]. Fibroblast cells are the most abundant type of cells in the pulmonary interstitium.…”

Section: Introductionmentioning

confidence: 99%

Propyl gallate induces cell death in human pulmonary fibroblast through increasing reactive oxygen species levels and depleting glutathione

Park¹

2023

Preprint

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Background Propyl gallate (PG) has demonstrated anti-growth effects on various cell types. This study aimed to investigate the impact of PG on reactive oxygen species (ROS) and glutathione (GSH) levels in primary human pulmonary fibroblast (HPF) cells. Additionally, the study explored the effects of N-acetyl cysteine (NAC), L-buthionine sulfoximine (BSO), and small interfering RNA (siRNAs) targeting antioxidant genes on ROS, GSH levels, and cell death in PG-treated HPF cells. Methods and Results Intracellular ROS and GSH levels were measured using different fluorescent probe dyes (H2DCFDA, DHE, MitoSOX™ Red and CMFDA) through flow cytometer analysis. PG treatment at concentrations ranging from 100 to 800 µM resulted in increased levels of total ROS and O2•− at early time points (30–180 min and 24 h). Higher concentrations of PG (800–1600 µM) led to an increased number of cells depleted of GSH at 24 h and reduced GSH levels at 30–180 min. PG treatment downregulated the activity of superoxide dismutase (SOD) and upregulated the activity of catalase in HPF cells. Treatment with 800 µM PG increased the number of apoptotic cells and cells with loss of mitochondrial membrane potential (MMP; ∆Ψm) as assessed by Annexin V-FITC/PI and rhodamine 123 staining, respectively. NAC treatment mitigated PG-induced cell death and loss of MMP in HPF cells, accompanied by a decrease in GSH depletion. Conversely, BSO exacerbated cell death and MMP loss induced by PG, independent of ROS and GSH depletion levels. Following transfection with siRNA, the HPF cells were exposed to PG treatment. The siRNAs against SOD1, SOD2, and catalase successfully attenuated cell death in PG-treated HPF cells. In contrast, siRNA against GSH peroxidase enhanced cell death. Conclusions PG induced cell death in HPF cells by increasing ROS levels and depleting GSH. NAC was found to decrease HPF cell death induced by PG, while BSO enhanced cell death. The findings suggest that modulating the antioxidant defense system can influence the cytotoxic effects of PG in HPF cells.

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“…Lung cancer is the leading cause of cancer-related deaths worldwide [ 29 ]. Recently, we reported that PG treatment inhibited the growth of lung cancer cells through apoptosis or GSH depletion [ 30 , 31 ]. In the present study, the anti-apoptotic effects of various pan-caspase, caspase-3, caspase-8, and caspase-9 inhibitors were investigated in PG-treated Calu-6 and A549 lung cancer cells in relation to changes in ROS and GSH levels.…”

Section: Introductionmentioning

confidence: 99%

The Anti-Apoptotic Effects of Caspase Inhibitors in Propyl Gallate-Treated Lung Cancer Cells Are Related to Changes in Reactive Oxygen Species and Glutathione Levels

Park

2022

Molecules

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Propyl gallate [3,4,5-trihydroxybenzoic acid propyl ester; PG] exhibits an anti-growth effect in various cells. In this study, the anti-apoptotic effects of various caspase inhibitors were evaluated in PG-treated Calu-6 and A549 lung cancer cells in relation to reactive oxygen species (ROS) and glutathione (GSH) levels. Treatment with 800 μM PG inhibited the proliferation and induced the cell death of both Calu-6 and A549 cells at 24 h. Each inhibitor of pan-caspase, caspase-3, caspase-8, and caspase-9 reduced the number of dead and sub-G1 cells in both PG-treated cells at 24 h. PG increased ROS levels, including O2∙−, in both lung cancer cell lines at 24 h. Generally, caspase inhibitors appeared to decrease ROS levels in PG-treated lung cancer cells at 24 h and somewhat reduced O2∙− levels. PG augmented the number of GSH-depleted Calu-6 and A549 cells at 24 h. Caspase inhibitors did not affect the level of GSH depletion in PG-treated A549 cells but differently and partially altered the depletion level in PG-treated Calu-6 cells. In conclusion, PG exhibits an anti-proliferative effect in Calu-6 and A549 lung cancer cells and induced their cell death. PG-induced lung cancer death was accompanied by increases in ROS levels and GSH depletion. Therefore, the anti-apoptotic effects of caspase inhibitors were, at least in part, related to changes in ROS and GSH levels.

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Propyl gallate decreases the proliferation of Calu‐6 and A549 lung cancer cells via affecting reactive oxygen species and glutathione levels

Cited by 9 publications

References 35 publications

High‐dose synthetic phenolic antioxidant propyl gallate impairs mouse oocyte meiotic maturation through inducing mitochondrial dysfunction and DNA damage

High‐dose synthetic phenolic antioxidant propyl gallate impairs mouse oocyte meiotic maturation through inducing mitochondrial dysfunction and DNA damage

Propyl gallate induces cell death in human pulmonary fibroblast through increasing reactive oxygen species levels and depleting glutathione

The Anti-Apoptotic Effects of Caspase Inhibitors in Propyl Gallate-Treated Lung Cancer Cells Are Related to Changes in Reactive Oxygen Species and Glutathione Levels

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