High cytotoxicity of a degraded TBBPA, dibromobisphenol A, through apoptotic and necrosis pathways

Suyama, Kyozo; Kesamaru, Hitoshi; Okubo, Takashi; Kasatani, Kazumi; Tomohara, Keisuke; Matsushima, Ayami; Nose, Takeru

doi:10.1016/j.heliyon.2023.e13003

Cited by 5 publications

(3 citation statements)

References 48 publications

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“…Following what was observed herein, vanadium compounds were previously reported to have cytotoxicity in vitro [26][27][28][29][30][31][32][33]. These results indicate that the cells might reach apoptosis through necrosis [40], making the compounds good candidates for potential cancer theranostics. The BJ fibroblasts registered significantly low viability, but as indicated by the other two assays, these values could be associated with either a lower number of cells or a lower number of mitochondria in the cells [41].…”

Section: Antitumor Activitysupporting

confidence: 77%

Decavanadate-Bearing Guanidine Derivatives Developed as Antimicrobial and Antitumor Species

Dumitrescu,

Maxim,

Badea

et al. 2023

IJMS

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To obtain biologically active species, a series of decavanadates (Hpbg)4[H2V10O28]·6H2O (1) (Htbg)4[H2V10O28]·6H2O; (2) (Hgnd)2(Hgnu)4[V10O28]; (3) (Hgnu)6[V10O28]·2H2O; and (4) (pbg = 1-phenyl biguanide, tbg = 1-(o-tolyl)biguanide, gnd = guanidine, and gnu = guanylurea) were synthesized and characterized by several spectroscopic techniques (IR, UV-Vis, and EPR) as well as by single crystal X-ray diffraction. Compound (1) crystallizes in space group P-1 while (3) and (4) adopt the same centrosymmetric space group P21/n. The unusual signal identified by EPR spectroscopy was assigned to a charge-transfer π(O)→d(V) process. Both stability in solution and reactivity towards reactive oxygen species (O2− and OH·) were screened through EPR signal modification. All compounds inhibited the development of Escherichia coli, Pseudomonas aeruginosa, Staphylococcus aureus, and Enterococcus faecalis bacterial strains in a planktonic state at a micromolar level, the most active being compound (3). However, the experiments conducted at a minimal inhibitory concentration (MIC) indicated that the compounds do not disrupt the biofilm produced by these bacterial strains. The cytotoxicity assayed against A375 human melanoma cells and BJ human fibroblasts by testing the viability, lactate dehydrogenase, and nitric oxide levels indicated compound (1) as the most active in tumor cells.

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Section: Antitumor Activitysupporting

confidence: 77%

Decavanadate-Bearing Guanidine Derivatives Developed as Antimicrobial and Antitumor Species

Dumitrescu,

Maxim,

Badea

et al. 2023

IJMS

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“…Moreover, Han et al [77] reported that TBBPA also caused apoptosis, mitochondrial dysfunction, and increased ROS in carp hepatocytes after exposure. Interestingly, it was also shown that degraded TBBPA (e.g., monoBr-BPA, diBr-BPA, and triBr-BPA) presented stronger toxicity to HeLa cells than parent TBBPA, leading to apoptosis [78]. Our results suggest that exposing mussels to 100 µg•L −1 of TBBPA raised the production of both caspase-3 and ubiquitin, suggesting that this concentration can lead to apoptosis and increased damaged proteins.…”

Section: Discussionmentioning

confidence: 50%

The Effects of Tetrabromobisphenol A (TBBPA) on the Mussel Mytilus galloprovincialis: A Multi-Biomarker Approach

Copeto,

Ganço,

Ferreira

et al. 2024

Oceans

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Tetrabromobisphenol A (TBBPA) is a fire-retardant containing bromine, produced in large quantities worldwide and extensively used in several industrial products. This compound was identified as a potential contaminant of the environment, causing toxicity to organisms. However, its toxicity remains poorly understood in marine bivalves. The first objective of this work was to evaluate the impact of TBBPA on mussels (Mytilus galloprovincialis) exposed for 28 days to various concentrations of TBBPA (0, 1, 10, and 100 µg·L−1), by assessing stress biomarkers’ responses (Glutathione S-transferase, superoxide dismutase, catalase, lipid peroxidation, total antioxidant capacity, total ubiquitin, caspase-3 and acetylcholinesterase). The results showed that lower concentrations (1 and 10 µg·L−1) were efficiently detoxified, as suggested by GST activities, which were supported by the responses of the other biomarkers. The most pronounced effects were observed in animals exposed to the highest concentration of TBBPA (100 µg·L−1), suggesting oxidative stress. Additionally, significant strong correlations were found between total antioxidant capacity and some biomarkers (superoxide dismutase and lipid peroxidation), showing that processes involved in oxidative stress fighting are working to avoid cell injury. In brief, mussels’ defense mechanisms were capable of dealing with exposure to the lower concentrations tested. Despite this, the risk of consuming shellfish or other fishery products contaminated with TBBPA should be a cause for concern.

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“…For example, TCBPA was found in 18.6% of serum samples from 150 female volunteers [7]. Various studies have evaluated the toxicological effects of TCBPA using in vitro and Am J Cancer Res 2024;14(3):1363-1375 in vivo models; these studies have indicated its potential for endocrine disruption, cytotoxicity, liver toxicity, and neurotoxicity [8]. For example, using zebrafish as an aquatic model organism, research has found that TCBPA has toxic effects on the cardiovascular and nervous systems of zebrafish [9].…”

Section: Introductionmentioning

confidence: 99%

Different effects of TCBPA exposure on liver cancer cells and liver cells: two sides of the coin

Wang

2024

Am J Cancer Res

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Tetrachlorobisphenol A (TCBPA), widely used as a substitute for tetrabromobisphenol A (TBBPA), has been detected in various environmental media. Therefore, a detailed evaluation of the toxicological properties of TCBPA is necessary. In this study, we used hepatoma and normal liver cell models in vitro to investigate the effects of TCBPA.Our findings indicate that TCBPA promotes the proliferation of liver cancer cells, as evidenced by MTT and EdU assays, and enhances the expression levels of molecules related to hepatoma proliferation. Further investigation into the molecular mechanism revealed that TCBPA-induced hepatoma proliferation is regulated by an NLRP3-mediated inflammatory process. Additionally, TCBPA was found to promote the epithelial-mesenchymal transition (EMT) process in liver cancer cells. Conversely, TCBPA inhibited the proliferation of normal liver cells. Mechanistic studies showed that TCBPA induced cell pyroptosis in normal liver cells by evaluating a series of related markers, including NLRP3, IL-1β, ASC, GASDMD, and Caspase 1. In vivo models further showed that TCBPA causes liver tissue damage. In summary, this study demonstrates that TCBPA has a dual effect: promoting the occurrence and development of liver tumor cells in vitro, while inhibiting the proliferation of normal liver cells, like two sides of a coin. These opposite cellular outcomes are regulated by NLRP3-mediated inflammatory processes, providing valuable insights for evaluating the potential health impacts of TCBPA.

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High cytotoxicity of a degraded TBBPA, dibromobisphenol A, through apoptotic and necrosis pathways

Cited by 5 publications

References 48 publications

Decavanadate-Bearing Guanidine Derivatives Developed as Antimicrobial and Antitumor Species

Decavanadate-Bearing Guanidine Derivatives Developed as Antimicrobial and Antitumor Species

The Effects of Tetrabromobisphenol A (TBBPA) on the Mussel Mytilus galloprovincialis: A Multi-Biomarker Approach

Different effects of TCBPA exposure on liver cancer cells and liver cells: two sides of the coin

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