In vitro cytotoxicity of bisphenol A to human gingival epithelial S-G cells

Harvey Babich, David Tipton

Research output: Contribution to journalArticle

8 Citations (Scopus)

Abstract

In vitro cell culture studies have noted that bisphenol A (BPA), acting as a xenoestrogen, stimulated human breast cancer cell proliferation in vitro. BPA is the precursor of many monomers, including bisphenol A dimethacrylate (Bis-DMA), which is used widely in resin-based dental composites and sealants. The detection of BPA in the saliva of patients in whom sealants had been applied 1 h earlier raised several health safety concerns. Studies on the in vitro response of normal human cells to BPA are lacking. By quantitating the in vitro cytotoxicity of BPA using cell culture assays combined with microscopy, the study presented herein provides a cytotoxicity profile of BPA toward normal human cells. The relative cytotoxicity of BPA, and, for comparative purposes, of other leachates from dental materials, toward human gingival epithelial (S-G) cells, gingival (GN) fibroblasts, and periodontal ligament (PDL) fibroblasts was evaluated with the neutral red (NR) assay. For the S-G and GN cells the sequence of potency was BPA, bisphenol glycidyl methacrylate (Bis-GMA) > Bis-DMA > triethylene glycol dimethacrylate (TEGDMA), but for the PDL fibroblasts the sequence was BPA, Bis-GMA > TEGDMA > Bis-DMA. More extensive studies focused on BPA and S- G cells. The midpoint NR cytotoxicity value of 0.2 mM BPA noted for a 24-h exposure of the S-G cells was similar to that noted with the 3-[4,5- dimethylthiazol-2-yl]-2,5-diphenyl tetrazolium bromide (MTT) and AlamarBlue metabolic assays. The lack of cytotoxicity as assayed by the release of lactic acid dehydrogenase (LDH) after a 3-h exposure of the S-G cells to BPA, indicated that the plasma membrane was not a prime target for BPA. Furthermore, the cytotoxicity of BPA was not potentiated in the presence of a P450 metabolic activating system. Subtoxic levels of BPA induced the formation of micronuclei and extensive vacuolization was noted upon exposure to highly toxic levels of BPA. Induction of cell death by apoptosis was evident with BPA exposure in serum-limited medium, with the extent of apoptosis dependent upon the concentration of BPA and the length of exposure.

Original languageEnglish (US)
Pages (from-to)233-244
Number of pages12
JournalIn Vitro and Molecular Toxicology: Journal of Basic and Applied Research
Volume12
Issue number4
StatePublished - Dec 1999

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Gastrin-Secreting Cells
Cytotoxicity
Bisphenol A-Glycidyl Methacrylate
Fibroblasts
Neutral Red
Periodontal Ligament
bisphenol A
In Vitro Techniques
Assays
Sealants
Ligaments
Cell culture
Cell Culture Techniques
Pit and Fissure Sealants
Apoptosis
Cells
Dental Materials
Dental composites
Poisons

All Science Journal Classification (ASJC) codes

  • Health, Toxicology and Mutagenesis
  • Toxicology

Cite this

In vitro cytotoxicity of bisphenol A to human gingival epithelial S-G cells. / Babich, Harvey; Tipton, David.

In: In Vitro and Molecular Toxicology: Journal of Basic and Applied Research, Vol. 12, No. 4, 12.1999, p. 233-244.

Research output: Contribution to journalArticle

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abstract = "In vitro cell culture studies have noted that bisphenol A (BPA), acting as a xenoestrogen, stimulated human breast cancer cell proliferation in vitro. BPA is the precursor of many monomers, including bisphenol A dimethacrylate (Bis-DMA), which is used widely in resin-based dental composites and sealants. The detection of BPA in the saliva of patients in whom sealants had been applied 1 h earlier raised several health safety concerns. Studies on the in vitro response of normal human cells to BPA are lacking. By quantitating the in vitro cytotoxicity of BPA using cell culture assays combined with microscopy, the study presented herein provides a cytotoxicity profile of BPA toward normal human cells. The relative cytotoxicity of BPA, and, for comparative purposes, of other leachates from dental materials, toward human gingival epithelial (S-G) cells, gingival (GN) fibroblasts, and periodontal ligament (PDL) fibroblasts was evaluated with the neutral red (NR) assay. For the S-G and GN cells the sequence of potency was BPA, bisphenol glycidyl methacrylate (Bis-GMA) > Bis-DMA > triethylene glycol dimethacrylate (TEGDMA), but for the PDL fibroblasts the sequence was BPA, Bis-GMA > TEGDMA > Bis-DMA. More extensive studies focused on BPA and S- G cells. The midpoint NR cytotoxicity value of 0.2 mM BPA noted for a 24-h exposure of the S-G cells was similar to that noted with the 3-[4,5- dimethylthiazol-2-yl]-2,5-diphenyl tetrazolium bromide (MTT) and AlamarBlue metabolic assays. The lack of cytotoxicity as assayed by the release of lactic acid dehydrogenase (LDH) after a 3-h exposure of the S-G cells to BPA, indicated that the plasma membrane was not a prime target for BPA. Furthermore, the cytotoxicity of BPA was not potentiated in the presence of a P450 metabolic activating system. Subtoxic levels of BPA induced the formation of micronuclei and extensive vacuolization was noted upon exposure to highly toxic levels of BPA. Induction of cell death by apoptosis was evident with BPA exposure in serum-limited medium, with the extent of apoptosis dependent upon the concentration of BPA and the length of exposure.",
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