Toxicokinetic of HEMA in guinea pigs

Reichl, Franz‐Xaver; Durner, Jürgen; Kehe, Kai; Manhart, Juergen; Folwaczny, Matthias; Kleinsasser, N.; Hume, W.R.; Hickel, Reinhard

doi:10.1016/s0300-5712(02)00050-7

Cited by 31 publications

(19 citation statements)

References 10 publications

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“…Therefore, enterohepatic recycling of [ 14 C]BisGMA and/or [ 14 C]BisGMA metabolite(s) cannot be excluded. Enterohepatic recycling and similar biological clearances have also been described for HEMA and TEGDMA in guinea pigs (Reichl et al, 2001(Reichl et al, , 2002. Analysis of the present data indicates the existence of similar mechanisms for uptake and biliary excretion for HEMA, TEGDMA, and BisGMA.…”

Section: Discussionsupporting

confidence: 79%

Distribution and Excretion of BisGMA in Guinea Pigs

et al. 2008

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Bisphenol-A-glycidyldimethacrylate (BisGMA) is used in many resin-based dental materials. It was shown in vitro that BisGMA was released into the adjacent biophase from such materials during the first days after placement. In this study, the uptake, distribution, and excretion of [14C]BisGMA applied via gastric and intravenous administration (at dose levels well above those encountered in dental care) were examined in vivo in guinea pigs to test the hypothesis that BisGMA reaches cytotoxic levels in mammalian tissues. [14C]BisGMA was taken up rapidly from the stomach and intestine after gastric administration and was widely distributed in the body following administration by each route. Most [14C] was excreted within one day as 14CO2. The peak equivalent BisGMA levels in guinea pig tissues examined were at least 1000-fold less than known toxic levels. The peak urine level in guinea pigs that received well in excess of the body-weight-adjusted dose expected in humans was also below known toxic levels. The study therefore did not support the hypothesis.

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Section: Discussionsupporting

confidence: 79%

Distribution and Excretion of BisGMA in Guinea Pigs

et al. 2008

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“…Consequently, non-crosslinked resin monomers can be leached out from the fillings by saliva, food or drinks 4,5) and reach the tissues of the oral cavity. These monomers can be inhaled or via the saliva reach the intestinal tract where they are absorbed by the small intestine and further metabolized [6][7][8][9][10] . Two main hypotheses how comonomers induce double strand breaks (DSBs) are currently discussed.…”

Section: Introductionmentioning

confidence: 99%

“…Therefore, the microscopic quantification of colocalizing γ-H2AX and 53BP1 foci has been used for NAC ameliorates dental composite-induced DNA double-strand breaks and chromatin condensation [39][40][41] . The metabolism of these substances was elucidated in animal studies using radioactively (C-14)-labeled (co)monomers [6][7][8][9] . It was noted that dental resin monomers can induce DSBs 29,30) and HEMA exposure can lead to apoptosis through oxidative DNA damage 42) , while Bis-GMA has been observed to induce morphological changes in human pulp cells including cellular contractions 43) .…”

Section: Introductionmentioning

confidence: 99%

NAC ameliorates dental composite-induced DNA double-strand breaks and chromatin condensation

Styllou

Hickel

et al. 2017

Dent. Mater. J.

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Released (co)monomers from dental composite components can induce DNA damage of which DNA double-strand breaks (DSBs) threaten genome integrity. Here, we tested whether the administration of the antioxidant N-acetylcysteine (NAC) is able to reduce the dental composite-induced DSBs in primary human gingiva fibroblasts. The dental composites Bis-GMA (bisphenol-Aglycerolate dimethacrylate), GMA (glycidyl methacrylate), HEMA (2-hydroxyethyl methacrylate) and TEGDMA (triethyleneglycol dimethacrylate) were found to induce co-localizing microscopic nuclear foci numbers of the DSB markers γ-H2AX and 53BP1 per cell in the order: GMA>Bis-GMA>TEGDMA>HEMA. Supplementation of (co)monomer-containing culture medium with NAC led to a significant reduction of resin-induced DSBs as well as to an amelioration of dental monomer-induced nuclear chromatin condensation in gingival fibroblasts. Thus, antioxidant treatment can reduce radical-induced chromatin and DNA damage and open avenues to mitigate genotoxic effects of dental composite compounds.

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“…In the GI, these compounds may interact with biological structures and metabolic pathways of cells and tissues. A systemic uptake of released resinous substances through the GI was shown in guinea pigs and mice [3,45]. Since there is no data available to date, it was of great importance to investigate the potential genotoxic effect of CQ and DMT in human intestinal cells.…”

Section: Caco-2 Cellsmentioning

confidence: 99%