Effect of 5-(p-hydroxyphenyl)-5-phenylhydantoin (p-HPPH) enantiomers, major metabolites of phenytoin, on the occurrence of chronic-gingival hyperplasia

in vivo and in vitro study

Ichiro Ieiri, W. Goto, S. Higuchi, K. Hirata, A. Toshitani, S. Imayama, Yukiko Ohyama, H. Yamada, K. Ohtsubo

研究成果: ジャーナルへの寄稿記事

17 引用 (Scopus)

抄録

The purpose of this study was to assess the possible role of the (R)- and (S)- enantiomers of the phenytoin metabolite p-HPPH in the pathogenesis of gingival hyperplasia (GH). About 98% of circulating p-HPPH is in the (S)-form. There were significant differences between patients with and without GH in (R)-p-HPPH level (0.055 vs 0.042 μg·ml-1), both enantiomer/racemate level ratios, and R/S enantiomeric ratio (0.0313 vs 0.0232); an increase in serum (R)-p-HPPH level was observed in patients with GH. In separate experiments, the effect of p-HPPH enantiomers on the proliferation of the normal human dermal fibroblast was studied. The in vitro study showed that (R)-p-HPPH selectively stimulated fibroblast growth. The results suggest that the least abundant metabolite, (R)-p-HPPH, is the most toxic with respect to gingival hyperplasia.

元の言語英語
ページ(範囲)51-56
ページ数6
ジャーナルEuropean Journal of Clinical Pharmacology
49
発行部数1-2
DOI
出版物ステータス出版済み - 11 1 1995

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Gingival Hyperplasia
Phenytoin
Fibroblasts
Poisons
In Vitro Techniques
5-phenylhydantoin
Skin
Growth

All Science Journal Classification (ASJC) codes

  • Pharmacology
  • Pharmacology (medical)

これを引用

Effect of 5-(p-hydroxyphenyl)-5-phenylhydantoin (p-HPPH) enantiomers, major metabolites of phenytoin, on the occurrence of chronic-gingival hyperplasia : in vivo and in vitro study. / Ieiri, Ichiro; Goto, W.; Higuchi, S.; Hirata, K.; Toshitani, A.; Imayama, S.; Ohyama, Yukiko; Yamada, H.; Ohtsubo, K.

:: European Journal of Clinical Pharmacology, 巻 49, 番号 1-2, 01.11.1995, p. 51-56.

研究成果: ジャーナルへの寄稿記事

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abstract = "The purpose of this study was to assess the possible role of the (R)- and (S)- enantiomers of the phenytoin metabolite p-HPPH in the pathogenesis of gingival hyperplasia (GH). About 98{\%} of circulating p-HPPH is in the (S)-form. There were significant differences between patients with and without GH in (R)-p-HPPH level (0.055 vs 0.042 μg·ml-1), both enantiomer/racemate level ratios, and R/S enantiomeric ratio (0.0313 vs 0.0232); an increase in serum (R)-p-HPPH level was observed in patients with GH. In separate experiments, the effect of p-HPPH enantiomers on the proliferation of the normal human dermal fibroblast was studied. The in vitro study showed that (R)-p-HPPH selectively stimulated fibroblast growth. The results suggest that the least abundant metabolite, (R)-p-HPPH, is the most toxic with respect to gingival hyperplasia.",
author = "Ichiro Ieiri and W. Goto and S. Higuchi and K. Hirata and A. Toshitani and S. Imayama and Yukiko Ohyama and H. Yamada and K. Ohtsubo",
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T2 - in vivo and in vitro study

AU - Ieiri, Ichiro

AU - Goto, W.

AU - Higuchi, S.

AU - Hirata, K.

AU - Toshitani, A.

AU - Imayama, S.

AU - Ohyama, Yukiko

AU - Yamada, H.

AU - Ohtsubo, K.

PY - 1995/11/1

Y1 - 1995/11/1

N2 - The purpose of this study was to assess the possible role of the (R)- and (S)- enantiomers of the phenytoin metabolite p-HPPH in the pathogenesis of gingival hyperplasia (GH). About 98% of circulating p-HPPH is in the (S)-form. There were significant differences between patients with and without GH in (R)-p-HPPH level (0.055 vs 0.042 μg·ml-1), both enantiomer/racemate level ratios, and R/S enantiomeric ratio (0.0313 vs 0.0232); an increase in serum (R)-p-HPPH level was observed in patients with GH. In separate experiments, the effect of p-HPPH enantiomers on the proliferation of the normal human dermal fibroblast was studied. The in vitro study showed that (R)-p-HPPH selectively stimulated fibroblast growth. The results suggest that the least abundant metabolite, (R)-p-HPPH, is the most toxic with respect to gingival hyperplasia.

AB - The purpose of this study was to assess the possible role of the (R)- and (S)- enantiomers of the phenytoin metabolite p-HPPH in the pathogenesis of gingival hyperplasia (GH). About 98% of circulating p-HPPH is in the (S)-form. There were significant differences between patients with and without GH in (R)-p-HPPH level (0.055 vs 0.042 μg·ml-1), both enantiomer/racemate level ratios, and R/S enantiomeric ratio (0.0313 vs 0.0232); an increase in serum (R)-p-HPPH level was observed in patients with GH. In separate experiments, the effect of p-HPPH enantiomers on the proliferation of the normal human dermal fibroblast was studied. The in vitro study showed that (R)-p-HPPH selectively stimulated fibroblast growth. The results suggest that the least abundant metabolite, (R)-p-HPPH, is the most toxic with respect to gingival hyperplasia.

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