Apoptosis Induction of Mouse Splenic Cells by Exposure to High-Level 17.BETA.-Estradiol and Endocrine Disrupting Chemicals

Sakazaki, Humitoshi; Ueno, Hitoshi; Nakamuro, Katsuhiko

doi:10.1248/jhs.50.248

Cited by 1 publication

(1 citation statement)

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“…In some previous papers, induction of apoptosis in vitro or in vivo by di-n-butyl phthalate, 11) di-2-ethylhexyl phthalate, [12][13][14] and 17β-estradiol 26,[31][32][33] were reported. These studies were generally carried out using much higher concentrations of the compounds than those used in our present study.…”

Section: Discussionmentioning

confidence: 99%

Apoptosis Inducing and Enhancing Activities of Environmental Estrogenic Compounds

Beppu

Nakadai

Igarashi

2006

JOURNAL OF HEALTH SCIENCE

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Effects of estrogenic compounds (bisphenolshowed an apoptosis-inducing activity significantly. 4-tert-Octylphenol (10 µ µ µ µ µM) exhibited an apoptosis-enhancing activity. In contrast, phthalate esters including di-n-butyl phthalate and di-2-ethylhexyl phthalate showed neither activity at 10 µ µ µ µ µM. Genistein (10 µ µ µ µ µM) significantly exhibited apoptosis-inducing and enhancing activities. On the other hand, 17β β β β β-estradiol did not show any of these activities at 10 nM, the concentration exerting the estrogenic activity comparable to or much higher than that of 10 µ µ µ µ µM of the test compounds. Effects of these estrogenic compounds on apoptosis were also investigated using mouse primary thymocytes. Mouse thymocytes similarly exposed to the estrogenic compounds in the absence or the presence of dexamethasone for 6 hr were characterized. In agreement with Jurkat cells, apoptosis-inducing or/and -enhancing activities were observed for the cells coincubated with bisphenol A, alkyl phenols, and genistein, but not those with di-2-ethylhexyl phthalate or 17β β β β β-estradiol. The apoptosis-inducing or/and -enhancing effects of the estrogenic compounds observed here appear to be due to their unidentified properties other than estrogenic activity.

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