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The Korean Journal of Pathology 2004;38(4): 228-237.
The Apoptotic Molecular Changes of Cellular Injury in Mouse Testis Induced by Endocrine Disrupting Chemicals.
Eun Hui Wang, Kweon Heang Lee, Ki Hwa Yang, Jinsuk Lee, Eun Sun Jung, Chang Suk Kang, Yeong Jin Choi
1Department of Clinical Pathology, The Catholic University of Korea, Seoul 150-713, Korea. mdyjchoi@catholic.ac.kr
2Department of Pharmacology, The Catholic University of Korea, Seoul 150-713, Korea.
3Korea Food & Drug Administration, Seoul, Korea.
BACKGROUND: Spermatogenesis is regulated by various cellular reactions, and especially cell proliferation and apoptosis. METHODS: We investigated the morphological changes and the apoptotic molecular changes in mouse testis induced by the endocrine disrupting chemicals. ICR mice were treated with bisphenol A (BPA), 2-bromopropane (2-BP) and diethylstilbesterol (DES). Histological examination and immunohistochemical staining, TUNNEL staining and RNAse protection assay were conducted. RESULTS: Testes treated with BPA showed normal spermatogenesis and the proliferation activity, and the density of the cells was similar with those in the control. 2-BP and DES groups, which showed a decrease of germ cells near the basal layer and degenerative changes. The proliferative activity identified by PCNA staining was significantly decreased in the 2-BP and DES groups (p<0.05). The apoptosis was significantly increased in the 2-BP group however, a significant decrease was noted in the BPA group (p<0.05). Among apoptosis-related molecules, the expression of Fas, Fas ligand, TRAIL, TNFp55 and caspase 1, 3, 6 and 8 were changed according to the change of the degree of apoptosis in all groups. CONCLUSIONS: Endocrine disrupting chemicals induced cellular injury in mouse testis through the changes of proliferative activity and apoptosis which was regulated by a number of apoptosis-related molecules. This probably results in the abnormality of spermatogenesis in mouse testis.
Key Words: Bisphenol A; 2-Bromopropane; Diethylstilbesterol; Spermatogenesis; Testis
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