The Apoptotic Molecular Changes of Cellular Injury in Mouse Testis Induced by Endocrine Disrupting Chemicals
Korean Journal of Pathology
;
: 228-237, 2004.
Article
in Korean
| WPRIM
| ID: wpr-148782
ABSTRACT
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.
Full text:
Available
Index:
WPRIM (Western Pacific)
Main subject:
Ribonucleases
/
Spermatogenesis
/
Testis
/
Apoptosis
/
Proliferating Cell Nuclear Antigen
/
Caspase 1
/
Cell Proliferation
/
Endocrine Disruptors
/
Fas Ligand Protein
/
Germ Cells
Type of study:
Prognostic study
Limits:
Animals
Language:
Korean
Journal:
Korean Journal of Pathology
Year:
2004
Type:
Article
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