Estrogenic Alkylphenols Induce Cell Death by Inhibiting Testis Endoplasmic Reticulum Ca2+ Pumps
| Autor: | Rita E. Godfrey, S Z Kahn, P. J. Hughes, Robert H. Michell, Jonathan G. Bilmen, Damon A. Lowes, Stephen C. Tovey, Christopher J. Kirk, H. McLELLAN, Francesco Michelangeli |
|---|---|
| Rok vydání: | 2000 |
| Předmět: |
Male
endocrine system Programmed cell death medicine.medical_specialty SERCA Biophysics Apoptosis Calcium-Transporting ATPases In Vitro Techniques Biology Endoplasmic Reticulum Biochemistry Sarcoplasmic Reticulum Calcium-Transporting ATPases chemistry.chemical_compound Estradiol Congeners Phenols BAPTA Internal medicine Testis medicine Animals Molecular Biology Sertoli Cells urogenital system Endoplasmic reticulum Cell Biology Sertoli cell Rats Nonylphenol medicine.anatomical_structure Endocrinology chemistry Microsome |
| Zdroj: | Biochemical and Biophysical Research Communications. 277:568-574 |
| ISSN: | 0006-291X |
| DOI: | 10.1006/bbrc.2000.3710 |
| Popis: | Industrial alkylphenols in the environment may act as "xenoestrogens" to disrupt testicular development and decrease male fertility. Amongst possible targets for these compounds are testicular Sertoli cells, which nurture the developing sperm cells. We demonstrate that SERCA 2 and 3 Ca(2+) pumps are relatively abundant in rat testis microsomal membranes, and also in Sertoli, myoid, and TM4 cells (a Sertoli cell line). A number of estrogenic alkylphenols such as nonylphenol, octylphenol, bisphenol A, and butylated hydroxytoluene all inhibit testicular Ca(2+) ATPase in the low micromolar concentration range. These agents also mobilize intracellular Ca(2+) in intact TM4 cells in a manner consistent with the inhibition of ER Ca(2+) pumps. Alkylphenols dramatically decrease the viability of TM4 cells, an effect that is reversed by either a caspase inhibitor or by BAPTA, and is therefore consistent with Ca(2+)-dependent cell death via apoptosis. We postulate that alkylphenols disrupt testicular development by inhibiting ER Ca(2+) pumps, thus disturbing testicular Ca(2+) homeostasis. |
| Databáze: | OpenAIRE |
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