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Variability of glutathione during the menstrual cycle - Due to estrogen effects on hepatocytes?
Linköping University, Faculty of Health Sciences. Linköping University, Department of Biomedicine and Surgery, Oncology. Östergötlands Läns Landsting, Centre of Surgery and Oncology, Department of Oncology UHL.
Linköping University, Faculty of Health Sciences. Linköping University, Department of Neuroscience and Locomotion, Pathology. Östergötlands Läns Landsting, Centre for Laboratory Medicine, Department of Clinical Pathology and Clinical Genetics.ORCID iD: 0000-0003-4075-159X
2004 (English)In: Free Radical Biology & Medicine, ISSN 0891-5849, Vol. 36, no 2, 145-151 p.Article in journal (Refereed) Published
Abstract [en]

Oxidative stress and alterations in the antioxidative defense system may be involved in carcinogenesis. We have previously shown that the levels of glutathione (GSH) in vivo in both breast tissue and subcutaneous fat were higher in the luteal phase compared with the follicular phase, suggesting an overall increase in GSH. This result was confirmed in the present study. Moreover, we exposed normal breast tissue in vivo, breast epithelial cells in vitro, and hepatocytes in culture to ovarian hormones. We found that local perfusion with estradiol, using microdialysis, in normal human breast tissue did not alter the local GSH levels in vivo. In vitro, treatment with estradiol and progesterone of normal human breast epithelial cells did not alter GSH levels. However, levels of GSH in hepatocytes were after 8 h estradiol exposure initially decreased, 76.6 ± 5% of control cells, p < .05, whereas 20 h exposure more than doubled GSH, 209 ± 26% compared with control cells, p < .01. Progesterone had no additional effect. Exposure of hepatocytes to estradiol increased the cellular content of γ-glutamylcysteine synthetase, the rate-limiting enzyme in GSH synthesis. In conclusion we suggest that estradiol affects the GSH homeostasis mainly by effects on hepatocytes, whereas local production in the breast is unaffected by estradiol.

Place, publisher, year, edition, pages
2004. Vol. 36, no 2, 145-151 p.
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Medical and Health Sciences
Identifiers
URN: urn:nbn:se:liu:diva-22675DOI: 10.1016/j.freeradbiomed.2003.10.028Local ID: 1965OAI: oai:DiVA.org:liu-22675DiVA: diva2:242988
Available from: 2009-10-07 Created: 2009-10-07 Last updated: 2017-08-30

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Dabrosin, CharlottaÖllinger, Karin

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Faculty of Health SciencesOncologyDepartment of Oncology UHLPathologyDepartment of Clinical Pathology and Clinical Genetics
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