The 8‐epimer of prostaglandin F2α, a marker of lipid peroxidation and oxidative stress, is decreased in the nipple aspirate fluid of women with breast cancer
Breast cancer (BC), a worldwide disease with increasing incidence, develops from ductal/lobular epithelium. Nipple aspirate fluid (NAF), secreted from the breast ducts and lobules, can be analyzed to assess breast metabolic activity. Whether lipid peroxidation in the mammary gland promotes or preven...
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Veröffentlicht in: | International journal of cancer 2007-05, Vol.120 (9), p.1971-1976 |
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Sprache: | eng |
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Zusammenfassung: | Breast cancer (BC), a worldwide disease with increasing incidence, develops from ductal/lobular epithelium. Nipple aspirate fluid (NAF), secreted from the breast ducts and lobules, can be analyzed to assess breast metabolic activity. Whether lipid peroxidation in the mammary gland promotes or prevents tumorigenesis is unclear. Malondialdehyde (MDA) and the 8‐epimer of Prostaglandin F2α (8‐iso‐PGF2α), two lipid peroxidation markers, were studied in milk (n = 10), NAF (n = 140) and plasma (n = 35) samples. MDA was detected in all plasma, in 80% of milk samples and in 95% of NAF samples. MDA levels in NAF and plasma were significantly higher than in milk (p = 0.016 and p = 0.029, respectively). We found no significant difference between levels of MDA in NAF samples from BC patients compared to healthy controls. 8‐iso‐PGF2α was detectable in all samples. 8‐iso‐PGF2α median levels in NAF were significantly higher than in both milk and plasma (p < 0.0001). The highest 8‐iso‐PGF2α levels were found in NAF from healthy women, significantly higher than in women with BC (p < 0.0001). No significant differences were found in both markers after the age‐adjustment. High levels of lipid peroxidation products in NAF suggest their in situ production in the nonlactating breast. Active lipid peroxidation may have a physiologic role in the normal mammary gland. Lower levels of 8‐iso‐PGF2α in NAF from BC patients suggest altered production of arachidonic acid metabolites during breast carcinogenesis. © 2006 Wiley‐Liss, Inc. |
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ISSN: | 0020-7136 1097-0215 |
DOI: | 10.1002/ijc.22522 |