Journal
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
Volume 477, Issue 4, Pages 575-580Publisher
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.bbrc.2016.06.087
Keywords
Arsenic; Reproduction; Endocrinology; Estrogen; Health; Molecular recognition
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Funding
- IISER Mohali
- Centre for Protein Science, Design and Engineering (CPSDE) [MHRD-14-0064]
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We report that arsenic trioxide (ATO) and 17-beta-estradiol (E2) abolish each other's independent cell signaling effects in respect of cell survival and proliferation/migration of breast cancer (MCF-7) cells. The possibility that this is due to binding of ATO to E2 was confirmed through difference absorption spectroscopy, chromatography-coupled voltammometry and 1-D H-1 and C-13 NMR spectroscopy. Binding leads to attenuation of E2's hydroxyl H-1 peaks at its C17 and C3 carbon positions. The results suggest that ATO and E2 can titrate each other's levels, potentially explaining why sustained arsenic exposure tends to be associated with delays in age of menarche, advanced age of menopause, poorer sperm quality, higher overall morbidity in men, and lower incidences of breast cancer in women in some arsenic-contaminated areas. (C) 2016 Elsevier Inc. All rights reserved.
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