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Effects of altered zinc availability on proliferation and oxidative stress in cultured cells
Author(s) -
Sankavaram Kavitha,
Grattan Bruce J,
Walker Robin,
Park Hea Jin,
Freake Hedley C
Publication year - 2009
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.23.1_supplement.216.2
Subject(s) - cell growth , oxidative stress , reactive oxygen species , zinc , cell culture , microbiology and biotechnology , cell , chemistry , biology , biochemistry , genetics , organic chemistry
Previous studies from our laboratory have demonstrated that primary and transformed cells differ in their homeostatic response to zinc deprivation. Altered zinc availability might also influence cellular proliferation and antioxidant defenses. In the present study, we examined the effects of zinc supplementation (15‐100 µM) and zinc deficiency induced by diethylenetriaminepentaacetic acid (DTPA, 25‐200 µM) on cell proliferation and reactive oxygen species (ROS). DTPA (50 µM) reduced cell proliferation in both MCF‐7 and MDA‐MB‐231 human breast cancer cells, but effects were greater and seen more quickly in MCF7 cells. 50 µM DTPA also reduced proliferation of H4IIE rat hepatoma cells, but did not affect cell number in primary hepatocytes. Zinc treatment (up to 50 µM) enhanced cell proliferation in MCF‐7 but not in MDA‐MB‐231 cells. It also increased proliferation of H4IIE cells, whereas a decline in cell number was found with primary hepatocytes. Cells were also observed for the generation of ROS. 48 hr incubation with DTPA significantly increased ROS in primary hepatocytes and MCF‐7 cells but not in H4IIE or MDA‐MB‐231 cells. Zinc induced ROS in both MCF‐7 and MDA cell lines but not in primary hepatocytes. Overall, while cellular responses differed, reduction of available zinc limited proliferation and addition stimulated growth. In some cells ROS were enhanced under both circumstances.