title: An in vitro examination of selenium-cadmium antagonism using primary cultures of rainbow trout (Oncorhynchus mykiss) hepatocytes.
abstract: The present study evaluated the ameliorative properties of selenium (Se) against cadmium (Cd)-induced oxidative stress, using isolated rainbow trout (Oncorhynchus mykiss) hepatocytes in primary culture as the model experimental system. Cadmium (Cd) is known to induce cytotoxic effects by disrupting cellular oxidative homeostasis. On the other hand, selenium (Se) is an essential component of biological antioxidative machinery, and thus may provide protection against the toxic insults of Cd by augmenting the cellular antioxidant response. However, Se, when present above the threshold concentration, can also induce reactive oxygen species (ROS) generation and cause oxidative damage. In this experiment, trout hepatocytes in primary culture were exposed to 100 µM Cd, alone or in combination with different concentrations (25-500 µM) of selenite (SeO3(2-)) or selenomethionine (SeMet) for 48 h. Our findings indicated that both chemical forms of Se, at the lowest concentration used (25 µM), significantly reduced Cd-induced cytotoxicity (measured as cell viability). In contrast, Se at higher concentrations (≥ 50 µM) did not offer any protection against a Cd induced decrease in cell viability. The reduced cytotoxicity of Cd in the presence of 25 µM selenite or SeMet was associated with reduced intracellular ROS production, recovery of the cellular thiol status (ratio of reduced and oxidized glutathione), and amelioration in the activities of major enzymatic antioxidants (superoxide dismutase, catalase, and glutathione peroxidase). Co-treatment of hepatocytes with Cd and pharmacological antioxidants (TEMPO and NAC) also reduced Cd-induced oxidative stress in trout hepatocytes. This provided further evidence that Se likely ameliorates Cd toxicity via different antioxidative mechanisms.
authors.affiliation: Department of Biology, University of Saskatchewan, 112 Science Place, Saskatoon, SK, Canada. Ankur.jamwal@usask.ca.
authors.forename: Ankur
authors.initials: A
authors.lastname: Jamwal
authors.affiliation: Department of Biology, University of Saskatchewan, 112 Science Place, Saskatoon, SK, Canada. Ankur.jamwal@usask.ca.
authors.forename: Mohammad
authors.initials: M
authors.lastname: Naderi
authors.affiliation: Department of Biology, University of Saskatchewan, 112 Science Place, Saskatoon, SK, Canada. Ankur.jamwal@usask.ca and Toxicology Centre, University of Saskatchewan, 44 Campus Drive, Saskatoon, SK, Canada.
authors.forename: Som
authors.initials: S
authors.lastname: Niyogi
mesh_terms: D000818:Animals; D002104:Cadmium / Q000633:toxicity*; D002470:Cell Survival / Q000187:drug effects; D002478:Cells, Cultured; D022781:Hepatocytes / Q000166:cytology*; D017686:Oncorhynchus mykiss / Q000378:metabolism*; D018384:Oxidative Stress / Q000187:drug effects*; D012643:Selenium / Q000378:metabolism* / Q000494:pharmacology*; D012645:Selenomethionine / Q000494:pharmacology; D018038:Sodium Selenite / Q000494:pharmacology
chemical_list: D002104:Cadmium; D012645:Selenomethionine; D012643:Selenium; D018038:Sodium Selenite