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.

Chronic Dietary Selenomethionine Exposure Induces Oxidative Stress, Dopaminergic Dysfunction, and Cognitive Impairment in Adult Zebrafish (Danio rerio)

“…For example, imbalance in Se concentrations in the brain has been implicated in the pathophysiology of several neurological diseases , and cognitive decline . There is now a general consensus that the primary mechanism underlying Se toxicity is oxidative stress, , which in turn is a major contributor to the neurodegeneration of the brain leading to cognitive decline …”

Antagonistic Interaction of Selenium and Cadmium in Human Hepatic Cells Through Selenoproteins

“…An increase in the expression of other selenoproteins such as GPx1 and SELENOK has also been correlated with a higher concentration of sodium selenite ( Rusolo et al, 2013 ). In the study by Jamwal et al (2016) , the GPx activity was significantly (∼35%) decreased in trout hepatocytes treated with Cd alone or in combination with a high concentration of selenite or SeMet (250 µM) relative to control cells. However, a partial recovery of the GPx activity was recorded in hepatocytes exposed to 100 µM Cd in combination with 25 µM selenite or SeMet.…”

Marine Fish Primary Hepatocyte Isolation and Culture: New Insights to Enzymatic Dissociation Pancreatin Digestion

“…Freshwater species (such as Oncorhynchus mykiss, Cyprinus carpio, Oreochromis niloticus Pelteobagrus fulvidraco, and Ctenopharyngodon idellus) are the most used fish models to assess the mode of action of environmental pollutants [14,45,46,48,51,[55][56][57][58][59]. However, in the context of marine environmental toxicology, marine fish primary hepatocytes are an interesting approach when assessing the effects of xenobiotics, such as polycyclic aromatic hydrocarbons (PAHs), since it increases the ecological and economic relevance to the studies.…”