Effects of acute and subchronic exposures to waterborne selenite on the physiological stress response and oxidative stress indicators in juvenile rainbow trout

Selenium (Se) is an essential element that may bioaccumulate to toxic levels. In fish, the major toxicity symptom is larval teratogenic deformities, but little is known about the effect of Se on other systems such as the physiological stress response and oxidative stress. To test the hypothesis that Se is a chemical stressor that causes toxicity through oxidative stress, juvenile rainbow trout were exposed to waterborne sodium selenite, and physiological stress response and stress-related parameters (plasma cortisol, glucose, T3 and T4, gill Na+/K+-ATPase, the ability of the head kidney to secrete cortisol, and condition factor) and hepatic oxidative stress indicators (reduced glutathione, glutathione peroxidase, and lipid peroxidation) were measured after 96 h (acute exposure to 0–2.67 mg/L Se) and 30 days (sub-chronic exposure to 0–0.16 mg/L).Acute exposure to waterborne sodium selenite significantly increased plasma cortisol levels (control = 0.01 ± 0.0 ng/mL, and 2.52 mg/L Se = 73.5 ± 22 ng/mL) and plasma glucose levels (control = 0.75 ± 0.1 mg/mL, and 3.60 mg/L Se = 1.64 ± 0.2 mg/mL), but gill Na+/K+-ATPase activities, plasma T3 and T4 levels, and condition factor were unchanged. The 96 h acute selenite exposure decreased hepatic reduced glutathione levels (control = 18.4 ± 1.5 μmol/mg protein, and 3.60 mg/L Se = 12.4 ± 1.1 μmol/mg protein). Lipid peroxidation levels (0.03–0.08 U/mg protein) and glutathione peroxidase (3.7–6.0 mU/mg protein) activities significantly varied with treatment. The 30 days sub-chronic exposure increased plasma cortisol, T3, and T4, but there was no effect on plasma glucose levels, gill Na+/K+-ATPase activity, the ability to secrete cortisol, and condition factor. The 30 days sub-chronic exposure to selenite did not alter antioxidant activities or lipid peroxidation levels.These experiments show, for the first time, that exposure to waterborne selenite up to 0.1 mg/L, activates the physiological stress response in fish but does not impair cortisol secretion after 30 days. The decrease in reduced glutathione in juvenile rainbow trout subjected to the acute sodium selenite exposure suggests that oxidative stress may play an important role in the effects of Se in fish.