Investigation of oxidative stress status and apoptotic markers of juvenile trout exposed to arsenic toxicity.

Abstract

Arsenic is one of the most abundant elements on earth. Arsenic, also called metalloid, is used as a raw material in many industries. Arsenic causes the acceleration of free radical production in the body and the resulting oxidative stress. In juvenile trout, the interactions of arsenic with metacomposition, biochemical analysis, and apoptosis stimuli were investigated. Results were demonstrated by several marker applications, including oxidative stress parameters, proinflammatory cytokine expressions, DNA damage, and apoptosis markers. In our study, arsenic was applied to juvenile trout (Oncorhynchus mykiss) at concentrations of 25, 50, and 75 mg/L for 96 h. After exposure, the brain tissues of the fish were collected and homogenized. SOD the GSH-Px, CAT, and MDA levels were determined by spectrophotometric methods in the supernatants from the brain tissues of the juvenile trout. Levels of NF-kB, TNF-α, IL-6, Nrf-2, GSH, caspase-3, AChE, and 8-OHdG were determined with an ELISA kit. When the brain tissues of the fish were examined after the study, it was found that the levels of NF-kB, TNF-α, IL-6, Nrf-2, Caspza-3, MDA, and 8-OHdG increased, and the levels of GSH, CAT, SOD, AChE, and GSH-Px decreased. It was found that oxidative stress occurred as a result of the effect of the heavy metal arsenic in the brain tissues of the fish after application.