Sodium dithionate (Na2S2O4) induces oxidative damage in mice mitochondria heart tissue

Abstract

Sodium dithionite (Na2S2O4) is an inorganic sodium salt, a bleaching agent that has a reducing agent role and is generally used as food additive or preservative in the production of diverse foods and beverages. The aim of this study is to determine the effects of Na2S2O4 on cardiac mitochondria damage and biochemical parameters in male mice. Na2S2O4 were administered orally at doses of 10, 20, 50 and 100 mg/kg to male mice for 45 days. Heart mitochondria were isolated for the evaluation of oxidative stress biomarkers such as mitochondrial function, reactive oxygen species (ROS), lipid peroxidation (LPO), protein carbonyl (PC) content, catalase activity (CAT) and glutathione content (GSH). Blood samples were collected and Creatine phosphokinase (CPK), Creatine kinase-MB (CK-MB) and Troponin I were quantified in the serum. Mitochondrial function was significantly (P < 0.001) decreased and oxidative stress biomarkers including, ROS, LPO and PC were significantly enhanced. Also, CAT activity and GSH content were significantly decreased by Na2S2O4-treated groups in heart mitochondria when compared to the control group. Na2S2O4 administration elevated the serum levels of CPK, CK-MB, and troponin I (especially, at high doses) compared with the control group. These findings suggest that Na2S2O4 induces mitochondria toxicity and cardiac damage especially at high doses with a dose-dependent manner.

Keywords

• Sodium dithionite
• Na2S2O4
• Cardiotoxicity
• Heart enzymes
• Oxidative stress
• Mitochondria toxicity