Dithiothreitol (DTT) rescues mitochondria from nitrofurantoin‐induced mitotoxicity in rat. Issue 12 (4th July 2016)

• Record Type: Journal Article
• Authors: Omidi, Mahmoud; Niknahad, Hossein; Mohammadi‐Bardbori, Afshin
• Is Part Of: Journal of biochemical and molecular toxicology. Volume 30:Issue 12(2016:Dec.)
• Page Start: 588
• Page End: 592
• Publication Date: 2016-07-04
• Subjects: dithiothreitol -- mitochondrial dysfunction -- nitrofurantoin -- oxidative stress; Biochemistry -- Periodicals; Molecular biology -- Periodicals; Toxicology -- Periodicals; 574
• DOI: 10.1002/jbt.21825
• Languages: English
• ISSNs: 1095-6670

Abstract

Abstract: Nitrofurantoin ( N ‐(5‐nitro‐2‐furfurylidine) 1‐amino‐hydantoine; NIT) is mainly used for the treatment of acute urinary tract infections. However, its administration can be associated with liver failure or cirrhosis. The aim of this study was to determine whether NIT is a mitochondrial toxicant, if so, what mechanism(s) is involved. The rat liver mitochondria were isolated and treated with different doses of NIT alone or in combination with a reagent of choice for protecting thiol groups, dithiothreitol (DTT). Several mitochondrial parameters, including succinate dehydrogenase activity (also called 3‐(4, 5‐dimethylthiazol‐2‐yl) 2, 5‐diphenyl tetrazolium bromide assay), lipid peroxidation, superoxide dismutase activity, Reduced glutathione (GSH), and oxidized glutathione (GSSG), and GSSG (oxidized glutathione) levels were determined. The results from this study showed that simultaneous treatment of mitochondria with NIT and DTT significantly reduces the toxicity. Here, we provide evidence that mitochondrial dysfunction followed by depletion of reduced glutathione can be reversed by DTT administration.