Dithiothreitol (DTT) rescues mitochondria from nitrofurantoin-induced mitotoxicity in rat.

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.

journal_name

J Biochem Mol Toxicol

authors

Omidi M,Niknahad H,Mohammadi-Bardbori A

doi

10.1002/jbt.21825

subject

Has Abstract

pub_date

2016-12-01 00:00:00

pages

588-592

issue

12

eissn

1095-6670

issn

1099-0461

journal_volume

30

pub_type

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