It is has been demonstrated that
mitochondrial dysfunction, oxidative stress, and chronic inflammatory process are associated with progress of
morbid obesity in human patients. For this reason, the searching for safe and effective
antiobesity drugs has been the subject of intense research. In this context, the organic
selenium compounds have attracted much attention due to their pharmacological properties, such as
antihyperglycemic,
antioxidant, and anti-inflammatory. The aim of this study was to evaluate the hepatoprotective action of
p-chloro-diphenyl diselenide (p-ClPhSe)2 , an organic
selenium compound, in a model of
obesity induced by
monosodium glutamate (
MSG) administration in rats. Wistar rats were treated during the first ten postnatal days with
MSG (4 g/kg by
subcutaneous injections) and received (p-ClPhSe)2 (10 mg/kg, intragastrically) from 90th to 97th postnatal day. Mitochondrial function,
purine content and the levels of
proteins involved in apoptotic (
poly [ADP-ribose] polymerase [PARP]) and inflammatory processes (inducible
nitric oxide synthases [iNOS] and p38) were determined in the liver of rats. The present study, demonstrated that postnatal administration of
MSG to male rats induced a
mitochondrial dysfunction, accompanied by oxidative stress and an increase in the
ADP levels, without altering the efficiency of phosphorylation in the liver of adult rats. Furthermore, the
MSG administration also induces hepatotoxicity, through an increase in PARP, iNOS, and p38 levels. (p-ClPhSe)2 treatment had beneficial effects against
mitochondrial dysfunction, oxidative stress, and modulated
protein markers of apoptosis and
inflammation in the liver of
MSG-treated rats. J. Cell. Biochem. 118: 2877-2886, 2017. © 2017 Wiley Periodicals, Inc.