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(p-ClPhSe)2 Reduces Hepatotoxicity Induced by Monosodium Glutamate by Improving Mitochondrial Function in Rats
Caroline B Quines1, Pietro M Chagas1, Diane Hartmann2
1Laboratório de Síntese, Reatividade e Avaliação Farmacológica e Toxicológica de Organocalcogênios, Centro de Ciências Naturais e Exatas, Departamento de Bioquímica e Biologia Molecular, Universidade Federal de Santa Maria, Santa Maria, CEP 97105-900, RS, Brazil.
Abstract:
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.
Insights
Organic selenium compounds, like p-chloro-diphenyl diselenide, show promise in combating obesity-related liver damage. This study found it protected rats from liver injury caused by monosodium glutamate, reducing oxidative stress and inflammation.
Area of Science:
- Biochemistry
- Toxicology
- Pharmacology
Background:
- Morbid obesity is linked to mitochondrial dysfunction, oxidative stress, and chronic inflammation.
- Organic selenium compounds possess antioxidant, anti-inflammatory, and antihyperglycemic properties.
- Developing safe and effective anti-obesity drugs is a significant research focus.
Purpose of the Study:
- To investigate the hepatoprotective effects of p-chloro-diphenyl diselenide ((p-ClPhSe)2) in a rat model of monosodium glutamate (MSG)-induced obesity.
- To assess the impact of (p-ClPhSe)2 on mitochondrial function, oxidative stress, and inflammatory markers in the liver.
Main Methods:
- Wistar rats were administered MSG during the early postnatal period to induce obesity.
- (p-ClPhSe)2 was administered intragastrically to rats from day 90 to 97 post-birth.
- Liver tissues were analyzed for mitochondrial function, purine content, and levels of apoptosis (PARP) and inflammation (iNOS, p38) related proteins.
Main Results:
- MSG administration induced mitochondrial dysfunction, oxidative stress, and increased ADP levels in rat livers.
- MSG treatment led to hepatotoxicity, evidenced by elevated levels of PARP, iNOS, and p38.
- (p-ClPhSe)2 treatment mitigated mitochondrial dysfunction, reduced oxidative stress, and modulated apoptosis and inflammation markers in MSG-treated rats.
Conclusions:
- Postnatal MSG administration causes significant liver damage, including mitochondrial dysfunction and inflammation, in adult rats.
- (p-ClPhSe)2 demonstrates notable hepatoprotective effects against MSG-induced liver injury.
- Organic selenium compounds like (p-ClPhSe)2 represent a potential therapeutic strategy for managing obesity-related liver complications.
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