Monosodium Glutamate Induces Cytotoxicity in Rat Liver via Mitochondrial Permeability Transition Pore Opening

The study investigated the effect of sodium glutamate on the production of reactive oxygen and nitrogen species (ROS/RNS) in kidney tissues of rats under conditions of acute desynchronization (AD) and lipopolysaccharide (LPS)-induced systemic inflammatory response (SIR) and, thus, contributed to a deeper understanding of the mechanisms involved in the development of renal dysfunction under these conditions. The experiment was conducted on 21 male Wistar rats (210-230 g), randomly divided into three groups: intact animals, a group exposed to AD modeling under LPS-induced systemic inflammatory response (Group II), and a group (Group 3) exposed to AD modeling under LPS-induced systemic inflammatory response, who received sodium glutamate in a dose of 20 mg/kg. The administration of sodium glutamate significantly increased the generation rate of the superoxide anion radical by 13.8% through microsomal monooxygenases, by 8.7% through the mitochondrial respiratory chain, and by 7.7% through leukocyte NADPH oxidase compared to Group 2. However, sodium glutamate did not affect the total NO synthase activity or the activity of its constitutive and inducible isozymes in the kidney homogenate compared to Group 2. The uncoupling index of constitutive NO synthases in kidney tissues also remained unchanged under the administration of sodium glutamate, but the peroxynitrites were 20.5% higher, and S-nitrosothiols were 11.6% higher, than in group 2. The findings indicate that sodium glutamate significantly increases oxidative-nitrosative stress in rat kidney tissues under AD and LPS-induced SIR, resulting in excessive ROS/RNS formation.

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Monosodium Glutamate Induces Cytotoxicity in Rat Liver via Mitochondrial Permeability Transition Pore Opening

Cited by 4 publications

References 27 publications

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Influence of Sodium Glutamate on Reactive Oxygen and Nitrogen Species Production in Kidney Tissues of Rats Under Acute Desynchronization and Lipopolysaccharide-Induced Systemic Inflammatory Response

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