Effects of Monopotassium Glutamate on Mitochondrial Membrane Permeability Transition and Lipid Peroxidation- an In-vitro Study

• E.O Adewoye

Stimulation of Mitochondrial Membrane Permeability Transition (MMPT) pore opening as well as membrane lipid peroxidation by apoptotic and necrotic stimuli has been identified as the possible effectors of cell death in numerous pathological disorders. Studies have reported that ingestion of monosodium glutamate (MSG) stimulate MMPT pore opening in vivo. Consumption of potassium supplements and salt substitutes may cause a shift in potassium homeostasis resulting in a number of complications like paralysis and cardiac arrhythmia. Monopotassium glutamate (MPG) is used generally as flavor enhancer in food and salt substitute by people who are sodium restricted but there is dearth of information on the effect of MPG on MMPT pore opening. This study was therefore designed to assess the in vitro effect of MPG on MMPT pore opening and lipid peroxidation. Liver mitochondria were prepared from liver excised from male Wistar rats (100-120g) under ether anesthesia. Varying concentration of potassium and sodium glutamate (100, 200, 300 and 400 μg/ml) were tested on MMPT and lipid peroxidation in rat liver. The MMPT pore was estimated by measuring mitochondrial swelling while lipid peroxidation was estimated spectrophotometrically. Data were analyzed by one-way ANOVA and level of significance taken at P<0.05. Monopotassium and monosodium glutamate did not induce MMPT pore opening but induced generation of lipid peroxides. Monopotassium glutamate induced higher percentage of lipid peroxidation (p<0.05) compared to MSG. Monopotassium glutamate significantly induced lipid peroxidation but did not stimulate mitochondrial membrane permeability transition pore opening.

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