• V Pavlovic, S Cekic, D Sokolovic, and B Djindjic.
• Institute of Physiology, Faculty of Medicine, University of Nis, Nis, Serbia and Montenegro. vojapav@yahoo.com
• Bratisl Med J. 2006 Jan 1; 107 (5): 185-91.

BackgroundMonosodium glutamate (MSG) is the sodium salt of glutamic acid, widely spread in modern nutrition. Numerous recent studies have shown the existence of glutamic receptors on different nonneuronal cells, which among others also include lymphocytes and thymocytes.ObjectivesThe current study was designed to evaluate the prolonged effect of MSG on rat thymocyte proliferation, apoptosis and expression of two apoptosis related proteins, Bel-2 and Bax.Material And MethodsWistar rats (male) were exposed to monosodium glutamate (MSG) (4 mg/g body wt, i.p.) for 6 consecutive days and sacrificed on 30th and 45th day after last MSG dose. Thymocyte proliferation was evaluated by measuring the expression of proliferating cell nuclear antigen by flow cytometry. Apoptosis was detected using the Annexin V-FITC/PI apoptosis detection kit and cells were analyzed using a flow cytometer. Expression of Bcl-2 and Bax proteins were determined with flow cytometry using respective monoclonal antibodies.ResultsThe current study results demonstrate that MSG significantly decreased thymocyte proliferation (p < 0.001) induced by ConA and increased apoptosis rate (p < 0.001) of the cells during examination period. MSG treatment induced down regulation of Bcl-2 protein while Bax protein levels were not significantly changed.ConclusionThese results indicate that MSG significantly modulates thymocyte proliferation by modulating the apoptosis rate of the cells. The temporal profile of Bcl-2 and Bax expression, after MSG treatment, suggest that down regulation of Bcl-2 protein and resulting change of Bcl-2/Bax protein ratio may be an important event in thymocyte apoptosis, triggered by MSG (Tab. 1, Fig. 3, Ref. 36).

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