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      Histochemical Studies of the Effects of Monosodium Glutamate on the Liver of Adult Wistar Rats

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          Abstract

          Background:

          Monosodium glutamate (MSG) is a commonly used food additive and there is growing concern that excitotoxins such as MSG play a critical role in the development of several hepatic disorders.

          Objectives:

          The histochemical effect of monosodium glutamate was investigated on the liver of adult Wistar rats.

          Methods:

          Adult male Wistar rats (n = 24), with an average weight of 230 g were randomly assigned into two treatment groups, (A & B) (n=16) and Control (C) (n=8). The rats in the treatment groups (A & B) received 0.04mg/kg and 0.08mg/kg of monosodium glutamate thoroughly mixed with the grower's mash, respectively on a daily basis for forty-two days. The 0.04mg/kg and 0.08mg/kg monosodium glutamate doses were chosen and extrapolated in this experiment based on the previous work done with the additive. The control group (C) received equal amount of feed (Growers’ mash) without monosodium glutamate added for the same period. The rats were given water ad libitum. Both the treatment and control rats were sacrificed by cervical dislocation on day forty-three of the experiment. The Liver was carefully dissected out and quickly fixed in Bouin's fluid for histochemical studies, while blood was collected for estimation of total protein, albumin, transaminasese (aspartate aminotransferase (AST) and alanine aminotransferase (ALT).

          Results:

          The histological findings showed changes like dilatation of the central vein, which contained lysed red blood cells, cyto-architectural distortions of the hepatocytes, atrophic and degenerative changes on the liver of the animals that received feed incoporated with monosodium glutamate. Furthermore, the biochemical parameters were significantly higher in the test than control groups (P < 0.0001). These changes were more severe in the group that had 0.08 mg/kg of monosodium glutamate mixed in their feed.

          Conclusion:

          These findings showed that monosodium glutamate consumption may have some deleterious effects on the liver of adult Wistar rats at higher doses and by extension may affect the functions of the liver.

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          Most cited references22

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          The toxicity/safety of processed free glutamic acid (MSG): a study in suppression of information.

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            Umami and appetite: effects of monosodium glutamate on hunger and food intake in human subjects.

            Subjects consumed soup (beef consomme) preloads of a fixed size containing different concentrations of monosodium L-glutamate (MSG). Effects on appetite following these preloads, and when no soup was consumed, were assessed in 3 studies. The soups supplemented with MSG were rated as more "pleasant," more "savoury" and more "satisfying" than soup with no added MSG. Compared with the no preload condition, consumption of the soups initially reduced appetitive motivational ratings and increased fullness ratings, but did not alter food intake in a test meal begun either 2 or 30 minutes later. This immediate inhibition of subjective motivation to eat was unaffected by MSG concentration. The failure of the soups to reduce subsequent food intake is presumably due to their low energy content (less than 10 kcal) and indicates that sensory stimulation alone is insufficient to reduce appetite. Indeed, the most important finding concerning MSG showed that motivation to eat recovered more rapidly following a lunchtime meal in which MSG-supplemented soup was served as the first course (compared both with the effect of unsupplemented soup and no preload). It is suggested tentatively that MSG through its stimulation of orosensory receptors and/or by improving the palatability of the soup may have influenced the metabolic disposal of nutrients consumed in the previous meal.
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              Myocardial ischemia: the pathogenesis of irreversible cell injury in ischemia.

              Cells made ischemic rapidly manifest many distinct structural and functional alterations as a consequence of the depletion of their energy stores. In attempting to determine which of these are causally related to the eventual cell death, the authors have emphasized the relationship to the reversibility of the ischemic injury. Two phenomena have consistently characterized irreversibly in contrast to reversibly injured ischemic cells: the inability to restore mitochondrial function and evidence of plasma membrane damage. Studies in the authors' laboratory are reviewed that have focused on the pathogenesis, biochemical nature, and the relationship to irreversible cell injury of both of these alterations. A number of mitochondrial abnormalities are related to changes in long-chain acyl-CoA metabolism with inhibition of adenine nucleotide translocation and potentiation of a Ca2+-dependent increase in the permeability of the inner mitochondrial membrane. These changes are reversible upon reoxygenation only when the large increase in intracellular Ca2+ content that accompanies the phospholipid depletion from other cellular membranes is prevented. This disorder in phospholipid metabolism is felt to be the critical lesion that produces irreversible cell injury in ischemia. It affects the endoplasmic and sarcoplasmic reticular membranes of liver and myocardial cells, respectively, and probably the plasma membranes of both. It is prevented by pretreatment with chlorpromazine. An activation of endogenous phospholipases by an elevated, cytosolic free Ca2+ ion concentration is suggested as the mechanism underlying this phospholipid disturbance. The central role of intracellular Ca2+ in the initiation and functional consequences of ischemic cell injury are emphasized.
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                Author and article information

                Journal
                Ann Med Health Sci Res
                Ann Med Health Sci Res
                AMHSR
                Annals of Medical and Health Sciences Research
                Medknow Publications & Media Pvt Ltd (India )
                2141-9248
                2277-9205
                Jan-Jun 2011
                : 1
                : 1
                : 21-29
                Affiliations
                [* ]Department of Anatomy, School of Basic Medical Sciences, College of Medical Sciences, University of Benin, Benin City, Edo State, Nigeria
                [** ]Department of Anatomy, Faculty of Basic Medical Sciences, College of Health Sciences, Delta State University, Abraka, Delta State, Nigeria
                Author notes
                Correspondence: Dr A. O. Eweka, Department of of Anatomy, School of Basic Medical Sciences, College of Medical Sciences, University of Benin, Benin City, Edo State, Nigeria
                Article
                AMHSR-1-21
                3507088
                23209951
                a4579e74-f64f-4148-a5d8-d169c7fa36e3
                Copyright: © Annals of Medical and Health Sciences Research

                This is an open-access article distributed under the terms of the Creative Commons Attribution-Noncommercial-Share Alike 3.0 Unported, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                : 24 September 2010
                : 14 December 2010
                : 15 December 2010
                Categories
                Original Article

                Medicine
                wistar rats,histochemical effect,monosodium glutamate,atrophic and degenerative changes,hepatocytes,liver enzymes

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