“…A similar degree of serum creatinine level increase had been previously reported following the oral exposure to a significantly higher amount of MSG [10]. …”
Section: Discussionsupporting
confidence: 81%
“…No data are available on the effects of MSG on the urinary apparatus and kidney function in humans. Of note, chronic oral MSG intake in rats leads to changes in antioxidant systems and renal markers including lipid peroxidation byproducts [10], in agreement with what observed in rats injected with MSG [11]. Moreover, dietary MSG increases the urinary pH in rats [12] and alkaline urine may influence the kidney capacity to secrete or reabsorb metabolites that contribute to stone formation, as in the case of calcium phosphate products [13].…”
Section: Introductionsupporting
confidence: 55%
“…In previous experiments, MSG supplementation either by injection [11] or oral intake [10,24] induced kidney damage but we report herein for the first time that the chronic consumption of dietary MSG causes obstructive nephropathy from urolithiasis in adult rats possibly via urine alkalinization which predispose to CaP precipitation.…”
Section: Discussionmentioning
confidence: 75%
“…Such moderate hydronephrosis resembles the effects of partial ureteral obstruction in rats [35] and obstructive nephropathy causes major changes in the tubulo-interstitial compartment of the kidney and renal interstitial fibrosis is a common long-term consequence [36]. We are convinced that this phenomenon may cause the kidney interstitial fibrosis observed in MSG-treated rats while oxidative stress secondary to MSG may also contribute [10] as reactive oxygen species induce the transmodulation of fibroblasts to myofibroblasts [37]. Tubular interstitial fibrosis is the strongest morphological predictor of clinical outcome in kidney disease, and is tightly associated to the progression of renal diseases [38].…”
BackgroundThe peritoneal injection of monosodium glutamate (MSG) can induce kidney injury in adult rats but the effects of long-term oral intake have not been determined.MethodsWe investigated the kidney histology and function in adult male Wistar rats that were fed ad
libitum with a standard rat chow pellet and water with or without the addition of 2 mg/g body weight MSG/day in drinking water (n=10 per group). Both MSG-treated and control animals were sacrificed after 9 months when renal function parameters, blood and urine electrolytes, and tissue histopathology were determined.ResultsMSG-treated rats were more prone to kidney stone formation, as represented by the alkaline urine and significantly higher activity product of calcium phosphate. Accordingly, 3/10 MSG-treated rats developed kidney stones over 9 months versus none of the control animals. Further, 2/10 MSG-treated rats but none (0/10) of the controls manifested hydronephrosis. MSG-treated rats had significantly higher levels of serum creatinine and potassium including urine output volume, urinary excretion sodium and citrate compared to controls. In contrast, MSG-treated rats had significantly lower ammonium and magnesium urinary excretion.ConclusionOral MSG consumption appears to cause alkaline urine and may increase the risks of kidney stones with hydronephrosis in rats. Similar effects in humans must be verified by dedicated studies.
“…A similar degree of serum creatinine level increase had been previously reported following the oral exposure to a significantly higher amount of MSG [10]. …”
Section: Discussionsupporting
confidence: 81%
“…No data are available on the effects of MSG on the urinary apparatus and kidney function in humans. Of note, chronic oral MSG intake in rats leads to changes in antioxidant systems and renal markers including lipid peroxidation byproducts [10], in agreement with what observed in rats injected with MSG [11]. Moreover, dietary MSG increases the urinary pH in rats [12] and alkaline urine may influence the kidney capacity to secrete or reabsorb metabolites that contribute to stone formation, as in the case of calcium phosphate products [13].…”
Section: Introductionsupporting
confidence: 55%
“…In previous experiments, MSG supplementation either by injection [11] or oral intake [10,24] induced kidney damage but we report herein for the first time that the chronic consumption of dietary MSG causes obstructive nephropathy from urolithiasis in adult rats possibly via urine alkalinization which predispose to CaP precipitation.…”
Section: Discussionmentioning
confidence: 75%
“…Such moderate hydronephrosis resembles the effects of partial ureteral obstruction in rats [35] and obstructive nephropathy causes major changes in the tubulo-interstitial compartment of the kidney and renal interstitial fibrosis is a common long-term consequence [36]. We are convinced that this phenomenon may cause the kidney interstitial fibrosis observed in MSG-treated rats while oxidative stress secondary to MSG may also contribute [10] as reactive oxygen species induce the transmodulation of fibroblasts to myofibroblasts [37]. Tubular interstitial fibrosis is the strongest morphological predictor of clinical outcome in kidney disease, and is tightly associated to the progression of renal diseases [38].…”
BackgroundThe peritoneal injection of monosodium glutamate (MSG) can induce kidney injury in adult rats but the effects of long-term oral intake have not been determined.MethodsWe investigated the kidney histology and function in adult male Wistar rats that were fed ad
libitum with a standard rat chow pellet and water with or without the addition of 2 mg/g body weight MSG/day in drinking water (n=10 per group). Both MSG-treated and control animals were sacrificed after 9 months when renal function parameters, blood and urine electrolytes, and tissue histopathology were determined.ResultsMSG-treated rats were more prone to kidney stone formation, as represented by the alkaline urine and significantly higher activity product of calcium phosphate. Accordingly, 3/10 MSG-treated rats developed kidney stones over 9 months versus none of the control animals. Further, 2/10 MSG-treated rats but none (0/10) of the controls manifested hydronephrosis. MSG-treated rats had significantly higher levels of serum creatinine and potassium including urine output volume, urinary excretion sodium and citrate compared to controls. In contrast, MSG-treated rats had significantly lower ammonium and magnesium urinary excretion.ConclusionOral MSG consumption appears to cause alkaline urine and may increase the risks of kidney stones with hydronephrosis in rats. Similar effects in humans must be verified by dedicated studies.
“…Similar findings were observed in rat kidney studies done by Abass and Abd El-Haleem (2011) and Dixit et al (2014). MSG generates reactive oxygen species (ROS) causing oxidative stress by endogenous antioxidants depletion in the kidneys, which leads to lipids, proteins, DNA, RNA oxidation, which in the end will produce cellular alterations (Paul et al, 2012, Sharma et al, 2014.…”
The study aims to assess the effect of monosodium glutamate (MSG) in Japanese quail (Coturnix japonica). It was done on one hundred and thirty-four quails were divided into four groups: one control group (C) and three experimental groups that received during 30 days a daily dose of 10 g (E1), 30 g (E2) and 50 g (E3) MSG/kg feed, respectively. It was noticed to the end of the experiment an improvement in growth performance for the group E1, while in groups E2 and E3 higher feed consumption and decreased average daily weight gain was observed. Hematological studies revealed significant changes for the groups E2 (decreased PCV, reduction of Hf/Lf ratio, due to heterophils decrease) and E3 (increased Hf/Lf ratio due to heterophils increase and lymphocytes reduction) compared to the control group (C). Hematobiochemical studies revealed significant increases in blood urea nitrogen (BUN), creatinine and uric acid in quails from E2 and E3. In the kidneys of birds from E2 and E3 birds, was observed a degradation of cortical and medullar cytoarchitecture and also necrosis and vacuolization of proximal and distal convoluted tubules cells were observed. Positive nuclei were showed by P53 staining, both in proximal and distal convoluted tubules, collecting tubules epithelium but also in some of Malpighi corpuscles. Bcl-2 revealed positivity in the cytoplasm of the proximal and distal convoluted tubules cells in varying proportions depending on the group suggesting the prooncogenic potential of MSG in dosages that exceed 30g/kg feed.
Adaptive response is the ability of an organism to better counterattack stress-induced damage in response to a number of different cytotoxic agents. Monosodium L-glutamate (MSG), the sodium salt of amino acid glutamate, is commonly used as a food additive. We investigated the effects of MSG on the life span and antioxidant response in Drosophila melanogaster (D. melanogaster). Both genders (1 to 3 days old) of flies were fed with diet containing MSG (0.1, 0.5, and 2.5-g/kg diet) for 5 days to assess selected antioxidant and oxidative stress markers, while flies for longevity were fed for lifetime. Thereafter, the longevity assay, hydrogen peroxide (H O ), and reactive oxygen and nitrogen species levels were determined. Also, catalase, glutathione S-transferase and acetylcholinesterase activities, and total thiol content were evaluated in the flies. We found that MSG reduced the life span of the flies by up to 23% after continuous exposure. Also, MSG increased reactive oxygen and nitrogen species and H O generations and total thiol content as well as the activities of catalase and glutathione S-transferase in D. melanogaster (P < .05). In conclusion, consumption of MSG for 5 days by D. melanogaster induced adaptive response, but long-term exposure reduced life span of flies. This study may therefore have public health significance in humans, and thus, moderate consumption of MSG is advocated by the authors.
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