Abstract
Animal studies suggest that chronic monosodium glutamate (MSG) intake induces kidney damage by oxidative stress. However, the underlying mechanisms are still unclear, despite the growing evidence and consensus that α-ketoglutarate dehydrogenase, glutamate receptors and cystine-glutamate antiporter play an important role in up-regulation of oxidative stress in MSG-induced renal toxicity. This review summaries evidence from studies into MSG-induced renal oxidative damage, possible mechanisms and their importance from a toxicological viewpoint.
Highlights
Monosodium glutamate (MSG) is a commonly-used additive in processed food and Asian cuisine to increase palatability
Published data indicate that renal fibrosis is associated with the chronic consumption of MSG [4] and oxidative stress is the main cause of kidney injury [5]
The increased level of α-ketoglutarate dehydrogenase has been found in the kidney of MSG-fed rats [5] and a strong consensus is being developed against αketoglutarate dehydrogenase, glutamate receptors, and cystine-glutamate antiporter for their potential role in the MSG-related renal oxidative stress
Summary
Monosodium glutamate (MSG) is a commonly-used additive in processed food and Asian cuisine to increase palatability. Published data indicate that renal fibrosis is associated with the chronic consumption of MSG [4] and oxidative stress is the main cause of kidney injury [5]. Decreased levels of major anti-oxidant enzymes and increased lipid peroxidation have been demonstrated in the kidneys of chronic MSG-exposed rats [10, 11].
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