BIOLOGICAL EFFECTS OF MONOSODIUM GLUTAMATE ON THE KIDNEYS AND POTENTIAL APPROACHES TO THEIR MITIGATION
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BIOLOGICAL EFFECTS OF MONOSODIUM GLUTAMATE ON THE KIDNEYS AND POTENTIAL APPROACHES TO THEIR MITIGATION

Published 2026-09-30

Authors:

Shevchenko K.V.
Poltava State Medical University image/svg+xml
https://orcid.org/0000-0003-1665-3236
Bilash S.M.
Poltava State Medical University image/svg+xml
https://orcid.org/0000-0002-8351-6090
Grygorenko A.S.
Poltava State Medical University image/svg+xml
https://orcid.org/0000-0003-2268-6384
Bieliaieva O.M.
Poltava State Medical University image/svg+xml
https://orcid.org/0000-0001-9060-4753
Bilash V.P.
Poltava State Medical University image/svg+xml
https://orcid.org/0000-0002-7178-3394
Onipko V.V.
Poltava State Agrarian University image/svg+xml
https://orcid.org/0000-0002-2260-971X
Pospielov S.V.
Poltava State Agrarian University image/svg+xml
https://orcid.org/0000-0003-0433-2996

Abstract:
The study provides a systematic analysis of scientific data on the biological effects of monosodium glutamate and the pathogenetic mechanisms underlying its impact on renal tissue. To achieve this aim, the findings of 41 experimental and review publications selected according to the PRISMA approach in PubMed, Web of Science, Scopus, and Google Scholar were summarised. Attention was focused on the functional, biochemical, molecular, and morphological manifestations of MSG-induced nephrotoxicity. Prolonged exposure to high doses of monosodium glutamate was found to be associated with increased creatinine, urea, and uric acid levels, impaired glomerular filtration, renal autoregulation, salt and water excretion, and regulation of water-electrolyte homeostasis. Oxidative and nitrosative stress is identified as a leading pathogenetic mechanism of injury and is characterised by enhanced lipid peroxidation, malondialdehyde accumulation, and depletion of glutathione and antioxidant enzymes. These alterations are accompanied by activation of pro-inflammatory signalling pathways, suppression of Nrf2, increased expression of NF-κB and cytokines, and initiation of caspase-dependent apoptosis. At the tissue level, glomerular injury, degeneration and necrosis of tubular epithelium, formation of hyaline casts, interstitial inflammatory infiltration, and fibrosis were described. The roles of the gut-kidney axis, metabolic abnormalities, and the dose- and time-dependent nature of toxicity were analysed. The effects of L-carnitine, protocatechuic acid, apocynin, omega-3 fatty acids, Nigella sativa, Ficus carica, Garcinia kola, Piper nigrum, and other nephroprotective agents were summarised. Their protective activity is associated with restoration of redox homeostasis, suppression of inflammation, limitation of apoptosis, and improvement of functional and structural renal parameters. The findings substantiate the biological risks of high and chronic monosodium glutamate consumption and provide a theoretical basis for developing strategies to prevent and correct alimentary nephropathy.
Keywords:
kidneys rats monosodium glutamate MSG E621 nephrotoxicity excretory system oxidative stress renal glomeruli tubular epithelium
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Publication:
«World of Medicine and Biology» Vol. 22 No. 97 (2026), pp. 258-266
UDC 616.61:615.212-085:664