Evidence map›Paper›PMID 37776396›Full record

ArticleBiological trace element research2024

Glutamine Defended the Kidneys Versus Lead Intoxication Via Elevating Endogenous Antioxidants, Reducing Inflammation and Carbonyl Stress, as well as Improving Insulin Resistance and Dyslipidemia.

Sina Mahdavifard, Najafzadeh Nowruz

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Article in Biological trace element research, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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1 · What the graph read from it

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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

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3 · Its place in the literature

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4 · The record

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5 · Who and what money

Authors and funding

2 authors.

Sina MahdavifardDepartment of Clinical Biochemistry, Ardabil University of Medical Sciences, Ardabil, Iran. sina.mahdavifard@arums.ac.ir.ORCID https://orcid.org/0000-0001-9878-2984
Najafzadeh NowruzResearch Laboratory for Embryology and Stem Cells, Department of Anatomical Sciences, School of Medicine, Ardabil University of Medical Sciences, Ardabil, Iran.ORCID https://orcid.org/0000-0001-8870-1255

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Kidneys are primarily sensitive to lead (Pb) poisoning due to their cardinal role in lead excretion. Then, we studied the effect of glutamine (Gln) on lead nephrotoxicity in rats by assessing the histopathological and biochemical parameters (the renal NF-kβ expression, metabolic profile, oxidative stress, inflammatory markers, methylglyoxal (MGO), and glyoxalase-I activity). Forty rats were allotted into four groups (ten rats in each): normal (N), Gln-treated N, Pb intoxication (Pbi), and Gln-treated Pbi. The treated groups took 0.1% Gln in drinking water for 1 month. To motivate lead poisoning, rats gained 50 mg/l lead acetate in drinking water for 1 month. Oxidative stress indices (total glutathione, its reduced and oxidized forms, their ratios, advanced protein oxidation products, malondialdehyde, and ferric ion reducing power) and inflammatory markers (renal nuclear factor-kβ expression, interleukin 1β level, and myeloperoxidase activity) were measured. Furthermore, metabolic profile (fasting blood sugar, insulin, insulin resistance, lipid profile, and atherogenic index) and renal dysfunction parameters were determined. Pb-induced renal histopathological alterations were investigated by a pathologist. In the kidney of Pbi rats, the glomerulus was damaged. Gln prevented kidney damage and reduced kidney dysfunction parameters. In addition, Gln decreased oxidative stress and inflammation in sera and kidney homogenates. In addition, it improved insulin resistance, dyslipidemia, and carbonyl stress (p < 0.001). Gln guarded the kidneys versus lead intoxication by improving insulin resistance and dyslipidemia, elevating antioxidant markers, and diminishing inflammation and carbonyl stress.

Indexed as

AntioxidantsDyslipidemiasGlutamineInflammationInsulin ResistanceKidneyOxidative StressAnimalsLead PoisoningMaleRatsRats, WistarAntioxidantsGlutaminecarbonyl stressGlutamineLead poisoningNephrotoxicityNuclear factor-kβ

Identifiers

PMID37776396

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.