ArticleClinical kidney journal2018
Metabolic adaptability in hexavalent chromium-treated renal tissue: an
Article in Clinical kidney journal, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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Who cites it
6 citing papers in PubMed, 27 citations in OpenAlex.
- Protective effects of thymoquinone against hexavalent chromium-ınduced nephrotoxicity: a multiparametric evaluation of oxidative stress, ınflammation, ferroptosis- and apoptosis-related markers.Molecular and cellular biochemistry · 2026Article
- Hexavalent Chromium and Hexavalent Uranium Induce Mitochondrial Damage and Transcriptomic Alterations in Chinese Soft-Shelled Turtle Embryo Fibroblasts.Biological trace element research · 2026Article
- Natural compounds attenuate combined chromium and arsenic-induced oxidative stress and nephritic apoptosis by activating the Nrf2/Keap1 signaling and associated xenobiotic metabolizing enzymes.Scientific reports · 2025Article
- Ameliorative effect of aqueous avocado seed extract against chromium-induced oxidative stress and cellular damage in rabbit kidney.Food science & nutrition · 2024Article
- Involvement of Tricarboxylic Acid Cycle Metabolites in Kidney Diseases.Biomolecules · 2021Review
- Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundHexavalent chromium [Cr(VI)], an environmental pollutant that originates mostly from anthropogenic sources, is a serious threat to human health. After entering into cells, Cr(VI) is capable of producing excessive free radicals and causing tissue damage. The present study aims to reveal the toxic manifestation of Cr(VI) on the metabolic activity of renal tissue.
methodsMale Swiss albino mice were treated orally with potassium dichromate (K
resultsCr(VI) suppresses the rate-limiting enzymes of the TCA cycle and oxidative phosphorylation indicating an inhibition of renal ATP production. It decreases protease activity by eliminating the protein substrates and alters the gluconeogenic pathway. Cr(VI) worsens the normophysiological attributes of renal tissue by enhancing the activity of alkaline phosphatase, pointing towards kidney disease. Histopathological observations confirmed these biochemical results through the presence of chronic tubular nephritis and altered glomerular structure. Cr(VI) retention occurs to a greater extent in renal tissue, which intensifies the toxic manifestation of this pollutant in the kidney.
conclusionsCr(VI) disrupts the metabolic interaction between carbohydrates and proteins in mammalian renal tissue.
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Registered trials
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