ArticleFree radical biology & medicine2010
Effects of age and calorie restriction on tryptophan nitration, protein content, and activity of succinyl-CoA:3-ketoacid CoA transferase in rat kidney mitochondria.
Article in Free radical biology & medicine, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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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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Who cites it
13 citing papers in PubMed, 21 citations in OpenAlex.
- The significance of the ketolytic gene OXCT1 in metabolism, intracellular signaling and disease development.Cellular and molecular life sciences : CMLS · 2026Review
- The Function and Mechanism of OXCT1 in Tumor Progression as a Critical Ketone Body Metabolic Enzyme.Biomolecules · 2025Review
- Molecular Mechanisms for Ketone Body Metabolism, Signaling Functions, and Therapeutic Potential in Cancer.Nutrients · 2022Review
- Metabolic and Signaling Roles of Ketone Bodies in Health and Disease.Annual review of nutrition · 2021Article
- Ketone Ester D-β-Hydroxybutyrate-(R)-1,3 Butanediol Prevents Decline in Cardiac Function in Type 2 Diabetic Mice.Journal of the American Heart Association · 2021Article
- A Ten-Day Grape Seed Procyanidin Treatment Prevents Certain Ageing Processes in Female Rats over the Long Term.Nutrients · 2020Article
- Ketone body 3-hydroxybutyrate mimics calorie restriction via the Nrf2 activator, fumarate, in the retina.Aging cell · 2018Article
- Multi-dimensional Roles of Ketone Bodies in Fuel Metabolism, Signaling, and Therapeutics.Cell metabolism · 2017Review
- Oxidative stress and the HIV-infected brain proteome.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2013Review
- Ketone body metabolism and cardiovascular disease.American journal of physiology. Heart and circulatory physiology · 2013Review
- Proteomic analysis of endogenous nitrotryptophan-containing proteins in rat hippocampus and cerebellum.Bioscience reports · 2012Article
- Redox modification of cell signaling in the cardiovascular system.Journal of molecular and cellular cardiology · 2012Review
- Senescence (ageing) @ 2011.Indian journal of dermatology · 2011Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
This study examined the protein targets of nitration and the consequent impact on protein function in rat kidney mitochondria at 4, 13, 19, and 24 months of age. Succinyl-CoA transferase (SCOT), a rate-limiting enzyme in the degradation of ketone bodies, was the most intensely reactive protein against anti-3-nitrotyrosine antibody in rat kidney mitochondria. However, subsequent mass spectrometric and amino acid analyses of purified SCOT indicated that tryptophan 372, rather than a tyrosine residue, was the actual site of simultaneous additions of nitro and hydroxy groups. This finding suggests that identification of nitrated tyrosine residues based solely on reactivity with anti-3-nitrotyrosine antibody can be potentially misleading. Between 4 and 24 months of age, the amounts of SCOT protein and catalytic activity, expressed per milligram of mitochondrial proteins, decreased by 55 and 45%, respectively. SCOT, and particularly its nitrated carboxy-terminal region, was relatively more susceptible to in vitro proteolysis than other randomly selected kidney mitochondrial proteins. The age-related decreases in SCOT protein amount and catalytic activity were prevented by a relatively long-term 40% reduction in the amount of food intake. Loss of SCOT protein in the aged rats may attenuate the capacity of kidney mitochondria to utilize ketone bodies for energy production.
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Registered trials
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