ArticleFree radical biology & medicine2000
Mitochondrial oxidative stress in mice lacking the glutathione peroxidase-1 gene.
Article in Free radical biology & medicine, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 73 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
73 citing papers in PubMed, 223 citations in OpenAlex.
- Identification of Proteomic Markers for Monitoring Direct Toxic Liver Injury (DTLI): Profiling Hepatoprotective Effects of Plant Polyphenols.International journal of molecular sciences · 2026Article
- Effects of different oxygen concentrations during intermittent hyperoxic training on endurance capacity in well-trained male mice.Physiological reports · 2026Article
- Exercise Training Stimulates the Release of Glutathione Peroxidase 1 (GPX1)-Enriched Extracellular Vesicles That Promote Angiogenesis.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Article
- Effects of Balanced Supplementation with Multiple Trace Elements on Oxidative Stress, Inflammation, and Immune Function in High-Fat Diet-Induced Rats.International journal of preventive medicine · 2025Article
- Strong associations of serum selenoprotein P with all-cause mortality and mortality due to cancer, cardiovascular, respiratory and gastrointestinal diseases in older German adults.European journal of epidemiology · 2024Article
- Unique features of KGN granulosa-like tumour cells in the regulation of steroidogenic and antioxidant genes.PloS one · 2024Article
- Article
- Oxidation State in Peritoneal Dialysis in Patients with Type 2 Diabetes Mellitus.International journal of molecular sciences · 2023Article
- Selenium-modified bone cement promotes osteoporotic bone defect repair in ovariectomized rats by restoring GPx1-mediated mitochondrial antioxidant functions.Regenerative biomaterials · 2023Article
- The role of glutathione peroxidase-1 in health and disease.Free radical biology & medicine · 2022Review
- Regulation of A-to-I RNA editing and stop codon recoding to control selenoprotein expression during skeletal myogenesis.Nature communications · 2022Article
- Hyperosmolality in CHO cell culture: effects on the proteome.Applied microbiology and biotechnology · 2022Article
- A Comprehensive Comparison of Different Selenium Supplements: Mitigation of Heat Stress and Exercise Fatigue-Induced Liver Injury.Frontiers in nutrition · 2022Article
- Mitochondrial Management of Reactive Oxygen Species.Antioxidants (Basel, Switzerland) · 2021Review
- Sulforaphane improves mitochondrial metabolism in fibroblasts from patients with fragile X-associated tremor and ataxia syndrome.Neurobiology of disease · 2021Article
- Ginsenoside Re Protects against Serotonergic Behaviors Evoked by 2,5-Dimethoxy-4-iodo-amphetamine in Mice via Inhibition of PKCδ-Mediated Mitochondrial Dysfunction.International journal of molecular sciences · 2021Article
- Catalytic Antioxidants in the Kidney.Antioxidants (Basel, Switzerland) · 2021Review
- PER1 interaction with GPX1 regulates metabolic homeostasis under oxidative stress.Redox biology · 2020Article
- The effect ofRSC advances · 2020Article
- Article
13 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Oxidative stress resulting from mitochondrially derived reactive oxygen species (ROS) has been hypothesized to damage mitochondrial oxidative phosphorylation (OXPHOS) and to be a factor in aging and degenerative disease. If this hypothesis is correct, then genetically inactivating potential mitochondrial antioxidant enzymes such as glutathione peroxidase-1 (Gpx1; EC 1.11.1.9) should increase mitochondrial ROS production and decrease OXPHOS function. To determine the expression pattern of Gpx1, isoform-specific antibodies were generated and mutant mice were prepared in which the Gpx1 protein was substituted for by beta-galactosidase, driven by the Gpx1 promoter. These experiments revealed that Gpx1 is highly expressed in both the mitochondria and the cytosol of the liver and kidney, but poorly expressed in heart and muscle. To determine the physiological importance of Gpx1, mice lacking Gpx1 were generated by targeted mutagenesis in mouse ES cells. Homozygous mutant Gpx1(tm1Mgr) mice have 20% less body weight than normal animals and increased levels of lipid peroxides in the liver. Moreover, the liver mitochondria were found to release markedly increased hydrogen peroxide, a Gpx1 substrate, and have decreased mitochondrial respiratory control ratio and power output index. Hence, genetic inactivation of Gpx1 resulted in growth retardation, presumably due in part to reduced mitochondrial energy production as a product of increased oxidative stress.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.