ArticleFEBS open bio2014
Senescence marker protein-30/superoxide dismutase 1 double knockout mice exhibit increased oxidative stress and hepatic steatosis.
Article in FEBS open bio, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 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
18 citing papers in PubMed, 40 citations in OpenAlex.
- The Role of Oxidative Stress and Cellular Senescence in the Pathogenesis of Metabolic Associated Fatty Liver Disease and Related Hepatocellular Carcinoma.Antioxidants (Basel, Switzerland) · 2023Review
- Ascorbate Is a Primary Antioxidant in Mammals.Molecules (Basel, Switzerland) · 2022Review
- Modulation of Oxidative Stress-Induced Senescence during Non-Alcoholic Fatty Liver Disease.Antioxidants (Basel, Switzerland) · 2022Review
- Superoxide Radicals in the Execution of Cell Death.Antioxidants (Basel, Switzerland) · 2022Review
- The Potential Role of Cellular Senescence in Non-Alcoholic Fatty Liver Disease.International journal of molecular sciences · 2022Review
- Review
- Ascorbate is a multifunctional micronutrient whose synthesis is lacking in primates.Journal of clinical biochemistry and nutrition · 2021Article
- Senescence Marker Protein 30 (SMP30): A Novel Pan-Species Diagnostic Marker for the Histopathological Diagnosis of Breast Cancer in Humans and Animals.International journal of molecular sciences · 2021Article
- Upregulation and stabilization of senescence marker protein-30 by epigallocatechin gallate againstJournal of clinical biochemistry and nutrition · 2021Article
- L-Carnitine counteracts in vitro fructose-induced hepatic steatosis through targeting oxidative stress markers.Journal of endocrinological investigation · 2020Article
- Influence of different concentrations of uric acid on oxidative stress in steatosis hepatocytes.Experimental and therapeutic medicine · 2018Article
- Article
- Stem Cell Replacement Improves Expression of SMP30 in db/db Mice.International journal of molecular sciences · 2015Article
- Oxidative stress and antioxidant therapy in traumatic spinal cord injuries.Romanian journal of anaesthesia and intensive care · 2014Article
- Palladium and platinum nanoparticles attenuate aging-like skin atrophy via antioxidant activity in mice.PloS one · 2014Article
- Superoxide dismutase 1 loss disturbs intracellular redox signaling, resulting in global age-related pathological changes.BioMed research international · 2014Review
- Preventive Effects of Vitamin C on Diethylnitrosamine-induced Hepatotoxicity inIn vivo (Athens, Greece)Article
- Study of Cellular Senescence and Vitamin D Deficiency in Nonalcoholic Fatty Liver Disease and The Potential Protective Effect of Vitamin D Supplementation.Journal of clinical and experimental hepatologyArticle
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Superoxide dismutase 1 (SOD1) is an antioxidant enzyme that converts superoxide anion radicals into hydrogen peroxide and molecular oxygen. The senescence marker protein-30 (SMP30) is a gluconolactonase that functions as an antioxidant protein in mammals due to its involvement in ascorbic acid (AA) biosynthesis. SMP30 also participates in Ca(2+) efflux by activating the calmodulin-dependent Ca(2+)-pump. To reveal the role of oxidative stress in lipid metabolism defects occurring in non-alcoholic fatty liver disease pathogenesis, we generated SMP30/SOD1-double knockout (SMP30/SOD1-DKO) mice and investigated their survival curves, plasma and hepatic lipid profiles, amounts of hepatic oxidative stress, and hepatic protein levels expressed by genes related to lipid metabolism. While SMP30/SOD1-DKO pups had no growth retardation by 14 days of age, they did have low plasma and hepatic AA levels. Thereafter, 39% and 53% of male and female pups died by 15-24 and 89 days of age, respectively. Compared to wild type, SMP30-KO and SOD1-KO mice, by 14 days SMP30/SOD1-DKO mice exhibited: (1) higher plasma levels of triglyceride and aspartate aminotransferase; (2) severe accumulation of hepatic triglyceride and total cholesterol; (3) higher levels of superoxide anion radicals and thiobarbituric acid reactive substances in livers; and (4) decreased mRNA and protein levels of Apolipoprotein B (ApoB) in livers - ApoB is an essential component of VLDL secretion. These results suggest that high levels of oxidative stress due to concomitant deficiency of SMP30 and/or AA, and SOD1 cause abnormal plasma lipid metabolism, hepatic lipid accumulation and premature death resulting from impaired VLDL secretion.
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