ArticleJournal of bioenergetics and biomembranes2006
Adaptations to oxidative stress induced by vitamin E deficiency in rat liver.
Article in Journal of bioenergetics and biomembranes, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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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.
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Who cites it
7 citing papers in PubMed, 22 citations in OpenAlex.
- Molecular basis of unique specificity and regulation of group VIA calcium-independent phospholipase APharmacology & therapeutics · 2023Review
- Loss of smooth muscle CYB5R3 amplifies angiotensin II-induced hypertension by increasing sGC heme oxidation.JCI insight · 2019Article
- CytochromeNPJ aging and mechanisms of disease · 2016Article
- Membrane-bound CYB5R3 is a common effector of nutritional and oxidative stress response through FOXO3a and Nrf2.Antioxidants & redox signaling · 2014Article
- Coenzyme Q10 deficiencies in neuromuscular diseases.Advances in experimental medicine and biology · 2009Review
- Selenium deficiency activates mouse liver Nrf2-ARE but vitamin E deficiency does not.Free radical biology & medicine · 2008Article
- The effects of a low vitamin E diet on dichloroacetate- and trichloroacetate-induced oxidative stress in the livers of mice.Journal of biochemical and molecular toxicologyArticle
Corrections and comments
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Authors and funding
3 authors at 3 institutions in 2 countries.
Funding
Abstract
Vitamin E deficiency in rats led to a sequence of antioxidant defense adaptations in the liver. After three weeks, alpha-tocopherol concentration was 5% of control, but ascorbate and ubiquinol concentrations were 2- to 3-fold greater than control. During the early phase of adaptation no differences in markers of lipid peroxidation were observed, but the activities of both cytochrome b5 reductase and glucose-6-phosphate dehydrogenase were significantly greater in deficient livers. By nine weeks, accumulation of lipid peroxidation end products began to occur along with declining concentrations of ascorbate, and higher NQO1 activities. At twelve weeks, rat growth ceased, and both lipid peroxidation products and cytosolic calcium-independent phospholipase A2 reached maximum concentrations. Thus, in growing rats the changes progressed from increases in both ubiquinol and quinone reductases through accumulation of lipid peroxidation products and loss of endogenous antioxidants to finally induction of lipid metabolizing enzymes and cessation of rat growth.
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Registered trials
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