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Research & Studies
There are 39 good studies at Choline. Here's a selection:
Abstracts with Choline - Phosphatidylcholine Research:
Epigenetic changes of the thioredoxin system in the tx-j mouse model and in patients with Wilson disease
Charles E Mordaunt Noreene M Shibata Dorothy A Kieffer Anna CzłonkowskaTomasz Litwin Karl H Weiss Daniel N Gotthardt Kristin Olson Dongguang WeiStewart Cooper ... Show more
Human Molecular Genetics, ddy262, https://doi.org/10.1093/hmg/ddy262
Published: 16 July 2018
Wilson disease (WD) is caused by mutations in the copper transporter ATP7B, leading to copper accumulation in the liver and brain. Excess copper inhibits S-adenosyl-L-homocysteine hydrolase, leading to variable WD phenotypes from widespread alterations in DNA methylation and gene expression. Previously, we demonstrated that maternal choline supplementation in the Jackson toxic milk (tx-j) mouse model of WD corrected higher thioredoxin 1 transcript levels in fetal liver. Here, we investigated the effect of maternal choline supplementation on genome-wide DNA methylation patterns in tx-j fetal liver by whole-genome bisulfite sequencing (WGBS). Tx-j Atp7b genotype-dependent differences in DNA methylation were corrected by choline for genes including, but not exclusive to, oxidative stress pathways. To examine phenotypic effects of postnatal choline supplementation, tx-j mice were randomized to one of six treatment groups: with or without maternal and/or continued choline supplementation, and with or without copper chelation with penicillamine (PCA) treatment. Hepatic transcript levels of thioredoxin 1 and peroxiredoxin 1 were significantly higher in mice receiving maternal and continued choline with or without PCA treatment compared to untreated mice. A WGBS comparison of human WD liver and tx-j mouse liver demonstrated a significant overlap of differentially-methylated genes associated with ATP7B deficiency. Further, eight genes in the thioredoxin pathway were differentially methylated in human WD liver samples. In summary, Atp7b deficiency and choline supplementation have a genome-wide impact, including on thioredoxin system-related genes, in tx-j mice. These findings could explain the variability of WD phenotype and suggest new complementary treatment options for WD.
Topic: oxidative stress - phenotype - homocysteine - gene expression - mutation -
choline - dna methylation - etus - genes - genome - genotype - hepatolenticular -degeneration - hydrolase - membrane transport proteins - milk - mothers -
penicillamine - thioredoxin - brain - copper - liver - mice - epigenetics -
copper chelation therapy
Phospholids protect the pancreas against alchohol-induced oxidative stress.
Free Radic Biol Med. 1999 Mar;26(5-6):609-19. PMID: 10218649
S I Aleynik, M A Leo, M K Aleynik, C S Lieber
Section of Liver Disease&Nutrition and Alcohol Research Center, Bronx VA Medical Center and Mt. Sinai School of Medicine, New York, NY 10468, USA.
Oxidative stress is considered to be a forerunner of pancreatitis. Since we had found polyenylphosphatidylcholine, a mixture of polyunsaturated phosphatidylcholines extracted from soybeans, to protect against hepatic oxidative stress, we now tested its effects on the pancreas. Sprague-Dawley rats were pair-fed for two months nutritionally adequate liquid diet containing ethanol (36% of energy) or isocaloric carbohydrate, with either polyenylphosphatidylcholine (3 g/1000 kcal) or safflower oil, with or without 5 g/1000 kcal carbonyl iron. Parameters of oxidative stress (F2-isoprostanes, 4-hydroxynonenal, reduced glutathione), ubiquinol-10, ubiquinol-9 and vitamin E, as well as phosphatidylcholine species, were assessed by GC/MS and/or HPLC. Alcohol feeding increased pancreatic 4-hydroxynonenal three-fold, F2-isoprostanes and ubiquinol-9 by more than 70%, whereas it decreased total phospholipids, several phosphatidylcholine species, ubiquinol-10 and glutathione, especially in iron fed rats. Polyenylphosphatidylcholine prevented the rise in 4-hydroxynonenal and F2-isoprostanes, the decrease in dilinoleoylphosphatidylcholine and oleoyllinoleoylphosphatidylcholine and opposed the alcohol-induced decrease of glutathione; alpha-tocopherol remained unchanged. Iron had no significant effect except for decreasing ubiquinol-10 in the pancreas and increasing aminotransferases in the plasma. Thus, the alcohol-induced oxidative stress in the pancreas was shown to be prevented by polyenylphosphatidylcholine which may act, in part, by correcting the depletion of several phosphatidylcholine species.
Article Published Date : Mar 01, 1999
Study Type : Animal Study
Substances : Phosphatidylcholine : CK(101) : AC(22)
Diseases : Alcohol Toxicity : CK(337) : AC(125), Oxidative Stress : CK(3871) : AC(1382), Pancreatic Diseases : CK(21) : AC(8)
Pharmacological Actions : Antioxidants : CK(8430) : AC(3132)
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