scholarly journals Vitamin E and hepatotoxic agents

1969 ◽  
Vol 23 (2) ◽  
pp. 309-317 ◽  
Author(s):  
J. Bunyan ◽  
M. A. Cawthorne ◽  
A. T. Diplock ◽  
J. Green
Keyword(s):  
Vitamin E ◽  
Fatty Liver ◽  
Orotic Acid ◽  
Lipid Peroxides ◽  
Fat Content ◽  
Liver Fat ◽  
Male Rats ◽  
Tocopheryl Acetate ◽  
Deficient Diet

1. Fatty liver was induced in 4-month-old male rats by oral dosing with ethanol. The marked increase in liver fat was not accompanied by a rise in lipid peroxides.2. Homogenates were prepared from the livers of vitamin E-deficient rats and incubated with ethanol. In the concentration range of 10–50 μl/3 ml, ethanol increased the production of malondialdehyde. Methanol, which is not a hepatotoxin, showed a similar effect at 10–35 μl/3 ml homogenate. These findings indicate that the pro-oxidative effect of alcohols in vitro is unrelated to their hepatotoxic action in vivo.3. Fatty liver was induced in 3.g-month-old, vitamin E-deficient male rats by oral dosingwith ethanol. The effect of pretreatment with vitamin E and N,N'-diphenyl-p-phenylenediamine (DPPD) was studied. D-α-Tocopheryl acetate, given as three doses of 350 mg/kg at 48, 24 and 2 h before the ethanol, failed to decrease the fat accumulation and seemed rather to increase the fat content of the liver. DPPD, given as three doses of 600 mg'kg at similar intervals before the ethanol dose, reduced the fat content of the liver almost to normal.4. Weanling rats of both sexes were given a vitamin E-deficient diet containing 1% orotic acid for 15 days to induce fatty liver. Dietary supplements of D-a-tocopheryl acetate (500 ppm), selenium (I ppm) or DPPD (100 ppm) did not reduce the lipid accumulation. Lipid peroxides and malondialdehyde levels were lower in the livers of animals treated with orotic acid than in controls, regardless of the presence of vitamin E.j. Liver necrosis was produced in 9-week-old female vitamin E-deficient rats by the intra-peritoneal injection of zoo mg thioacetamide. Promethazine hydrochloride (Phenergan), given intraperitoneally as two doses (25 mg/kg at the same time as the thioacetamide and 12.5 mg/kg 6 h later), markedly reduced the necrosis. D-α-Tocopheryl acetate, given as two oral doses of 1000mg/kg 48 h and 24 h before the thioacetamide, tended to exacerbate the necrosis.6. The results are discussed in relation to the question of lipid peroxidation as a cause of hepatotoxicity.

scholarly journals Preventive Effects of Dehydroepiandrosterone Acetate on the Fatty Liver Induced by Orotic Acid in Male Rats.

1998 ◽  
Vol 47 (4) ◽  
pp. 257-260 ◽  
Author(s):  
Hirohiko GOTO ◽  
Shuji YAMASHITA ◽  
Takashi MAKITA
Keyword(s):  
Fatty Liver ◽  
Orotic Acid ◽  
Male Rats ◽  
Preventive Effects

scholarly journals Quantification of Hepatorenal Index for Computer-Aided Fatty Liver Classification with Self-Organizing Map and Fuzzy Stretching from Ultrasonography

2015 ◽  
Vol 2015 ◽  
pp. 1-9 ◽  
Author(s):  
Kwang Baek Kim ◽  
Chang Won Kim
Keyword(s):  
Fatty Liver ◽  
Hepatic Steatosis ◽  
Learning Algorithm ◽  
Fat Content ◽  
Liver Fat ◽  
Self Organizing Map ◽  
Liver Fat Content ◽  
Computer Aided ◽  
Good Set ◽  
Self Organizing

Accurate measures of liver fat content are essential for investigating hepatic steatosis. For a noninvasive inexpensive ultrasonographic analysis, it is necessary to validate the quantitative assessment of liver fat content so that fully automated reliable computer-aided software can assist medical practitioners without any operator subjectivity. In this study, we attempt to quantify the hepatorenal index difference between the liver and the kidney with respect to the multiple severity status of hepatic steatosis. In order to do this, a series of carefully designed image processing techniques, including fuzzy stretching and edge tracking, are applied to extract regions of interest. Then, an unsupervised neural learning algorithm, the self-organizing map, is designed to establish characteristic clusters from the image, and the distribution of the hepatorenal index values with respect to the different levels of the fatty liver status is experimentally verified to estimate the differences in the distribution of the hepatorenal index. Such findings will be useful in building reliable computer-aided diagnostic software if combined with a good set of other characteristic feature sets and powerful machine learning classifiers in the future.

scholarly journals Sequestration of Vitamin E by Liver Fat in vivo, in vitro and in Women with Hepato-steatosis

2020 ◽  
Vol 4 (Supplement_2) ◽  
pp. 1696-1696
Author(s):  
Pierre-Christian Violet ◽  
Ifechukwude Ebenuwa ◽  
Stacey Chung ◽  
Jeffrey Atkinson ◽  
Danny Manor ◽  
...  
Keyword(s):  
Liver Disease ◽  
Vitamin E ◽  
High Fat Diet ◽  
Alpha Tocopherol ◽  
Liver Fat ◽  
Slight Reduction ◽  
High Fat ◽  
High Vitamin

Abstract Objectives Hepato-steatosis (HS) due to obesity is now the most common cause of chronic liver disease in the Americas and Western Europe. The only means to prevent disease is avoidance of obesity. α-Tocopherol at doses of 800 I.U. daily was reported to have partial treatment effects for NASH. Because alpha tocopherol is a fat-soluble vitamin, we hypothesized that excess fat in liver, as found in HS, could act unintentionally sequester vitamin E, thereby altering its normal physiology and contributing to development of NASH. Using oral and intravenous deuterated tocopherols, evidence showing HS altered a-tocopherol physiology was reported based on pharmacokinetics studies in obese women with HS. Here we further tested the sequestration hypothesis in vitro, and in vivo. Methods In vitro, we investigated effects of fat on intracellular vitamin E localization. Control human and mouse hepatocytes and hepatocytes pre-loaded with fat were incubated with fluorescent α-tocopherol (BDP-α-tocopherol). In vivo experiments were performed using mice fed a high fat diet with different vitamin E doses. Results Compared to controls, fat- loaded cells contained more a-tocopherol, and BDP-a-tocopherol was specifically localized into intracellular fat droplets. In cells incubated with BDP a-tocopherol, we found that fat loading decreased a-tocopherol release. Induced expression of TPP, which mediates vitamin E intracellular disposition under normal conditions, was not observed in fat loaded cells, further confirming vitamin E was trapped in fat. Livers of mice fed high fat diet had more vitamin E compared to controls. By further increasing vitamin E content of the high fat diet, we observed a reduction in liver size and liver fat in the high vitamin E group. Using a mouse metabolic chamber, we observed a slight reduction of oxygen consumption rate in the high vitamin E group compared to controls. Conclusions Considered together, these findings imply that fat in the liver may produce unrecognized hepatic vitamin E sequestration, which could drive liver disease. These results are consistent with the possibility that increased vitamin E intake might, if begun at an early stage, restore vitamin E physiology, potentially decreasing or preventing progression of HS to NASH. Funding Sources NIH intramural program (DK053213–14).

scholarly journals Some effects of vitamin E and selenium deprivation on tissue enzyme levels and indices of tissue peroxidation in rainbow trout (Salmo gairdneri)

1985 ◽  
Vol 53 (1) ◽  
pp. 149-157 ◽  
Author(s):  
J. G. Bell ◽  
C. B. Cowey ◽  
J. W. Adron ◽  
Aileen M. Shanks
Keyword(s):  
Rainbow Trout ◽  
Vitamin E ◽  
Peroxidase Activity ◽  
Cumene Hydroperoxide ◽  
Dietary Vitamin ◽  
Salmo Gairdneri ◽  
Deficient Diet ◽  
Exudative Diathesis ◽  
Malondialdehyde Formation

1. Duplicate groups of rainbow trout (Salrno gairdnert) (mean weight 11 g) were given for 40 weeks one of four partially purified diets that were either adequate or low in selenium or vitamin E or both.2. Weight gains of trout given the dually deficient diet were significantly lower than those of trout given a complete diet or a diet deficient in Se. No mortalities occurred and the only pathology seen was exudative diathesis in the dually deficient trout.3. There was significant interaction between the two nutrients both with respect to packed cell volume and to malondialdehyde formation in the in vitro NADPH-dependent microsomal lipid peroxidation system.4. Tissue levels of vitamin E and Se decreased to very low levels in trout given diets lacking these nutrients. For plasma there was a significant effect of dietary vitamin E on Se concentration.5. Glutathione (GSH) peroxidase (EC 1. 1 1. 1.9) activity in liver and plasma was significantly lower in trout receiving low dietary Se but was independent of vitamin E intake. The ratios of hepatic GSH peroxidase activity measured with cumene hydroperoxide and hydrogen peroxide were the same for all treatments. This confirms the absence of a Se-independent GSH peroxidase activity in trout liver.6. Se deficiency did not lead to any compensatory increase in hepatic GSH transferase (EC 2. 5. 1. 18) activity; values were essentially the same in all treatments.7. Plasma pyruvate kinase (EC 2. 7. 1.40) activity increased significantly in the trout deficient in both nutrients. This was thought to be due to leakage of the enzyme from the muscle and may be indicative of incipient (subclinical) muscle damage.

scholarly journals Kupffer cell depletion protects against the steatosis, but not the liver damage, induced by marginal-copper, high-fructose diet in male rats

2015 ◽  
Vol 308 (11) ◽  
pp. G934-G945 ◽  
Author(s):  
Ming Song ◽  
Dale A. Schuschke ◽  
Zhanxiang Zhou ◽  
Wei Zhong ◽  
Jiayuan Zhang ◽  
...  
Keyword(s):  
Fatty Liver ◽  
Regulatory Element ◽  
Critical Role ◽  
Deionized Water ◽  
Male Rats ◽  
Sprague Dawley ◽  
Deficient Diet ◽  
High Fructose Diet ◽  
Triglyceride Accumulation ◽  
High Fructose

High-fructose feeding impairs copper status and leads to low copper availability, which is a novel mechanism in obesity-related fatty liver. Copper deficiency-associated hepatic iron overload likely plays an important role in fructose-induced liver injury. Excess iron in the liver is distributed throughout hepatocytes and Kupffer cells (KCs). The aim of this study was to examine the role of KCs in the pathogenesis of nonalcoholic fatty liver disease induced by a marginal-copper high-fructose diet (CuMF). Male weanling Sprague-Dawley rats were fed either a copper-adequate or a marginally copper-deficient diet for 4 wk. Deionized water or deionized water containing 30% fructose (wt/vol) was also given ad libitum. KCs were depleted by intravenous administration of gadolinium chloride (GdCl3) before and/or in the middle of the experimental period. Hepatic triglyceride accumulation was completely eliminated with KC depletion in CuMF consumption rats, which was associated with the normalization of elevated plasma monocyte chemoattractant protein-1 (MCP-1) and increased hepatic sterol regulatory element binding protein-1 expression. However, hepatic copper and iron content were not significantly affected by KC depletion. In addition, KC depletion reduced body weight and epididymal fat weight as well as adipocyte size. Plasma endotoxin and gut permeability were markedly increased in CuMF rats. Moreover, MCP-1 was robustly increased in the culture medium when isolated KCs from CuMF rats were treated with LPS. Our data suggest that KCs play a critical role in the development of hepatic steatosis induced by marginal-copper high-fructose diet.

scholarly journals Effects of protein and vitamin E on haemoglobin formation in rats

1968 ◽  
Vol 22 (4) ◽  
pp. 751-755 ◽  
Author(s):  
J. Bunyan ◽  
J. Green ◽  
M. A. Cawthorne
Keyword(s):  
Vitamin E ◽  
Dietary Supplement ◽  
Tocopheryl Acetate ◽  
Dietary Vitamin ◽  
Deficient Diet ◽  
Growth Depression ◽  
Low Protein ◽  
Protein Diets ◽  
Severe Growth ◽  
Haemolysis Test

1. Young rats were given, for 9 weeks, vitamin E-deficient diets containing either 20% or 10% casein, with and without a dietary supplement of 350 ppm D-α-tocopheryl acetate. For the next 5 weeks the casein content of the low-protein diets was decreased to 7%.2. The low-protein diets induced severe growth depression.3. The dialuric acid-induced haemolysis test showed that the rats given the 20% casein vitamin E-deficient diet were depleted of vitamin E, but that the rate of depletion on the lowcasein diet was slower.4. Haemoglobin levels were slightly decreased by the 10% casein diets after 9 weeks, but this difference was not found after 14 weeks, comparing 20% and 7% casein. Dietary vitamin E had no effect on haemoglobin levels or erythrocyte counts.

scholarly journals Noninvasive Quantification of Hepatic Steatosis: Relationship Between Obesity Status and Liver Fat Content

2014 ◽  
Vol 6 (1) ◽  
pp. 16-24 ◽  
Author(s):  
S. C. McLeay ◽  
G. A. Morrish ◽  
T. K. Ponnuswamy ◽  
B. Devanand ◽  
M. Ramanathan ◽  
...  
Keyword(s):  
Fatty Liver ◽  
Hepatic Steatosis ◽  
Liver Volume ◽  
Fat Content ◽  
Liver Fat ◽  
Normal Body Mass Index ◽  
Liver Fat Content ◽  
Total Liver Volume ◽  
Total Liver ◽  
Obese Subjects

The aim of this study was to assess and compare fat content within the liver for normal (body mass index (BMI) < 25 kg/m2), overweight (25-30 kg/m2) and obese (≥ 30 kg/m2) subjects using a noninvasive, non-contrast computed tomography (CT) quantification method. Adult subjects aged 18-60 yrs scheduled to undergo CT examination of the abdominal region were recruited for this study, stratified across BMI categories. Liver volume, fat content, and lean liver volume were determined using CT methods. A total of 100 subjects were recruited, including 30 normal weight, 31 overweight, and 39 obese. Total liver volume increased with BMI, with mean values of 1138 ± 277, 1374 ± 331, and 1766 ± 389 cm3 for the normal, overweight, and obese, respectively (P < 0.001), which was due to an increase in both liver fat content and lean liver volume with BMI. Some obese subjects had no or minimal hepatic fat content. The prevalence of mild fatty liver in this study of 100 subjects was overestimated for all BMI categories using a range of qualitative diagnostic measures, with predicted prevalence of fatty liver in obese subjects ranging from 76.9% for liver-to-spleen ratio ≤ 1.1 to 89.7% for liver attenuation index (liver HU - spleen HU) ≤ 40, compared to 66.7% by quantification of fat content. Results show that total liver volume increases with BMI, however, not all obese subjects display fatty infiltration of the liver. CT quantification of liver fat content may be suitable for accurate diagnosis of hepatic steatosis in clinical practice and assessment of donor livers for transplantation.

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