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1.
The modulatory role of dietary vitamin A on the carcinogen metabolizing enzymes was studied in masheri extract and benzo[a]pyrene-treated rats. Weanling male Sprague-Dawley rats were fed vitamin A deficient (SR-) and vitamin A sufficient (SR+) semisynthetic diets for 12 weeks. ME/B[a]P treatment significantly increased the phase I activating enzymes in both SR- and SR+ groups. However, a higher percentage increase in enzyme activities was observed in both liver and lung of the SR- animals compared to the SR+ groups. Glutathione content and activity of glutathione S-transferase were decreased in both liver and lung of SR- animals on treatment with either ME or B[a]P. In the SR+ group, an increase in GSH content and GST activity was observed following the ME/B[a]P treatment. The hepatic pool of vitamin A was depleted while that of vitamin C was increased after ME or B[a]P treatment in both SR- and SR+ groups. 相似文献
2.
U J Nair N Ammigan J R Kulkarni S V Bhide 《Indian journal of experimental biology》1991,29(3):256-258
Activities of several drug metabolising enzymes in the small intestine were investigated in Swiss mice, Sprague Dawley rats and Syrian Golden Hamsters fed 10% masheri, a pyrolysed tobacco product, in diet, for 20 months. The basal levels of enzymes in proximal (PI), medium (MI) and distal (DI) parts of the intestine in the three species were similar. However, the levels of cytochrome P-450, benzo(a) pyrene hydroxylase (B(a)OH) and glutathione S-transferase (GST) were highest in hamsters followed by rat and mice. Upon treatment with masheri, significant induction of cytochrome P-450 and B(a)PH was observed in PI and DI of all the three species. However, GSH and GST was depleted upon masheri treatment in all the three species again only in proximal and distal parts of the intestine. Thus increase in activating enzymes together with depletion in GSH-GST system upon exposure could be an important factor in the susceptibility of the small intestine to hazardous xenobiotic exposure. 相似文献
3.
Studies on the modulation of the carcinogen metabolizing enzymes on treatment with masheri extract (ME) and benzo (a) pyrene (B (a)P), were carried out in male Sprague Dawley rats (12 weeks old) fed a nutritionally adequate standard diet. Injection (ip) of ME and B (a) P at 3/4 LD50 dose given in 3 doses at 24 hr interval increased the phase I activating enzymes, viz. cytochrome P-450, benzo (a) pyrene hydroxylase and benzphetamine demethylase while both ME and B (a) P significantly depleted glutathione content and decreased glutathione-S transferase activity. Furthermore, the same treatment of ME and B (a) P significantly depleted the hepatic vitamin A pool while a concommittant increase in vitamin C content was observed. 相似文献
4.
Female rats were used to investigate the comparative role of vitamin A and beta-carotene (dietary or injected) on growth, feed intake and reproduction. After 3 wk of vitamin A and beta-carotene depletion, rats were assigned to one of six groups: 1) CON = fed 5% NRC recommended level of vitamin A (= 60 mug retinol equivalent (RE)/kg diet); 2) VA = fed 100% of vitamin A (= 1200 mug RE/kg diet); 3) HVA = fed 150% of vitamin A; 4) VA+C = fed 100% of vitamin A + 1.2mg beta-carotene; 5) VA+IC = fed 100% of vitamin A + injected weekly with 8.37 mg of beta-carotene; and 6) VA+IVA = fed 100% of vitamin A + injected weekly with 1400 IU of vitamin A. The level of vitamin A and beta-carotene in dam blood and liver reflected the level of supplementation. No difference in feed intake or body weight was observed. Although mean litter size was similar for all groups, mean pup weight at birth was lowest for deficient rats. Pup mortality through 2 wk postpartum was lower for groups receiving higher levels of either vitamin A or beta-carotene. However, supplemental beta-carotene did not influence growth or reproductive performance. Therefore, low intakes in vitamin A or beta-carotene had no effect on feed intake, growth or reproduction in female rats but decreased fetal growth and increased mortality among pups. 相似文献
5.
Zhou X Xie M Niu C Sun R 《Comparative biochemistry and physiology. Part A, Molecular & integrative physiology》2003,135(2):263-270
We studied the effect of dietary vitamin C on growth, liver vitamin C and serum cortisol levels in stressed and unstressed juvenile soft-shelled turtles. Turtles were fed with vitamin C supplementation at dosages of 0, 250, 500, 2500, 5,000 or 10,000 mg/kg diet for 4 weeks. Vitamin C supplementation exerted significant effects on specific growth rate and liver vitamin C concentrations. The specific growth rate peaked in the group fed at 500 mg/kg diet, while liver vitamin C levels increased with increasing dietary vitamin C levels. Serum cortisol concentrations did not differ between groups of turtles fed diets supplemented with vitamin C in the range of 0-10,000 mg/kg. After acid stress, hepatic vitamin C levels were unaffected, while serum cortisol in the control group was significantly elevated (P<0.01). The other five groups of turtles did not show significant changes in serum cortisol compared with pre-stress levels. 相似文献
6.
Effect of dietary vitamin C on the growth performance and innate immunity of juvenile cobia (Rachycentron canadum) 总被引:1,自引:0,他引:1
This study was conducted to evaluate the effects of dietary vitamin C on growth performance, hematologic parameters and innate immune responses in juvenile cobia, Rachycentron canadum. Seven practical diets were formulated to contain 0.0 (as the basal diet), 13.6, 27.2, 54.4, 96.6, 193.4 and 386.5 mg ascorbic acid equivalent kg(-1) diet. Each diet was fed to triplicate groups of juvenile cobia with initial body weight of 5.5 g in 500-L cylindrical fiberglass tank. The results of 8 weeks feeding trial showed that typical vitamin C-deficient signs such as spinal deformation and body nigrescence were observed in the fish fed the basal diet. Fish fed the basal diet had significantly lower weight gain, specific growth rate (SGR), protein efficiency ratio (PER) and feed efficiency (FE) than those fed the diets supplemented with vitamin C, but no significant differences were observed among diets supplemented with vitamin C. However, survival rate was significantly affected by the dietary vitamin C levels, fish fed the basal diet had lower survival rate than those fed the diets supplemented with vitamin C. The ascorbic acid concentration in liver was correlated positively with the dietary vitamin C levels, however, the thiobarbituric acid reactive substances (TBARS) concentrations in liver was not significantly affected by the dietary vitamin C levels, although, fish fed the basal diet had the highest TBARS values among all treatments. The activities of serum lysozyme, superoxide dismutase (SOD), alkaline phophatase (AKP) and total immunoglobulin (Ig) were significantly influenced by the dietary vitamin C levels, fish fed the basal diet had lower lysozyme, SOD, AKP and total Ig than those fed diets supplemented with vitamin C. The serum glucose and triglyceride concentrations were significantly affected by the dietary vitamin C levels. Fish fed the basal diet had lower red blood cell and hemoglobin values than those fed the vitamin C supplemented diets. The challenge experiment with Vibrio harveyi showed that lower cumulative survival was in fish fed the unsupplemented diet, the cumulative survival were significantly increased with increase of the dietary ascorbic acid levels from 13.6 to 96.6 mg kg(-1), while the cumulative survival reached plateau when dietary ascorbic acid levels increased from 96.6 to 386.5 mg kg(-1). These results indicated that dietary vitamin C did significantly influence on growth performance and immune response of juvenile cobia. 相似文献
7.
Effect of physical restraint on oxidative stress in mice fed a selenium and vitamin E deficient diet
Physical restraint has been associated with increased oxidative damage to lipid, protein, and DNA. The purpose of this experiment
was to determine whether physical restraint would further exacerbate oxidative stress in mice fed a selenium (Se) and vitamin
E (VE) deficient diet. Three-week-old mice were fed a Torula yeast diet containing adequate or deficient Se and VE. Menhaden
oil was added to the deficient diet to impose an additional oxidative stress. After 4 wk feeding, half the mice in each group
were restrained for 5 d in well-ventilated conical tubes for 8 h daily. Mice fed the Se and VE deficient diets had increased
liver thiobarbituric acid-reactive substance (TBARS) levels and decreased liver glutathione peroxidase (GPX1) activity and
α-tocopherol levels. Plasma corticosterone levels were elevated in restrained mice fed the deficient diet compared to unrestrained
mice fed the adequate diet. Restraint had no effect on liver TBARS or α-tocopherol levels. Liver GPX1 activity, however, was
lower in restrained mice fed the adequate diet. In addition, liver superoxide dismutase (SOD) activity was lower in the restrained
mice fed the adequate or deficient diet. Thus, under our conditions, Se and VE deficient diet, but not restraint, increased
lipid peroxidation in mice. Restraint, however, decreased antioxidant protection in mice due to decreased activities of GPX1
and SOD enzymes. 相似文献
8.
We have studied the effects of dietary vitamin E supplement on the clinical signs and pathological changes in GAD (gracile axonal dystrophy) mice. The control diet contained 2 mg of dl-alpha-tocopheryl acetate (2 I.U.) and vitamin E-supplemented diet contained 58.5 mg of dl-alpha-tocopheryl nicotinate (50 I.U.), per 100 mg of feed. The diet was given to normal (gad/+) and GAD (gad/gad) mice from 21 to 130 days of age. During the feeding, there was no improvement in clinical signs in the GAD mice fed the vitamin E-supplemented diet. The gracile nucleus of the medulla oblongata and the gracile fascicules of the spinal cord were investigated for pathology at 130 days of age, and alpha-tocopherol was also assayed in the serum, liver, brain and spinal cord at that time. There were no pathological differences in the gracile nucleus and fascicules between the GAD mice fed the control and vitamin E-supplemented diet. The alpha-tocopherol levels in the serum and target organs in the control GAD mice were not significantly different from those in control normal mice, showing that GAD mice could absorb and transport alpha-tocopherol. In the supplemented GAD mice, no significant increases in alpha-tocopherol levels were observed in the liver, brain or spinal cord. Particularly, the percentage increase of alpha-tocopherol level in the liver of GAD mice was very low in comparison with that in normal mice, even though the liver can store vitamin E. Thus it may be that the capacity to store vitamin E is lowered in GAD mice. Further studies are needed to investigate in detail the vitamin E metabolism in the mutant mice. 相似文献
9.
目的: 探讨利拉鲁肽联合维生素D对高脂诱导非酒精性脂肪肝(NAFLD)小鼠的影响及其潜在机制。方法: C57BL/6小鼠随机平均分为对照组、NAFLD模型组、利拉鲁肽组、维生素D组和利拉鲁肽联合维生素D组,每组10只。对照组普通饲料连续喂养12 周; 模型组高脂饲料连续喂养12周; 利拉鲁肽组、维生素D组和联合组均高脂饲料连续喂养12周, 从第9周起上述3组小鼠分别腹腔注射0.6 mg/(kg·d)利拉鲁肽、灌胃250 mg/(kg·d)维生素D和腹腔注射0.6 mg/(kg·d)利拉鲁肽及灌胃250 mg/(kg·d)维生素D。喂养至12周后,收集各组小鼠血液和肝组织进行生化及病理检测;并采用免疫印迹方法检测各组小鼠肝组织AMP活化蛋白激酶(AMPK)磷酸化水平。结果: 与模型组相比,利拉鲁肽或维生素D单独或联合治疗均可改善NAFLD小鼠肝脏脂质积累(甘油三酯: 6.0±0.7 vs 3.8±0.3, 3.9±0.3和2.1±0.2,P均<0.05;胆固醇:1.4±0.5 vs 0.9±0.2, 0.8±0.2和0.5±0.1,P均<0.05)和脂肪变性(NAFLD活动评分:2.4±0.3 vs 1.0±0.2, 0.9±0.1和0.6±0.1,P均<0.05);此外与利拉鲁肽或维生素D组相比,利拉鲁肽联合维生素D治疗效果更明显,而且可能与调节胰岛素抵抗和AMPK磷酸化相关。结论: 结果表明,维生素D可增强利拉鲁肽对高脂诱导NAFLD的治疗效果,其机制可能与调节胰岛素抵抗和AMPK磷酸化有关。 相似文献
10.
Ping-Hsiao Shih Yin-Ching Chan Jiunn-Wang Liao Ming-Fu Wang Gow-Chin Yen 《The Journal of nutritional biochemistry》2010,21(7):598-605
In the present study, we evaluated the beneficial effect of mulberry extracts (ME), which are rich in phenolics and anthocyanins, on the induction of antioxidant enzymes and on the promotion of cognition in senescence-accelerated mice (SAMP). Six-month old SAMP8 and SAMR1 mice were fed a basal diet supplemented with 0.18% and 0.9% ME for consecutive 12 weeks. The results showed that the mice fed the ME supplement demonstrated significantly less amyloid β protein and showed improved learning and memory ability in avoidance response tests. ME-treated mice showed a higher antioxidant enzyme activity and less lipid oxidation in both the brain and liver, as compared to the control mice. Furthermore, treatment with ME decreased the levels of serum aspartate aminotransferase, alanine aminotransferase, triglyceride and total cholesterol that increase with ageing. The hepatoprotective effect of ME appeared to occur through a mechanism related to regulation of the mitogen-activated protein kinases and activation of the nuclear factor-erythroid 2 related factor 2, where the latter regulates the induction of phase 2 antioxidant enzymes and reduction of oxidative damage. Overall, supplementation of ME might be advantageous to the induction of an antioxidant defense system and for the improvement of memory deterioration in ageing animals. 相似文献
11.
Effect of genistein supplementation on tissue genistein and lipid peroxidation of serum, liver and low-density lipoprotein in hamsters 总被引:4,自引:0,他引:4
The aim of this study was to investigate the effects of genistein supplementation in a vitamin E-deficient diet on the genistein concentrations and the lipid oxidation of serum, liver and low-density lipoprotein (LDL) of hamsters. Thirty-six male hamsters were randomly divided into three groups and fed a vitamin E-deficient semisynthetic diet (AIN-76) containing different levels of genistein, i.e., G0 (control group, genistein-free diet), G50 (50 mg genistein/kg diet) and G200 (200 mg genistein/kg diet) for 5 weeks. The concentrations of genistein in serum and liver significantly increased with the increase of genistein supplementation. The vitamin E contents in LDL were higher in hamsters fed G50 or G200 diets than in hamsters fed genistein-free diet. Genistein supplementation to hamsters significantly reduced the propagation rate during conjugated diene formation of LDL oxidation, and the lag time of LDL oxidation in hamsters fed G200 diets was significantly lower than that of G0 diets. In addition, genistein supplementation significantly raised serum total antioxidant capacity and decreased the thiobarbituric acid-reactive substances (TBARS) of LDL and liver in hamsters. However, no significant differences in TBARS were found in serum, irrespective of genistein addition. On the other hand, the relative contents of polyunsaturated fatty acids in LDL were decreased after genistein supplementation. There was a negative correlation between lag time and P/S ratio, and a positive correlation between lag time and vitamin E contents. These data demonstrate that genistein supplementation markedly increased its concentrations in body tissues and reduced oxidative stress of lipid oxidation of serum, liver and LDL. 相似文献
12.
Toxoplasmosis, particularly toxoplasmic encephalitis, has emerged as a major cause of morbidity and mortality in patients with acquired immunodeficiency syndrome. Patients infected with human immunodeficiency virus typically experience chronic oxidative stress, and concurrent infection with the intracellular parasite Toxoplasma gondii would be expected to further exacerbate this condition. The present study was conducted to determine whether vitamin E and selenium supplementation might be beneficial in a murine model of toxoplasmosis. To investigate the effect of these antioxidants on the severity of parasitic infection. Swiss Webster (SW) or C57Bl/6J mice infected with oocysts of the ME49 strain of T. gondii were maintained on diets containing no vitamin E or selenium, no vitamin E and 8 ppm selenium, 400 IU/kg vitamin E plus 8 ppm selenium, or vitamin E and selenium at the levels present in standard rodent chow (16 IU/kg and 0.2 ppm, respectively). The results of the study showed that increased dietary supplementation with vitamin E and selenium resulted in trends toward increased tissue cyst number, tissue pathology, and weight loss during infection. In contrast, both resistant SW and susceptible C57Bl/6J mice fed a deficient diet (complete absence of vitamin E and selenium) showed the lowest mean numbers of tissue cysts and very little evidence of tissue pathology during chronic infection. 相似文献
13.
Ibrahim W Lee US Szabo J Bruckner G Chow CK 《The Journal of nutritional biochemistry》1999,10(11):674-678
The purpose of this study was to determine the effects of dietary fat, vitamin E, and iron on oxidative damage and antioxidant status in kidneys of mice. Sixty 1-month-old male Swiss-Webster mice were fed a basal vitamin E-deficient diet that contained either 8% fish oil + 2% corn oil or 10% lard with or without 1 g all-rac-alpha-tocopherol acetate or 0.74 g ferric citrate per kilogram of diet for 4 weeks. Significantly (P < 0.05) higher levels of lipid peroxidation products, thiobarbituric acid reactants (TBAR), and conjugated dienes were found in the kidneys of mice fed with fish oil compared with mice fed lard irrespective of vitamin E status. Mice maintained on a vitamin E-deficient diet had significantly higher renal levels of TBAR, but not conjugated dienes, than the supplemented group. Fish oil fed mice receiving vitamin E supplementation had lower levels of alpha-tocopherol than did mice in the lard fed group. Significantly higher levels of ascorbic acid were also found in the kidneys of mice fed with fish oil than were found in mice fed lard. The levels of protein carbonyls and glutathione (GSH), and activities of catalase, superoxide dismutase, selenium (Se)-GSH peroxidase, and non-Se-GSH peroxidase were not significantly altered by dietary fat or vitamin E. Dietary iron had no significant effect on any of the oxidative stress and antioxidant indices measured. The results obtained provide experimental evidence for the pro-oxidant effect of high fish oil intake in mouse kidney and suggest that dietary lipids play a key role in determining cellular susceptibility to oxidative stress. 相似文献
14.
Mohamed AI Hussein AS Bhathena SJ Hafez YS 《The Journal of nutritional biochemistry》2002,13(7):435-441
The effect of dietary fats with varying degrees of unsaturation in the presence of different concentrations of vitamin E on tissue lipid levels was studied in rats. Rats were fed either menhaden oil, olive oil or coconut oil at 15% levels with either 0.1, 0.3 or 0.6 mg/g of vitamin E as alpha-tocopherol for four weeks. Rat serum and liver were analyzed for total cholesterol, HDL-cholesterol, triacylglycerol and phospholipids. In addition, fatty acid composition of serum lipids was also analyzed. Serum total cholesterol and triacylglycerol were significantly lower in rats fed menhaden oil than in those fed olive or coconut oil, while the HDL-cholesterol was significantly higher in serum of rats fed menhaden and olive oil than in those fed coconut oil. Levels of vitamin E in the diet had only a significant effect on serum cholesterol and liver phospholipids. The Pearson correlation coefficient showed a significant positive relationship between serum triacylglycerol and total cholesterol, and a negative correlation between triacylglycerol and HDL-cholesterol, and between total and HDL-cholesterol.In the liver, total cholesterol was significantly higher in rats fed coconut oil than in rats fed menhaden oil. Total liver phospholipids were lower in rats fed either coconut oil or olive oil compared to those fed menhaden oil, especially with higher levels of vitamin E intake. Higher levels of vitamin E in the diet appear to increase triacylglycerol and phospholipids in livers of rats fed menhaden oil. In the liver a significant negative correlation was observed between phospholipids and cholesterol. The type and degree of unsaturation (polyunsaturated fatty acids in menhaden oil, monounsaturated fatty acids in olive oil and saturated fatty acids in coconut oil) significantly affected plasma and tissue lipids. 相似文献
15.
Palsdottir V Olsson B Borén J Strandvik B Gabrielsson BG 《Prostaglandins, leukotrienes, and essential fatty acids》2011,85(3-4):179-188
We have previously reported that essential fatty acid deficiency (EFAD) during suckling in mice resulted in an adult lean phenotype and a resistance to diet-induced obesity. We now hypothesized that postnatal EFAD would cause long-term effects on lipid metabolism. C57BL/6 mice were fed an EFAD or a control diet from the 16th day of gestation and throughout lactation. The pups were weaned to standard diet (STD) and at 15 weeks of age given either high fat diet (HFD) or STD. Lipoprotein profiles, hepatic lipids, fatty acids and mRNA expression were analyzed in 3-week-old and 25-week-old offspring. At weaning, the EFAD pups had higher cholesterol levels in both plasma and liver and 6-fold higher concentrations of hepatic cholesterol esters than control pups. Adult EFAD offspring had higher levels of hepatic cholesterol and linoleic acid, but lower levels of dihomo-γ-linolenic acid and Pparg mRNA expression in the liver. In addition, HFD fed EFAD offspring had lower plasma total cholesterol, lower hepatic triglycerides and lower liver weight compared to controls fed HFD. In conclusion, early postnatal EFAD resulted in short-term alterations with increased hepatic cholesterol accumulation and long-term protection against diet-induced liver steatosis and hypercholesterolemia. 相似文献
16.
H. Wen A. S. Yan Q. Gao M. Jiang Q. W. Wei 《Zeitschrift fur angewandte Ichthyologie》2008,24(5):534-538
The present experiment was conducted to determine the dietary vitamin A requirement of juvenile Amur sturgeon (Acipenser schrenckii) by formulating seven semipurified diets containing 10, 258, 510, 1050, 2020, 4100 and 8300 IU vitamin A (as retinol acetate) kg?1 diet, respectively. Each experimental diet was fed to triplicate groups of 20 juveniles each with initial average weights of 12.09 ± 0.22 g in 405‐L aquaria and maintained at 25.0 ± 2.0°C for 8 weeks. Fish fed the basal diet (10 IU vitamin A kg?1 diet) exhibited poor appetite and activity, whereas these signs were not observed in any group fed vitamin A‐supplemented diets. Weight gain, feed efficiency and hepatosomatic index increased significantly with increases in the dietary vitamin A level, reaching a peak with the vitamin A 1050 IU kg?1 diet, and then decreasing. Muscle chemical compositions were not affected by the dietary vitamin A levels. Vitamin A concentrations in liver and muscle increased significantly as the vitamin A levels increased within a range of 10~4100 IU kg?1 diet; above this level there were no significant changes. Broken‐line regression analysis of weight gain and liver vitamin A concentration against the dietary vitamin A level showed that juvenile Amur sturgeon required a minimum of 923 IU vitamin A kg?1 in the diet for maximal growth, and 1981 IU kg?1 for highest liver vitamin A accumulation. 相似文献
17.
A possible role of intracellular Ca2+ and participation of calmodulin in cellular metabolism in endotoxin-poisoned mice were investigated. The levels of calcium in liver cytosol and liver mitochondria fractions in poisoned mice were markedly higher 18-48 hr after endotoxin injection than in the control mice. On the other hand, the levels of serum calcium in the poisoned mice were about 20% lower at 18 hr than in the controls. The serum calcium levels in mice injected with 50 and 100 micrograms of endotoxin showed no dose-response effect, but a dose-response effect was observed at a dose of 200-400 micrograms. The serum Ca2+ levels in endotoxin-tolerant mice were similar to those in the control mice. The levels in mice injected with glucocorticoid-antagonizing factor mice were about 14% lower at 3 hr than in the controls. The mice fed a vitamin D3- and calcium-free diet showed a higher mortality rate in the early stage (12-18 hr) of endotoxication than that of the mice fed a normal diet. The lipid peroxide levels and Ca2+-ATPase activity in the liver mitochondria fraction in endotoxin-poisoned mice showed a higher level than those of the control mice. There was little or no difference in the levels of serum glucose between the mice injected with calmodulin antagonist (trifluoperazine, TFP) plus endotoxin and those given endotoxin alone. However, the liver glycogen levels in TFP plus endotoxin-treated mice were markedly higher than that in mice given endotoxin alone. Furthermore, calcium antagonist (verapamil) plus endotoxin-treated mice had about a 40% higher survival rate after 72 hr than those given endotoxin alone. The findings suggest that there is a possibility of participation of the Ca2+-calmodulin system in carbohydrate metabolic disorders during endotoxemia and that the changes in intracellular Ca2+ may result in various metabolic disorders. 相似文献
18.
Several oxidative stressors (dietary selenium deficiency, dietary vitamin E deficiency coupled with fish oil feeding, genetic reduction of glutathione peroxidase activity) allow a normally benign coxsackievirus B3 (CVB3/0) to damage heart muscle in host mice. This study investigated whether dietary iron overload, another oxidant stress, would also permit CVB3/0 to exert a cardiopathologic effect in vitamin E-deficient (-VE) mice. Four groups of mice were fed either a -VE or a +VE diet containing either an adequate or an excessive (30x) amount of iron. After 4 weeks of feeding, the mice were inoculated with CVB3/0 and heart damage was assessed at various times postinfection. Mice fed a diet sufficient in VE with excess iron developed heart damage equivalent to mice fed a diet deficient in vitamin E without excess iron. However, severe heart damage occurred in the group fed a diet deficient in VE with excess iron, which was the most pro-oxidative diet. The highest heart viral titers were found in mice fed the -VE/excessive iron diet. However, the extent of heart damage did not always correlate with the formation of TBARS in liver homogenates. Further research is needed to clarify the role of oxidative stress and iron overload in determining the course of viral infection. 相似文献
19.
Iron status in rats fed a purified diet without vitamin A 总被引:3,自引:0,他引:3
A. C. Beynen K. W. Sijtsma G. J. Van Den Berg A. G. Lemmens C. E. West 《Biological trace element research》1992,35(1):81-84
The effect of vitamin A deficiency on iron status was investigated in rats. After 28 d of feeding either low or high vitamin
A diets (0 vs 4000 IU of vitamin A per kg feed), the final body weight was slightly but significantly lowered by the low vitamin
A diet. Plasma retinol concentrations were decreased in rats fed diets low in vitamin A. Marginal vitamin A deficiency produced
slightly, but significantly lower blood hemoglobin concentrations; it did not clearly affect hematocrit. The concentration
of iron in liver was significantly higher when diets low in vitamin A were fed while significantly lower levels were observed
in femur. 相似文献
20.
The influence of dietary vitamin E and Santoquin on lipid peroxidation and liver regeneration in partially-hepatectomized rats was studied. Rats were fed either a basal 10% tocopherol-stripped corn oil diet, the basal diet plus 40 mg dl-alpha-tocopheryl acetate/kg, or the basal diet plus 2 g Santoquin (6-ethoxy-1,2-dihydro-2,2,4-trimethylquinoline)/kg. After 6 weeks, rats fed the antioxidant-deficient diet produced more of the lipid peroxidation product, pentane, than did the rats fed antioxidants. Partial hepatectomy was performed after six and one-half weeks or ten weeks of feeding the diets. At 3 and 6 days after surgery, pentane production was significantly elevated over pre-surgery levels in rats fed the antioxidant-deficient or vitamin E-supplemented diets, but not in rats fed the Santoquin-supplemented diet. Six days after surgery, there were fewer thiobarbituric acid reactants in regenerating liver of Santoquin-fed rats than of vitamin-E fed rats or antioxidant-deficient rats. There was no increase in the 6-day level of thiobarbituric acid reactants over the 3-day level in livers of rats fed Santoquin, while there was an increase in livers of the antioxidant-deficient and vitamin E-supplemented rats. Liver sulfhydryl levels were higher at 3 and 6 days post surgery in the Santoquin-fed rats than in the antioxidant-deficient or vitamin E-supplemented rats. Plasma gamma-glutamyl-transpeptidase activity was not different among the groups of rats. Between the third and sixth day following surgery, liver regeneration was significantly stimulated in Santoquin-fed, but not vitamin E-fed rats. After 11 days, a stimulatory, but not statistically significant, effect of vitamin E was found. Although DNA content of liver was higher at 6 days than at 3 days post surgery, it was not different among the dietary groups, indicating that cell proliferation rather than hypertrophy had occurred. Partial hepatectomy could have altered the ability of the liver to metabolize pentane, thus explaining part of the increased production of pentane. However, the results obtained support the interpretation that elevated levels of dietary antioxidants can be beneficial in terms of reduced lipid peroxidation and increased rates of liver regeneration following liver surgery. 相似文献