Green tea catechin improves microsomal phospholipase A2 activity and the arachidonic acid cascade system in the kidney of diabetic rats

The purpose of this study was to investigate the effects of green tea catechin on the microsomal phospholipase A2 activity and arachidonic acid cascade in the kidneys of streptozotocin-induced diabetic rats. Sprague-Dawley male rats weighing 100 +/- 10 g were assigned randomly to one normal and three streptozotocin-induced diabetic groups. The diabetic groups were the DM-0C group (n = 10), fed a catechin-free diet, the DM-0.25C group (n = 10), fed a 0.25 g catechin per 100 g diet, and the DM-0.5C group (n = 10), fed a 0.5 g catechin per 100 g diet. The kidney microsomal phospholipase A2 activity was higher in the diabetic groups than in the normal group, while it was lower in the DM-0.25C and DM-0.5C groups than in the DM-OC group. The percentage of phosphatidylcholine hydrolysed in the kidney microsomes was not significantly different between any of the four groups. The percentage of phosphatidylethanolamine hydrolysed in the kidney microsomes was progressively higher in the DM-0.5C, DM-0.25C and DM-OC groups, respectively, compared to the normal group. The formation of thromboxane A2 was significantly higher while the formation of prostacyclin was lower in kidney microsomes of the streptozotocin-induced diabetic groups compared with the normal group, but this condition was improved by catechin supplementation. Kidney microsomal vitamin E concentrations were progressively lower in the DM-0.5C, DM-0.25C, and DM-0C groups, respectively, compared to the normal group. The kidney thiobarbituric acid reactive substance (TBARS) contents became higher in the DM-0C and DM-0.25C groups as compared with the normal group, whereas the DM-0.5C group did not differ from the normal group. Kidney function appears to be improved by green tea catechin supplementation due to its antithrombus action, which in turn controls the arachidonic acid cascade system.     

Effects of green tea catechin on prostaglandin synthesis of renal glomerular and renal dysfunction in streptozotocin-induced diabetic rats

The purpose of the present study was to investigate the effects of green tea catechin on prostaglandin synthesis of renal glomerular and renal dysfunction in rats with streptozotocin-induced diabetes. Sprague-Dawley rats weighing 100 +/- 10 g were randomly assigned to one normal group and three groups with streptozotocin-induced diabetes. The diabetic groups were classified to a catechin-free diet (DM group), a 0.25% catechin diet (DM-0.25C group) and a 0.5% catechin diet (DM-0.5C group) according to the levels of catechin supplement in their diet. The animals were maintained on an experimental diet for 4 weeks. At this point, they were injected with streptozotocin to induce diabetes. They were killed on the sixth day. The catechin supplementation groups (DM-0.25C, DM-0.SC groups) showed a decrease in thromboxane A2 synthesis but an increase in prostacyclin synthesis, compared to the DM group. The ratio of prostacyclin/thromboxane A2 was 53.3% and 38.1% lower in the DM and DM-0.25C groups, respectively, than in the normal group. The ratio in the DM-0.5C group did not differ from that in the normal group. The glomerular filtration rate in catechin feeding groups (DM-0.25C and DM-0.5C groups) was maintained at the normal level. The urinary beta2-microglobulin content in the DM-0.5C group was significantly lower than that in the normal group. On the sixth day after induction of diabetes, the urinary microalbumin content in the DM, DM-0.25C and DM-0.5C groups had increased 5.40, 4.02, 3.87 times, respectively, compared with the normal group. In conclusion, kidney function appears to be improved by green tea catechin supplementation due to its antithrombotic action, which in turn controls the arachidonic acid cascade system.     

Effects of green tea catechin on phospholipase A2 activity and antithrombus in streptozotocin diabetic rats.

The purpose of this study was to investigate the effects of dietary green tea catechin on phospholipase A2 (PLA2) activity and the antithrombotic reaction of platelets in streptozotocin (STZ)-diabetic rats. Sprague-Dawley male rats weighing 100 +/- 10 g were randomly divided into one normal and three STZ-diabetic groups, which were subdivided into catechin-free group (DM-0C), 0.5% catechin group (DM-0.5C) and 1% catechin group (DM-1C). The activity level of platelet phospholipase A2 was higher in the diabetic groups than in the normal group, while it was lower in DM-0.5C and DM-1C than in DM-0C. The activity of platelet cyclooxygenase in DM-0C was 1.1-fold as high as in the normal group, but was significantly reduced by catechin supplementation. The platelet thromboxane A2 (TXA2) formation became higher in DM-0C as compared to the normal group, but not in DM-0.5C and DM-1C. The synthesis of aortic prostacyclin (PGI2) was lower in DM-0C and DM-0.5C than in the normal group. The PGI2/TXA2 ratio was decreased to 55% in DM-0C, but was restored by catechin supplementation. These results indicate that STZ-diabetic rats are sensitive to platelet aggregation and thrombosis, and that the abnormality can be improved by dietary catechin.     

Effects of vitamin E on renal dysfunction in chronic cadmium-poisoned rats

Cadmium is a highly toxic metal that can be ingested or inhaled from a variety of industrial and dietary sources. The purpose of this study was to investigate the effects of vitamin E on renal dysfunction and blood pressure changes in chronic cadmium-poisoned rats. Sprague-Dawley rats weighing 100 +/- 10 g were randomly assigned to one control group and three cadmium-poisoned groups. Cadmium groups were assigned to dietary groups according to levels of vitamin E supplementation: vitamin E-free diet (Cd-0E group), 40 mg of vitamin E/kg of diet (Cd-40E group), and 400 mg of vitamin E/kg of diet (Cd-400E group). The animals were raised for 20 weeks, and cadmium was supplied in the drinking water at 50 ppm Cd(2+). The morphological changes observed by both light and electron microscopy revealed mitochondria and tubule epithelial cell edema in the Cd-0E group, yet this was alleviated with the highest level of vitamin E supplementation (Cd-400E group). The urinary beta(2)-microglobulin levels indicated that glomerular injury was higher in the Cd-poisoned groups than in the control group, but were lowered by vitamin E supplementation. Although the glomerular filtration rate (GFR) of the Cd-0E group was significantly lower than that of the control group, the vitamin E-supplemented groups exhibited a similar GFR to the control group, suggesting that vitamin E protected the kidney from functional damage. Angiotensin converting enzyme activity, and blood pressure, and heart rate were all significantly higher in the Cd-poisoned group, but each remained nearly normal with vitamin E supplementation. Accordingly, these results indicate that vitamin E supplementation in chronic cadmium-poisoned rats normalized renal dysfunction and blood pressure regulation.     

Effects of vitamin E on toxicity by minute amounts of paraquat fed continuously to rats

The effects of vitamin E on toxicity by minute amounts of paraquat fed continuously for some period to rats were investigated. Two experiments were carried out as experiments 1 and 2. In both experiments, weaning rats were divided at first into two groups; one group was given a vitamin E-deficient diet, and the other a vitamin E-supplemented control diet (50 mg alpha-tocopherol/kg of diet). They were fed on these diets for 40 days. After that, in both experiments, the rats that had been fed the vitamin E-deficient diet were further divided into two groups, which were either given a paraquat-added diet (+PQ-E) or continuously fed the same vitamin E-deficient diet (-E). The amount of paraquat added was 250 mg of methyl viologen per kg of diet. After the addition of paraquat, these two groups were pair-fed. In experiment 1, paraquat was given to all the rats fed the vitamin E-supplemented control diet (+PQ+E). In experiment 2, rats fed the control diet were divided into paraquat-added (+PQ+E) and non-paraquat-added (+E) groups, similar to those of vitamin E-deficient rats. These two groups were also pair-fed thereafter. In both experiments, about 35 days after paraquat addition, they were sacrificed. Plasma and liver alpha-tocopherol contents were measured by HPLC, and liver peroxidation value was measured by chemiluminescence and the TBA method. And, as parameters of vitamin E deficiency, plasma pyruvate kinase and GOT activities and alpha-cysteine proteinase inhibitor (alpha-CPI) level were measured. When the analyzed values were compared between paraquat-added and the corresponding not-added control groups (+PQ-E vs. -E, +PQ+E vs. +E), the following results were obtained. In experiment 1, the values of plasma and liver alpha-tocopherol levels were significantly lower in the +PQ-E group than those of the -E group; however, liver peroxidation values and values of the three parameters of vitamin E deficiency were not different significantly. In experiment 2, the value of liver alpha-tocopherol level was significantly lower in the +PQ+E group than that of the +E group.(ABSTRACT TRUNCATED AT 400 WORDS)     

The influence of linoleate and vitamin E from sunflower seed oil on platelet function and prostaglandin production in the common marmoset monkey

Vitamin E and linoleate, both of which are found in high concentrations in sunflower seed oil, were examined independently for their influence on general and blood-vascular parameters in vitamin E-deficient common marmosets. A vitamin E-deficient diet (-E, 4 micrograms/g) was supplemented with either 40 micrograms/g vitamin E (+E), vitamin E stripped sunflower oil (+10% SSO-E), or SSO (+10% SSO w/w) in a 2 x 2 factorial designed experiment, and the diets fed for 9 months to 4 even groups of common marmosets. Vitamin E deficiency was associated in marmosets with a loss of skeletal muscle mass and of body weight, enhanced peroxidative haemolysis of erythrocytes, increased white blood cell counts, and in the SSO-E group a relative neutrophilia. Platelet reactivity was increased with vitamin E deficiency, and to a greater degree with the SSO-E group. Aortic prostacyclin production was significantly increased by the addition of vitamin E, linoleate and both as SSO to the deficient diet, the effects being additive. Fatty acid changes associated with the different treatments reflected the influence of high linoleate and vitamin E treatments. The platelet and aortic arachidonate value in the SSO-E group showed the lowest and most variable value, and this was associated with greatest platelet aggregability. An adequate vitamin E intake is essential for stabilising high PUFA diets and biomembranes and enhancing the protective role of prostacyclin in blood vessels against thrombogenesis.     

持续性硬膜外阻滞对妊娠高血压综合征患者血管活性因子的影响

目的探讨持续性硬膜外阻滞前后妊娠高血压综合征(简称“妊高征”)患者外周血血管活性因子一氧化氮(NO)、内皮素(ET)、前列环素(PGI2)、血栓素(TXA2) 水平的变化。方法选择剖宫产的妊高征孕妇(PIH组)和正常晚期妊娠孕妇(NLP组) 各30例,分别于硬膜外阻滞前及阻滞完善后测血压并抽取静脉血,测定外周血中NO、ET、 PGI2及TXA2的浓度变化。结果阻滞前PIH组NO和PGI2浓度显著低于NLP组 (P<0．01);而ET和TXA2浓度明显高于NLP组(P<0．01);阻滞后PIH组和NLP组NO、 PGI2浓度显著高于阻滞前(P<0．01);而ET和TXB2浓度麻醉前、后比较,差异无显著性 (P<0．05)。结论血浆中NO、PGI2浓度降低,ET、TXA2浓度升高是妊高征发病的重要原因之一;持续性硬膜外阻滞可使孕妇体内血管舒张因子(NO、PGI2)水平上升,而对血管收缩因子(ET,TXA2)影响不明显,可安全应用于妊高征孕妇剖宫产手术麻醉中。     

Kidney injury induced by lipid peroxide produced by vitamin E deficiency and GSH depletion in rats

Four-week-old Wistar male rats were fed a vitamin E (VE)-deficient (0E) or a VE-sufficient (10E) diet for 6 weeks and then intraperitoneally treated with buthionine sulfoximine (BSO) at 1 mmol/kg body weight once a day for 3 days. Glutathione (GSH) depletion by BSO treatment caused injuries especially in the kidneys of VE-deficient rats. The kidney weight increased in the VE-deficient rats after BSO treatment (0E-BSO). It was observed that the epithelial cells of the renal tubules in this group were strongly impaired and the injuries were necrosis and desquamation. No injury was observed in the kidneys of the BSO-untreated 0E group and the 10E groups. The TBA value of the kidney of 0E-BSO group was lower than that of the BSO-untreated 0E group, but the lipofuscin content of the kidney of the 0E-BSO group was 10 times higher than that of the BSO-untreated 0E group. These results suggest that the kidney injuries in rats may be caused by lipid peroxidation induced by vitamin E deficiency and glutathione depletion.     

硒和维生素E对前列环素和血栓素合成的调控机制

前列环素（ＰＧＩ２）和血栓素（ＴＸＡ２）是一对生物功能相反的强烈的细胞生理调节剂，其生物合成是由花生四烯酸经前列腺素合酶催化生成ＰＧＨ２，再在前列环素合酶和血栓素合酶的作用下分别异构为ＰＧＩ２和ＴＸＡ２。由于过氧化物对前列腺素合酶、前列环素合酶和血栓素合酶的催化活性有不同影响，所以能控制体内过氧化物水平的抗氧化剂硒和维生素Ｅ对ＰＧＩ２和ＴＸＡ２的合成具有调控作用。硒和维生素Ｅ缺乏促进ＰＧＩ２／ＴＸＡ２比值下降，补硒和维生素Ｅ可以纠正这种作用     

Dietary vitamin E supplementation does not inhibit Candida albicans intestinal translocation in rats.

Candida albicans translocation was determined in rats receiving a normal or vitamin E-supplemented and deficient diet submitted to mesenteric ischemia and reperfusion (MIR). The antioxidant effect of vitamin E on lipid peroxidation was also assessed. The animals were divided into six groups submitted to different diets for 30 d. Groups N, NI, NC and NIC were submitted to a normal diet and used as controls, and groups VITE and DEFE received a vitamin E-supplemented and vitamin E-deficient diet, respectively. Groups NIC, VITE and DEFE were submitted to MIR, inoculated with Candida albicans and sacrificed 24 h after the surgical procedure. The antioxidant effect of vitamin E was determined in the liver and gut mucosa using the TBARS method. Candida albicans translocation was assessed in lymph node, liver and kidney specimens. The results showed that lipid peroxidation was lower (p < 0.05) in the vitamin E-supplemented group. However, vitamin E supplementation did not protect the rats against Candida albicans translocation (the translocation in the Group VITE was 100% for lymph nodes).     

Combined selenium and vitamin E deficiency causes fatal myopathy in guinea pigs

Selenium and vitamin E deficiencies were studied as part of an evaluation of oxidant defenses in guinea pigs. Male guinea pigs (100-120 g) were fed a control diet (C) or the diet without selenium (0 Se), without vitamin E (0 E), or without either selenium or vitamin E (0 Se-0 E). Between d 30 and 35, 7 of 13 guinea pigs fed the 0 Se-0 E diet were euthanized because of severe weakness of their extremities. No guinea pigs in the other diet groups developed weakness. Guinea pigs from each group were killed on d 37. Selenium deficiency and vitamin E deficiency were verified by measurement of glutathione peroxidase and alpha-tocopherol. Creatine phophokinase (CPK) activity was greater than controls in both groups fed vitamin E-deficient diets, but the increase was greater in the 0 Se-0 E group than in the 0 E group. Muscle F(2)-isoprostanes were greater than controls in both groups fed vitamin E-deficient diets with the level in the 0 Se-0 E group greater than that in the 0 E group. Histologic muscle necrosis was severe in the 0 Se-0 E group, minimal in the 0 E group and absent from other groups. The diets used in this study induced selenium and vitamin E deficiencies in guinea pigs. The study demonstrates that combined selenium and vitamin E deficiency results in a fatal myopathy in guinea pigs that is associated with lipid peroxidation in the affected muscle. This nutritional myopathy is much more severe than the myopathy that occurs with vitamin E deficiency alone.     

The influence of dietary vitamin E and calcium status on intestinal tumors in rats.

Male Sprague-Dawley rats were fed from weaning low (1-5 ppm) and normal (26-50 ppm) vitamin E diets for 30-34 weeks. Dietary fat was also varied from 5% (Experiment 1) to 20% (Experiments 2 and 3). Intestinal tumors were induced by 1,2-dimethylhydrazine given subcutaneously as 10 weekly doses at 20 mg/kg body wt. Tumor incidence was lower by 30% and burden was 25%-50% lower for low vitamin E rats than for vitamin E-replete rats. This result was independent of the fat content of the diet. In Experiment 3, vitamin E and calcium were assessed for their influence on intestinal tumors at two levels, with dietary vitamin E at 5 and 50 ppm and calcium at 0.2% and 1.0% in a 2 x 2 factorial experiment. The high calcium-low vitamin E diet produced the greatest fall in tumor incidence and burden relative to the other treatments. In this experiment, vitamin E deficiency reduced tumor incidence and calcium supplementation reduced tumor burden, with a significant interaction of the two. However, this group also showed evidence of reduced food intake and kidney change (calcification), which may have confounded the result. This points to a risk associated with this combination of nutrients at these levels in long-term experiments.     

Effect of green tea catechin on arachidonic acid cascade in chronic cadmium-poisoned rats

The purpose of this study was to investigate the effect of green tea catechin on the cyclooxygenase and lipoxygenase pathways in chronic cadmium-poisoned rats. Sprague-Dawley male rats weighing 100 +/- 10 g were randomly assigned to one normal and three cadmium-poisoned groups. The cadmium groups were classified as catechin-free diet group (Cd-0C), 0.25% catechin diet group (Cd-0.25C) and 0.5% catechin diet group (Cd-0.5C), in accordance with the level of catechin supplement. The phospholipase A2 activity was remarkably increased 117% in the Cd-0C group and 60% in the Cd-0.25C group compared with the normal group, and the level in the Cd-0.5C group was the same as the normal group. Activity of platelet cyclooxygenase increased 284% in the Cd-0C group, 147% in the Cd-0.25C group and 193% in the Cd-0.5C group. The synthesis of platelet thromboxane A2 (TXA2) increased 157% in the Cd-0C group and 105% in the Cd-0.25C group, compared with the normal group. The Cd-0.5C group showed the same level as the normal group. Prostacyclin (PGI2) formation in the aorta decreased 24% in the Cd-0C group and 18% in the Cd-0.25C group. The ratio of PGI2/TXA2, the thrombocyte synthesis index, decreased 70% in the Cd-0C group and 59% in the Cd-0.25C group. The activity of 5'-lipoxygenase in the polymorphonuclear leukocyte was increased 40% in the Cd-0C group as compared with the normal group. Catechin-supplemented Cd-0.25C and Cd-0.5C groups showed the level of the normal group. In this study, the observed content of leukotriene B4, which induces the inflammatory process, increased 54% in the Cd-0C group, and in catechin-supplemented groups, showed the same level as in the normal group. The serum peroxide value increased 60% in the Cd-0C group compared with the normal group; but in the Cd-0.5C group, it showed the level of the normal group. These results indicate that chronic cadmium poisoning in rats accelerates arachidonic acid metabolism. Inhibition of arachidonic acid metabolism due to catechin supplementation, however, decreases platelet aggregation and inflammatory action. In conclusion, it would appear that green tea catechin supplementation in chronic cadmium-poisoned rats inhibits the arachidonic acid cascade by regulating the activity of phospholipase A2.     

Modulation by dietary vitamin E of I-compounds (putative indigenous DNA modifications) in rat liver and kidney

I(indigenous)-compounds are age-related, carcinogen adduct-like, putative indigenous DNA modifications detectable by 32P-postlabeling assay in untreated animals. To investigate the origins of these DNA derivatives, we examined the effects of dietary vitamin E, a natural antioxidant, on I-compounds of rat liver and kidney DNA. Weanling female Sprague-Dawley rats were fed Draper's diets containing 0, 100, 1000, or 10,000 mg/kg alpha-tocopheryl acetate for 6 mo. The DNA from four individual rats of each group was analyzed by a nuclease P1-enhanced version of the 32P-postlabeling assay for DNA adducts. The amount of vitamin E in the liver was measured by high performance liquid chromatography. Rats fed vitamin E-deficient diet (0 mg/kg) showed identical profiles and similar levels of I-compounds as those fed the 100 mg/kg diet. Most I-spots were significantly intensified and one tissue-specific extra spot was found in both liver and kidney DNA of rats fed the 1000 or 10,000 mg/kg vitamin E diet. However, one of the five major I-spots detected in the kidney was weaker in the 1000 and 10,000 mg/kg groups than in the 0 and 100 mg/kg groups. These results show that formation of most I-compounds was not affected by vitamin E-deficient diet, and that long-term feeding of diet containing high levels of vitamin E may cause metabolic alterations leading to an increased formation of DNA-reactive (potentially mutagenic or carcinogenic) electrophiles.     

维生素E等药物抗动脉粥样硬化的作用

目的　探寻维生素E、氨氯地平、辛伐他汀抗动脉粥样硬化 (AS)的共同机制。方法　在高胆固醇饮食基础上建立兔AS模型 ,随机分组 ,检测各组兔主动脉AS面积、全血超氧化物歧化酶 (SOD)活力、血清丙二醛 (MDA)含量及血清脂质浓度。结果　与模型组相比 ,3组用药组主动脉AS面积均显著减少 (P <0 0 1) ,SOD活力明显升高 (P<0 0 1) ,MDA含量下降 (P <0 0 1) ,且以辛伐他汀组变化最显著。辛伐他汀组血清总胆固醇 (TC)、低密度脂蛋白胆固醇 (LDL -C)、甘油三脂 (TG)较模型组显著降低 (P <0 0 1)。结论　脂质过氧化物减少和SOD活力增加可能是维生素E、氨氯地平、辛伐他汀抗AS作用的共同机制。     

Polygonatum rhizoma affects antioxidant defense systems without changing mRNA expression in diet-induced hypercholesterolemic rabbits

This study was conducted to determine the antioxidant effects of a Polygonatum extract compared with the major antioxidant, vitamin E, in rabbits fed a high-cholesterol diet. Rabbits were given a high-cholesterol (0.5%, wt/wt) diet with vitamin E (0.03%, wt/wt) or a Polygonatum extract (0.05%, wt/wt) for 8 weeks. The body weight gain (g/week) was only significantly increased only in the high-cholesterol-fed control group, yet the relative liver weight was significantly lower in the Polygonatum group compared with the other groups. The supplementation of vitamin E and Polygonatum extract led to an increase in the hepatic catalase (CAT) activity without any change in superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) activities. Hepatic total glutathione content was significantly higher in the Polygonatum group than in the other groups. The level of hepatic mitochondrial H(2)O(2) was significantly lower in the two supplemented groups compared with the control group, whereas the level of cytosolic H(2)O(2) was only significantly lower in the Polygonatum group than in the control group. The level of plasma thiobarbituric acid-reactive substances (TBARS) was only significantly lower in the vitamin E group, whereas the level of hepatic TBARS was slightly lower in the Polygonatum group than in the other groups. In the case of the high-density lipoprotein-related antioxidant enzyme, vitamin E supplementation produced the highest plasma paraoxonase (PON) activity compared with the other groups, although there was no difference in the hepatic PON activity among the groups. Meanwhile, the plasma vitamin E concentration was significantly higher in the vitamin E and Polygonatum groups than in the control group; however, plasma vitamin A concentration did not differ significantly between the groups. As regards the mRNA expressions of hepatic antioxidant enzymes, the vitamin E and Polygonatum extract supplementation had no effect on the SOD, CAT, GSH-Px, and PON mRNA expression. Accordingly, these results indicate that the Polygonatum extract had a positive effect on the antioxidant defense system based on decreasing the content of hepatic TBARS and hydrogen peroxide, increasing the CAT activity and total glutathione level in the liver, and sparing the plasma vitamin E. Thus, further studies on the functional components in Polygonatum extract and their biological efficacies are needed.     

Response of B-6 vitamers in plasma, erythrocytes and tissues to vitamin B-6 depletion and repletion in the rat

We determined the response patterns of B-6 vitamers in blood and tissues to vitamin B-6 depletion and repletion. B-6 vitamers were measured in plasma, erythrocytes, liver, muscle, kidney, heart, brain, spleen and lung by reverse-phase high performance liquid chromatography in male rats pair-fed control or vitamin B-6-deficient diets for 2 or 4 wk, or for 4 wk followed by 1 wk of repletion with the control diet (n = 4/group). Food intake (15.6 +/- 0.3 g/d, mean +/- SEM; n = 28) and body weight (190 +/- 2 and 290 +/- 5 g at wk 0 and 5, respectively; n = 28) of control groups were not different from those of deficient groups throughout the study. After 2 wk of vitamin B-6 depletion, tissue concentrations of pyridoxal phosphate (PLP) and pyridoxamine phosphate (PMP) were about 50% and 10-40% lower, respectively, in the deficient than in the control group (except for spleen PMP); in plasma and erythrocytes, PLP and pyridoxal concentrations were about 90% lower in the deficient group. Differences in vitamer concentrations between control and deficient groups were not larger after 4 wk of depletion than after 2 wk. Vitamer concentrations in plasma, erythrocytes and all tissues returned to control levels after 1 wk of repletion with the control diet. These results demonstrate that B-6 vitamers in blood and tissues of the rat respond quickly and reversibly to changes in dietary vitamin B-6, with larger percentage changes occurring in plasma and erythrocytes than in tissues.     

Influence of sesame oil on blood glucose, lipid peroxidation, and antioxidant status in streptozotocin diabetic rats

The present study was carried out to assess the influence of sesame oil on blood glucose, lipid peroxidation, and status of antioxidants in normal and streptozotocin (STZ) diabetic rats. Diabetes was induced in adult female albino Wistar rats weighing 180-200 g by administration of STZ (40 mg/kg of body weight) intraperitonially. Both normal and diabetic rats were fed with a commercial diet containing 2% oil supplemented with 6% sesame oil for 42 days. Diabetic rats had elevated levels of blood glucose (322.61 +/- 9.49 mg/dL), glycosylated hemoglobin, vitamin E, thiobarbituric acid-reactive substances (TBARS), and lipid hydroperoxides and decreased levels of hemoglobin, vitamin C, and reduced glutathione (GSH). An increase in glucose-6-phosphatase and fructose-1,6-bisphosphatase activities and a decrease in hexokinase activity were observed in liver and kidney tissues. When diabetic rats fed with sesame oil were compared with diabetic rats, a significant reduction in levels of blood glucose (222.02 +/- 8.27 mg/dL), glycosylated hemoglobin, TBARS, and lipid hydroperoxides and glucose-6-phosphatase and fructose-1,6-bisphosphatase activities and an elevation in hemoglobin, vitamin E, and GSH levels and hexokinase activity were observed. Thus, sesame oil consumption influences beneficially the blood glucose, glycosylated hemoglobin, lipid peroxidation, and antioxidant levels in diabetic rats.     

Bioavailability of vitamin E in rats fed graded levels of pectin

Dietary pectin at levels of 0, 3, 6 and 8% was fed ad libitum to rats for 8 wk to evaluate whether the bioavailability of vitamin E fed at 0.001% of the diet was affected by pectin. Rats fed 3% pectin were not different in any vitamin E parameters from those fed 0% pectin. By the end of the study body weights were significantly lower in the 6 and 8% pectin groups after adjusting for their nonsignificant trend of lower food intake. At wk 8, liver vitamin E levels were reduced in the 6 and 8% pectin group compared to values at the start of the study. Both groups had significantly higher red blood cell hemolysis compared to 0% pectin at 8 wk. Fecal fat excretion was not different among the diet groups, but weights of the small and large intestines were significantly increased in rats fed 6 or 8% pectin compared to those fed 0 or 3%. Our results show that 6 and 8 but not 3% dietary pectin decreased vitamin E availability in rats.     

氧化固醇对不同硒状态大鼠前列环素和内皮素的影响

目的 :　研究不同硒量下氧化固醇对血浆前列环素 (PGI2 )和内皮素 (ET)水平的影响。方法 :　采用低硒饲料饲养大鼠 1 3 w后 ,从尾静脉注射氧化固醇 (Ch- Ox) 3 β,5 α,6 β-三羟胆固醇 (3 - triol) ,2 4 h后采用放射免疫法测定其血浆 PGI2 、血栓烷 A2 (TXA2 )和 ET水平。结果 :　低硒组血硒含量及谷胱甘肽过氧化物酶 (GSH- Px)活性显著低于对照组 (P<0 .0 1 ) ,血浆 PGI2 水平也显著低于对照组 (P<0 .0 5 ) ,但其血浆脂质过氧化物 (LPO)水平及血浆 TXA2 水平显著高于对照组 (P<0 .0 5和 P<0 .0 1 ) ,从而导致 PGI2 /TXA2 比值显著低于对照组 (P<0 .0 1 )。对照 +3 -triol组血浆 PGI2 、TXA2 及 PGI2 /TXA2 与对照组相比均无显著性差异。虽然低硒 +3 - triol组血浆PGI2 与对照 +3 - triol组相比无显著性差异 ,但其血浆 TXA2 显著高于对照 +3 - triol组 (P<0 .0 0 1 )。低硒组与对照组相比 ,血浆 ET水平略有降低 ,差异不显著。对照组注射 3 - triol后血浆 ET水平显著升高 (P<0 .0 5 ) ,而低硒组注射 3 - triol后血浆 ET显著低于对照 +3 - triol组 (P<0 .0 5 )。给低硒 1 0 w的大鼠饮水补硒可一定程度上减小这些变化。结论 :　低硒和 Ch- Ox影响 PGI2 、TXA2 的浓度 ,使 PGI2 /TXA2 比值降低 ,Ch- Ox还使