Supplementation of fenugreek leaves reduces oxidative stress in streptozotocin-induced diabetic rats

Trigonella foenum-graecum, commonly known as fenugreek, is a traditional medicinal plant of the Leguminoseae family in India. The antioxidant effect of fenugreek leaves was evaluated in the streptozotocin-induced diabetic rat model. The antioxidant effect was evaluated by estimating thiobarbituric acid-reactive substances and reduced glutathione and measuring the activities of catalase and superoxide dismutase in liver, heart, and kidney in diabetic rats. Fenugreek leaf powder supplementation significantly lowered lipid peroxidation and significantly increased the antioxidant system in diabetic rats. The effect at a dose of 1 g/kg of body weight of fenugreek leaf powder was similar to that of glibenclamide. Insulin restores all the parameters to near normal values. Thus, fenugreek leaf powder reduces oxidative stress in experimental diabetes.     

Panax ginseng reduces oxidative stress and restores antioxidant capacity in aged rats

Nutritional antioxidants interact with cells in an active mode, including retrieving and sparing one another, to diminish oxidative stress. However, the intracellular balance of prooxidants and antioxidants becomes unbalanced, favoring prooxidants during the aging process. One hypothesis is that an aging-associated increase in oxidative stress is the primary cause of aging. Hence, the research hypothesis for this study is that Korean red ginseng reduces oxidative stress in vivo. Therefore, we investigated the efficacy of Korean red ginseng water extract (GWE) in reducing aging-associated oxidative stress by measuring lipid peroxidation and antioxidant levels in older rats compared with young rats. We observed a significant increase in the markers for oxidative damage (eg, lipid peroxidation) and markers for vital organ damage (eg, aspartate aminotransferase, alanine aminotransferase, urea, and creatinine levels) in aged rats. The oxidative damage was accompanied by a significant decrease in enzymatic antioxidants such as superoxide dismutase, catalase, glutathione peroxidase, glutathione reductase, and glutathione-S-transferase, and nonenzymatic antioxidants such as reduced glutathione, vitamin E, and vitamin C. Aged rats fed a diet supplemented with Korean red ginseng water extract had significantly less oxidative damage, possibly by enhancing the enzymatic and nonenzymatic antioxidants status. Our data suggest that consumption of Korean red ginseng reduces lipid peroxidation and restores antioxidant capacity by suppressing oxidative stress in rats.     

Soy isoflavone supplementation alleviates oxidative stress and improves systolic blood pressure in male spontaneously hypertensive rats

The aim of this study was to investigate the protective effect of isoflavone against hypertension, via the mitigation of oxidative stress and prevention of nitric oxide (NO, a potent vasodilator) reduction, in spontaneously hypertensive rats (SHR). The 8 wk-old male SHR were divided into two groups, and fed a casein-based high fat diet (120 g fat, 1 g cholesterol/kg diet) for 30 d, either with or without 10 g of soy powder (containing 31.2% of isoflavones)/kg. During the 30-d study period, tail systolic blood pressures (BP) in the control SHR group increased, from 162.4 +/- 2.3 to 177.9 +/- 5.4 mmHg (p<0.05), while the isoflavone-supplemented group benefited from a clear antihypertensive effect (160.1 +/- 1.8 to 160.2 +/- 4.9 mmHg). The serum NO and total radical trapping antioxidant potential (TRAP) were elevated in the isoflavone group. The isoflavone group also experienced a significant decrease in oxidative DNA damage in leukocytes, using comet assay. DNA damage correlated positively with incremental BP during the study, and systolic BP at the end of the study (p<0.01). Our results indicate that soy isoflavone has an antihypertensive effect, possibly through the amelioration of oxidative stress, and the augmentation of NO production, in SHR.     

Soy protein affects serum insulin and hepatic SREBP-1 mRNA and reduces fatty liver in rats

The consumption of soy protein was shown to reduce blood lipids in humans and other animal species. Furthermore, it was shown that the ingestion of soy protein maintains normal insulinemia. Thus, the purpose of the present study was to determine whether soy protein affects the synthesis of lipids in the liver through sterol-regulatory element binding protein-1 (SREBP-1) due to modulation of insulin levels. We first conducted a short-term study in which rats were fed a diet containing 18 g/100 g soy protein or casein for 10 d. Rats fed soy protein had significantly lower serum insulin concentrations than rats fed casein, and this response was accompanied by an elevation in hepatic SREBP-1 mRNA that was 53% lower than that in rats fed casein at d 10. The increase in SREBP-1 mRNA occurred 30 min after consumption of the casein mean, and increased steadily for the next 2 h. We then conducted a second study to assess the long-term effect of soy protein consumption for 150 d on hepatic SREBP-1 expression. Long-term consumption of soy protein maintained normal insulin concentrations compared with rats fed casein, which were hyperinsulinemic. Thus, rats fed the soy protein diet had significantly lower expression of SREBP-1 mRNA than rats fed the casein diet. Soy protein intake also reduced the expression of fatty acid synthase (FAS) and malic enzyme, leading to low hepatic lipid depots of triglycerides and cholesterol, whereas rats fed the casein diet developed fatty liver. These data suggest that soy protein regulates SREBP-1 expression by modulating serum insulin concentration, thus preventing the development of fatty liver.     

Long-term high protein intake does not increase oxidative stress in rats

The maximum dietary protein intake that does not cause adverse effects in a healthy population is uncertain. We tested whether a high protein intake enhances oxidative stress. Adult rats were adapted to different casein-based diets containing either an adequate (13.8%; AP), medium (25.7%; MP), or high (51.3%; HP) level of crude protein; a fourth group received a HP diet but no RRR-alpha-tocopherol acetate (HP-toc). After 15 wk of feeding, plasma protein carbonyl concentration, liver lipid peroxide levels [thiobarbituric acid-reacting substances (TBARS)], reduced glutathione (GSH) status and leucine kinetics ([1-(13)C]leucine) were measured. Higher concentrations of protein carbonyls and TBARS were found in rats fed the AP and the HP-toc diets compared with those fed the MP and HP diets (P: < 0.05). GSH concentrations in plasma did not differ but total blood GSH concentrations were significantly (P: < 0.05) lower in rats fed the HP-toc diet compared with those fed the AP, MP and HP diets. Liver GSH concentrations were significantly (P: < 0.01) lower in rats fed the AP diet compared with the other groups. Rates of postabsorptive leucine oxidation (LeuOX) and flux (Q(Leu)) were positively correlated with the dietary protein level (for AP, MP, and HP, respectively: LeuOX, 74.9 +/- 28.5, 109 +/- 35.2, 142.3 +/- 38.4 micromol/(kg. h); Q(Leu), 425 +/- 102, 483 +/- 82, 505 +/- 80 micromol/(kg. h). Only HP-toc resulted in a significantly greater protein breakdown (PB(Leu)) and Q(Leu). No difference was seen in nonoxidative leucine disposal. Long-term intake of high protein diets did not increase variables of oxidative stress, in contrast to our initial hypothesis. An unexpected finding was that adequate protein feeding (AP) may in fact induce oxidative stress.     

Folic acid supplementation reduces oxidative stress and hepatic toxicity in rats treated chronically with ethanol

Folate deficiency and hyperhomocysteinemia are found in most patients with alcoholic liver disease. Oxidative stress is one of the most important mechanisms contributing to homocysteine (Hcy)-induced tissue injury. However it has not been examined whether exogenous administration of folic acid attenuates oxidative stress and hepatic toxicity. The aim of this study was to investigate the in vivo effect of folic acid supplementation on oxidative stress and hepatic toxicity induced by chronic ethanol consumption. Wistar rats (n = 32) were divided into four groups and fed 0%, 12%, 36% ethanol, or 36% ethanol plus folic acid (10 mg folic acid/L) diets. After 5 weeks, chronic consumption of the 36% ethanol diet significantly increased plasma alanine transaminase (ALT) (P < 0.05) and aspartate transaminase (AST) (P < 0.05), triglycerides (TG) (P < 0.05), Hcy (P < 0.001), and low density lipoprotein conjugated dienes (CD) (P < 0.05) but decreased total radical-trapping antioxidant potential (TRAP) (P < 0.001). These changes were prevented partially by folic acid supplementation. The 12% ethanol diet had no apparent effect on most parameters. Plasma Hcy concentration was well correlated with plasma ALT (r = 0.612^**), AST (r = 0.652^*), CD (r = 0.495^*), and TRAP (r = -0.486^*). The results indicate that moderately elevated Hcy is associated with increased oxidative stress and liver injury in alcohol-fed rats, and suggests that folic acid supplementation appears to attenuate hepatic toxicity induced by chronic ethanol consumption possibly by decreasing oxidative stress.     

Vitamin E reduces glucocorticoid-induced oxidative stress in rat skeletal muscle

The purpose of this study was to investigate the effect of vitamin E on oxidative stress in the skeletal muscle of glucocorticoid-treated rats. Male Sprague-Dawley rats (5 weeks of age) were fed a basal diet or a diet supplemented with vitamin E (5,000 mg DL-alpha-tocopheryl acetate/kg diet) for 10 d. The rats of both diet groups received subcutaneous injections of corticosterone (CTC) (0, 25, and 100 mg/kg body weight/d) during the final 4 d. Weights of the extensor digitorum longus and gastrocnemius (GAST) muscles were dose-dependently reduced by CTC. However, the muscle weight losses in rats fed the vitamin E diet were smaller than those in rats fed the basal diet. Protein carbonyl content in the GAST muscle, which was determined as an index of oxidatively modified protein, was increased by 100 mg of CTC, and the increment was significantly (p < 0.01) reduced by vitamin E supplement. Hyperglycemia was induced by 100 mg of CTC, but it was not affected by vitamin E. Lipid peroxide (TBARS) in plasma and in GAST muscle was elevated by 100 mg of CTC, and vitamin E significantly (p < 0.001) suppressed the formation of TBARS in the muscle. The change in TBARS paralleled that in protein carbonyl. These results show that CTC leads to oxidative stress in rat skeletal muscles and that vitamin E has roles in reducing the oxidative stress which causes muscle atrophy.     

Standardized Bacopa monnieri extract ameliorates acute paraquat-induced oxidative stress,and neurotoxicity in prepubertal mice brain

Objectives: Bacopa monnieri (BM), an ayurvedic medicinal plant, has attracted considerable interest owing to its diverse neuropharmacological properties. Epidemiological studies have shown significant correlation between paraquat (PQ) exposure and increased risk for Parkinson's disease in humans. In this study, we examined the propensity of standardized extract of BM to attenuate acute PQ-induced oxidative stress, mitochondrial dysfunctions, and neurotoxicity in the different brain regions of prepubertal mice.

Methods: To test this hypothesis, prepubertal mice provided orally with standardized BM extract (200?mg/kg body weight/day for 4 weeks) were challenged with an acute dose (15?mg/kg body weight, intraperitoneally) of PQ after 3 hours of last dose of extract. Mice were sacrificed after 48 hours of PQ injection, and different brain regions were isolated and subjected to biochemical determinations/quantification of central monoamine (dopamine, DA) levels (by high-performance liquid chromatography).

Results: Oral supplementation of BM for 4 weeks resulted in significant reduction in the basal levels of oxidative markers such as reactive oxygen species (ROS), malondialdehyde (MDA), and hydroperoxides (HP) in various brain regions. PQ at the administered dose elicited marked oxidative stress within 48 hours in various brain regions of mice. However, BM prophylaxis significantly improved oxidative homeostasis by restoring PQ-induced ROS, MDA, and HP levels and also by attenuating mitochondrial dysfunction. Interestingly, BM supplementation restored the activities of cholinergic enzymes along with the restoration of striatal DA levels among the PQ-treated mice.

Discussion: Based on these findings, we infer that BM prophylaxis renders the brain resistant to PQ-mediated oxidative perturbations and thus may be better exploited as a preventive approach to protect against oxidative-mediated neuronal dysfunctions.     

Soy protein reduces serum cholesterol by both intrinsic and food displacement mechanisms

The apparently smaller LDL cholesterol (LDL-C)-lowering effect of soy in recent studies has prompted the U.S. FDA to reexamine the heart health claim previously allowed for soy products. We therefore attempted to estimate the intrinsic and extrinsic (displacement) potential of soy in reducing LDL-C to determine whether the heart health claim for soy continues to be justified. The intrinsic effect of soy was derived from a meta-analysis using soy studies (20-133 g/d soy protein) included in the recent AHA Soy Advisory. The extrinsic effect of soy in displacing foods higher in saturated fat and cholesterol was estimated using predictive equations for LDL-C and NHANES III population survey data with the substitution of 13-58 g/d soy protein for animal protein foods. The meta-analysis of the AHA Soy Advisory data gave a mean LDL-C reduction of 0.17 mmol/L (n = 22; P < 0.0001) or 4.3% for soy, which was confirmed in 11 studies reporting balanced macronutrient profiles. The estimated displacement value of soy (13-58 g/d) using NHANES III population survey data was a 3.6-6.0% reduction in LDL-C due to displacement of saturated fats and cholesterol from animal foods. The LDL-C reduction attributable to the combined intrinsic and extrinsic effects of soy protein foods ranged from 7.9 to 10.3%. Thus, soy remains one of a few food components that reduces serum cholesterol (>4%) when added to the diet.     

Aspartame induced cardiac oxidative stress in Wistar albino rats

Aspartame (non-nutritive sweetener) is consumed by millions of people in products like beverages, instant breakfasts, desserts, breathe mints, sugar free chewing gum, vitamins, and pharmaceutical. On a weight basis, metabolism of aspartame generates approximately 50% phenylalanine, 40% aspartic acid and 10% methanol. The detailed mechanisms of their effects on cardiac tissue are still unclear. The present study aimed to clarify whether longer time aspartame consumption has any effect on heart of Wistar albino rats. Animals were randomly divided into 4 groups of 6 animals (group-1: control, group-2: folate deficient diet fed animals, group-3: control animals treated with aspartame, group-4: folate deficient diet fed animals treated with aspartame). Aspartame was given orally (40 mg/kg·bw/day), dissolved in normal saline and for 90 days. Since human beings have very low hepatic folate content, the folate deficient diet fed animals were used to mimic the human methanol metabolism. Aspartame consumption increased significantly plasma corticosterone level, suggesting that aspartame may act as a chemical stressor. There was a significant increase in lipid peroxidation, nitric oxide and protein carbonyl, and significant decrease in protein thiol, cardiac membrane bound ATPases (Na⁺, K⁺, Ca⁺⁺, Mg⁺⁺), enzymatic (SOD, CAT, GPX, G6PD, GR) and non-enzymatic antioxidants (GSH, Vit-C, Vit-E) as well as a significant increase in heart rate and heart marker enzymes (CK and CK-MB). It may be due to excessive generation of free radicals, which impairs cardiac function. Aspartame metabolite methanol or formaldehyde may be the causative factors behind these changes. However, up regulation of Hsp70 in immunohistochemical analysis of cardiac tissue might be a protective response to oxidative stress induced by aspartame metabolites and structural damages in cardiac tissue.     

Chronic ginseng consumption attenuates age-associated oxidative stress in rats

The antioxidant properties of North American ginseng (Panax quinquefolium) were investigated in young and old rats fed a ginseng-supplemented diet for 4 mo. Female Fischer 344 rats at 4 (Y, n = 38) or 22 (O, n = 25) mo of age were randomly divided into three groups and fed either a AIN-93G formula-based control diet (C) or a diet containing 0.5 g/kg (low dose, L) or 2.5 g/kg (high dose, H) dry ginseng power for 4 mo. Oxidant generation, measured with 2'7'-dichlorofluorescin (DCFH), was significantly lowered with ginseng feeding in the homogenates of heart, soleus, and the deep portion of vastus lateralis muscle (DVL) (P < 0.05) in both Y and O rats, and the effects were dose dependent. Superoxide dismutase activity was elevated in heart and DVL of H rats, and in soleus of L rats (P < 0.05). H rats showed higher glutathione peroxidase activity in DVL and soleus muscle (P < 0.05), and elevated citrate synthase activity in the heart of both age groups and DVL of Y rats (P < 0.05). Neither the H nor L diet affected age-dependent lipid peroxidation in the heart or muscle, but protein carbonyl content was attenuated with the H diet in the heart (P < 0.05) and with both the L and H diets in DVL (P < 0.01). We conclude that ginseng supplementation can prevent age-associated increase in oxidant production and oxidative protein damage in rats. These protective effects are explained in part by elevated antioxidant enzyme activities in the various tissues.     

六氯苯对大鼠机体氧化损伤和抗氧化酶活性的影响

目的 研究六氯苯（HCB）对大鼠的毒性作用,探讨HCB中毒的氧化应激机制.方法 2个染毒组分别以含HCB 2.5%（低剂量组）、20.0%（高剂量组）的饲料染毒大鼠14 d,测定血清中碱性磷酸酶等11项血清学指标;测定大脑（皮层、海马）、肝脏和血清中丙二醛（MDA）水平、总超氧化物歧化酶（T-SOD）、过氧化氢酶（CAT）和谷胱甘肽过氧化物酶（GSH-Px）活力.结果 （1）高剂量HCB染毒组大鼠大脑皮层、海马、肝和血清中MDA含量均高于对照组,低剂量染毒组海马和血清中MDA也较对照组明显增加,差异有统计学意义（P＜0.01或P＜0.05）.（2）2个剂量组大鼠大脑皮层和海马中T-SOD活力明显增加,与对照组比较,差异有统计学意义（P＜0.01）;但高剂量组大鼠血清T-SOD活力却明显降低,与对照组比较,差异有统计学意义（P＜0.01）.（3）高剂量染毒组大鼠海马CAT活力高于对照组,差异有统计学意义（P＜0.01）.（4）高剂量染毒组大鼠大脑皮层、海马和低剂量染毒组海马中GSH-Px活力高于对照组,差异有统计学意义（P＜0.01）,但两组大鼠肝脏中GSH-Px活力却明显降低,与对照组比较,差异有统计学意义（P＜0.01）.（5）2个剂量染毒组大鼠血清白蛋白、总胆固醇都较对照明显增加,而血清碱性磷酸酶活力却明显降低,与对照组比较,差异有统计学意义（P＜0.01）.结论 HCB可导致大鼠机体氧化损伤、抗氧化酶活力改变,氧化应激是其重要的毒作用机制.     

Central microinjection of phytohormone abscisic acid changes feeding behavior,decreases body weight,and reduces brain oxidative stress in rats

Objectives: Natural products have a potential role on food intake in mammals. It has been reported that phytohormone abscisic acid (ABA) has a regulatory role on metabolic processes. Here, the effects of ABA on feeding behavior and brain oxidative stress were investigated in male Wistar rats.

Methods: ABA was injected intracerebroventricularly. Experimental groups were included (n = 9): control (received no injection), ABA vehicle (received normal saline), and ABA-treated groups were injected with different doses of ABA (2.5, 5, and 10 μg/rat for 7 days). Daily cumulative daytime and nighttime food consumption, meal frequency, meal duration, and alteration in body weight were recorded. At the end of behavioral experiment, catalase and peroxidase activity and malondialdehyde (MDA) and hydrogen peroxide (H₂O₂) levels were assayed.

Results: The results showed that ABA (5 and 10 μg) increased the meal frequency. Moreover, ABA could decrease body weight and MDA and H₂O₂ levels and increased the catalase and peroxidase activities in diencephalon. It also decreased the MDA concentration in the brain stem.

Discussion: Taken together, ABA has an important effect on feeding behavior and body weight in rats likely via increasing antioxidant capacity. However, further studies are still required to determine the underlying mechanisms of ABA on the feeding behavior.     

DEHP对大鼠睾丸氧化应激和血清睾酮水平影响

目的 探讨邻苯二甲酸二乙基己酯（DEHP）对青春期雄性大鼠睾丸及性激素的影响及潜在机制。方法 18日龄SD大鼠24只,按体重随机分为4组（对照组、低、中、高剂量DEHP组）,每组6只。DEHP染毒剂量分别为250、500和750 mg/kg,经口连续染毒30 d;颈部脱臼处死,收集血清,分离睾丸组织;测定血清睾酮、黄体生成素（LH）和卵泡刺激素（FSH）等性激素水平及睾丸组织中谷胱甘肽过氧化物酶（GSH-Px）、超氧化物歧化酶（SOD）、丙二醛和5α-还原酶（5α-R）活性。结果 DEHP处理组,大鼠睾丸和附睾脏器系数降低,睾丸曲精小管管腔缩小,结构坍塌,部分细胞膜破裂,细胞排列紊乱;与对照组比较,高剂量DEHP组大鼠血清睾酮和LH水平[分别为（115.04±14.21） pg/mL、（23.42±3.12） mIU/mL]降低,中、高剂量DEHP组大鼠血清FSH水平[分别为（5.49±0.42）、（4.63±0.51） IU/L]下降,差异有统计学意义（P<0.05）;与对照组比较,高剂量DEHP组大鼠睾丸组织中GSH-Px和SOD活力[分别为（728.3±95.3）、（835.8±151.2） U/mg pro]降低,而中、高剂量DEHP组大鼠睾丸组织中丙二醛含量[分别为（79.6±13.9）、（90.6±4.0） nmol/mg pro]和5α-R2活性[分别为（415.9±112.7）、（415.9±147.8） IU/mg pro]升高,差异有统计学意义（P<0.05）。结论 DEHP暴露后,大鼠睾丸发生氧化应激,并通过诱导5α-R2活性降低血清睾酮水平。     

Municipal landfill leachate induces hepatotoxicity and oxidative stress in rats

Human beings are more often exposed to complex mixtures of hazardous chemicals than single toxicant. The present study investigated the effects of Olushosun municipal landfill leachate (OMLL) from Ojota in Lagos State of Nigeria on hepatic function and some biomarkers of oxidative stress in adult rats. Physicochemical characteristic analysis of OMLL showed that while total alkalinity, total acidity, total hardness, biochemical oxygen demand and chemical oxygen demand were 3-fold, 2-fold, 4-fold and 1-fold, respectively, concentrations of heavy metals analysis showed that copper, lead, cadmium, arsenic, cobalt, chromium and mercury were 9-fold, 4-fold, 21-fold, 1320-fold, 7-fold, 5-fold and 4-fold, respectively, higher than acceptable limits by regulatory authorities. The OMLL was administered at 0, 10, 20, 30 and 40% concentrations to adult male rats for 14 days. Following exposure, serum was collected for serum biochemistry assays and liver was collected to determine the antioxidant status. Exposure of animals to 10, 20, 30 and 40% OMLL resulted in 3%, 31%, 52% and 83% increase in aspartate aminotransferase activity, whereas it elevated alanine aminotransferase activity by 10%, 25%, 30% and 49%, respectively, when compared with the control. While OMLL administration significantly increased catalase activity, a sequential decrease in reduced glutathione level and in superoxide dismutase and glutathione-S-transferase activities with concomitant increase in malondialdehyde level were observed, when compared with the control. Collectively, the hepatotoxicity of OMLL could be due to the induction of oxidative stress and may suggest possible health hazards in subjects with occupational or environmental exposure.     

明日叶查尔酮对糖尿病大鼠氧化应激影响

目的 探讨明日叶查尔酮（AC）对2型糖尿病大鼠氧化应激水平的影响。方法 雄性Wistar大鼠高脂饲料喂养加链脲佐菌素腹腔注射建立2型糖尿病模型,将造模成功大鼠随机分为糖尿病模型组、AC 30、10、5 mg/kg组及对照组,每日经口灌胃AC连续4周,检测空腹血糖、血清胰岛素、超氧化物歧化酶（SOD）、丙二醛（MDA）、总抗氧化能力、氧化型低密度脂蛋白（ox-LDL）和胰腺组织病理改变等指标。结果 糖尿病模型组大鼠血糖与胰岛素水平分别为（17.30±3.57）mmol/L和（38.28±4.97）mU/L,MDA和ox-LDL含量分别为（12.00±1.32）nmol/mL和（23.05±2.87）ng/mL,均明显高于对照组（P<0.05）,与糖尿病模型组比较,AC 30 mg/kg组大鼠血糖[（7.00±2.55）mmol/L]、胰岛素[（29.50±5.31）mU/L]、MDA[（9.96±0.65）nmol/mL]和ox-LDL[（15.36±1.70）ng/mL]均明显降低,差异均有统计学意义（P<0.05）,胰岛细胞损伤程度减轻。结论 AC对2型糖尿病大鼠氧化应激和胰岛细胞损伤有一定抑制作用。     

Suppression of oxidative stress by grape seed supplementation in rats

Polyphenol-rich grape seeds have a beneficial effect on human health. The present study was performed to investigate the effects of grape seeds on antioxidant activities in rats. Male Sprague-Dawley rats were randomly divided into a control diet group (C), a high-fat diet group (HF), a 5% grape seed-supplemented control diet group (G), and a 5% grape seed-supplemented high-fat diet group (HG). Dietary supplementation with grape seeds reduced serum concentrations of lipid peroxides compared with those in the C and HF groups. The hepatic level of lipid peroxides decreased significantly in the grape seed groups compared with that in the C and HF groups. Superoxide dismutase activity in the G group increased significantly compared with that in the C group. Catalase activity tended to be higher by feeding grape seeds. The grape seed diet increased glutathione peroxidase activity in the C group. Glutathione-S-transferase activity increased significantly in the G group compared with that in the C group. Hepatic content of total glutathione increased significantly in the HG group but decreased significantly in the HF group. The ratio of reduced glutathione and oxidized glutathione increased by feeding the grape seed diet. Total vitamin A concentration was significantly higher in HG group than in other groups. Liver tocopherol content of the G and HG groups was significantly higher than that of the control groups. These results suggest that dietary supplementation with grape seeds is beneficial for suppressing lipid peroxidation in high fat-fed rats.     

Dietary conjugated linoleic acid reduces lipid peroxidation by increasing oxidative stability in rats

The antioxidative effect of conjugated linoleic acid (CLA) was examined by determining lipid peroxidation and antioxidative enzyme activities. Male Sprague-Dawley rats were fed one of the experimental diets-normal diet, vitamin E-deficient control diet, 0.5% CLA vitamin E-deficient diet, or 1.5% CLA vitamin E-deficient diet for 5 wk. Hepatic thiobarbituric acid reactive substances (TBARS) were increased in the vitamin E-deficient control group, but they were was significantly lowered in the CLA groups. Similarly, hepatic glutathione peroxidase activity was increased in the vitamin E-deficient diet and reduced by CLA supplementation. In addition, CLA caused a significant decrease in superoxide dismutase activity while having no effect on catalase activity. Analyses of the fatty acid composition revealed that dietary CLA was incorporated into hepatic microsomal membrane dose-dependently. Compared to the vitamin E-deficient control, CLA resulted in significantly higher saturated and monounsaturated fatty acids (palmitic and oleic acids) while lowering levels of oxidation-susceptible polyunsaturated fatty acids (linoleic, linolenic, and arachidonic acids) in both plasma and hepatic membrane. The concentrations of plasma cholesterol and triacylglycerol (TG) were lower in the 1.5% CLA group than in other groups. These results suggest that dietary CLA has antiatherosclerotic and antioxidant activity by increasing oxidative stability in plasma and hepatic membrane in the vitamin E-deficient rats.