Hepatic GSH-Px Activities Research Articles

Reducing oxidative stress and hepatoprotective effect of water extracts from Pu-erh tea on rats with high-fat diet

Reducing oxidative stress and hepatoprotective effect of Pu-erh tea water extracts on rats fed with high-fat diet were researched for explaining health care of Pu-erh tea. Fifty SD rats were divided into five groups. The body weight was measured once a day. The malondialdehyde (MDA) and glucose (Glu) levels and the activities of alanine aminotransferase (ALT), aspartate aminotransferase (AST), nitric oxide synthase (NOS), and pyruvate kinase (PK) in serum were determined. Furthermore, the hepatic glycogen level (HGL) and the activities of hepatic total superoxide dismutase (T-SOD), catalase (CAT), and glutathione peroxidase (GSH-Px) were also measured after continuous administration for 12 weeks. The result demonstrated that Pu-erh extract caused the decreases in body weight, fat index, MDA and NOS levels, and the increases in hepatic T-SOD, CAT and GSH-Px activities, indicating that the extract may be due to inhibiting the increases of body weight and fat index, reducing oxidant stress state and inhibiting lipid peroxidation, thus decreasing the activities of ALT and AST, and protecting the liver in rat. Meanwhile, the extracts could increase the production of hepatic glycogen and the activity of PK, and reduce glucose level, protecting the liver from the diseases associated with type II diabetes.

Hepatotoxicity and endothelial dysfunction induced by high choline diet and the protective effects of phloretin in mice

The involvement of choline and its metabolite trimethylamine-N-oxide (TMAO) in endothelial dysfunction and atherosclerosis has been repeatedly confirmed. Phloretin, a dihydrochalcone flavonoid usually present in apples, possesses a variety of biological activities including vascular nutrition. This study was designed to investigate whether phloretin could alleviate or prevent high choline-induced vascular endothelial dysfunction and liver injury in mice. Mice were provided with 3% high choline water and given phloretin orally daily for 10 weeks. The high choline-treated mice showed the significant dyslipidemia and hyperglycemia with the impaired liver and vascular endothelium (p < 0.01). Administration of phloretin at 200 and 400 mg/kg bw significantly reduced the choline-induced elevation of serum TC, TG, LDL-C, AST, ALT, ET-1 and TXA2 (p < 0.01), and markedly antagonized the choline-induced decrease of serum PGI2, HDL-C and NO levels. Furthermore, phloretin elevated hepatic SOD and GSH-Px activities and decreased hepatic MDA levels of the mice exposed to high choline water. Moreover, histopathological test with the H&E and Oil Red O staining of liver sections confirmed the high choline diet-caused liver steatosis and the hepatoprotective effect of phloretin. These findings suggest that high choline causes oxidative damage, and phloretin alleviate vascular endothelial dysfunction and liver injury.

Optimization Extraction ofCrassostrea gigasPolysaccharides and its Antioxidant Activity and Hepatoprotective Against BCG-LPS-Induced Hepatic Injury in Mice

A active oyster polysaccharide (AOP) was extracted from oyster tissues by ultrasonic assisted extraction. The optimal extraction conditions were 20 min at pH 8, 60C with 40 W and water to solid ratio of 10, and with this method 42.73 ± 2.34 (mg/g) of AOP yield was obtained. Additionally, the antioxidant and hepatoprotective activities of AOP were investigated. The results showed that AOP exhibited strong antioxidant effects, which included scavenging activities against DPPH radicals and hydrogen oxide with IC50 values of 3.08 and 11.18 mg/mL, respectively. For hepatoprotective activities against BCG-LPS-induced hepatic injury in mice, AOP was shown to effectively improved the liver index, spleen index and thymus index, reduced the serum levels of ALT and AST. Treatment with AOP significantly increased hepatic SOD and GSH-Px activity, GSH. The levels of TNF-α and IL-1β in BCG/LPS-induced mice liver homogenates were decreased markedly by treatment with AOP. Practical Applications This work provides an alternative way for aquatic products processing enterprises to evaluate oyster polysaccharide quality and bioactivity. AOP have been shown to have potential for nutritional or pharmaceutical applications. AOP may have hepatoprotective effects against BCG-LPS -induced liver injury, which was related to its antioxidative and immunomodulatory effects.

Experimental study on intervention effect of Grifola frondosa on nonalcoholic steatohepatitis

To study the preventive effect of Grifola frondosa on nonalcoholic steatohepatitis (NASH). The rat model of NASH was established by feeding high-fat diets for 12 weeks and intervened with 0.5 g · kg(-1) · d(-1) and 1.0 g · kg(-1) · d(-1) of C. frondosa powder suspensions. The degrees of hepatocyte fatty degeneration and inflammation were observed under the optical microscope with routine HE staining. The NAFLD activity scores (NAS) were calculated. Serum ALT, AST and hepatic TG and CHOL were tested by the biochemical method. The hepatic MDA was examined by thiobarbituric acid method. The hepatic SOD was tested by the xanthine oxidase test. The hepatic GSH-PX activity was determined by the dithio-nitrobenzoic acid method. Hepatic TNF-α and IL-6 were detected by the enzyme-linked immunosorbent assay (ELISA). The NASH model group induced by high-fat diets showed higher hepatic NAS, ser- um ALT, AST, CHOL and hepatic TG, CHOL, MDA, TNF-α, IL-6 (P < 0.01 or P < 0.05) and lower serum TG and hepatic SOD, GSH-PX (P < 0.01, P < 0.05) than the normal control group. After being intervened with different doses of G. frondosa, the NASH group revealed significantly lower hepatic NAS, serum ALT and hepatic TG, CHOL, MDA, TNF-α and IL-6 (P < 0.05) and higher hepatic SOD, GSH-PX (P < 0.05) than the model group. G. frondosa may prevent the further development of NASH by improving the disorder of lipid metabolism in rats with NASH induced by high-fat diets, relieving the level of oxidative stress and reducing the generation of inflammatory cytokines.

Porcine Splenic Hydrolysate has Antioxidant Activity in vivo and in vitro.

The antioxidant capacity of porcine splenic hydrolysate (PSH) was studied in vitro and in vivo. Peptide hydrolysates were prepared, using the proteolytic enzyme Alcalase®. The molecular weights of PSH were 37,666, 10,673, 6,029, and 2,918 g/mol. Rats were fed a 5% (w/v) PSH diet, instead of a casein diet, for 4 wk. The food intake, body weight gain, and liver weight of rats in the PSH group were similar to those in the control (CONT) group. There were no differences in the serum total cholesterol, triglyceride, total protein, or albumin levels between PSH and CONT groups. However, the level of in vivo hepatic lipid peroxidation in PSH group was significantly lower than that in CONT. In vivo hepatic catalase and glutathione peroxidase activities in the PSH group were significantly higher than those in the control group. The in vitro protein digestibility of PSH was lower than that of casein. The in vitro trolox equivalent antioxidant capacity of PSH was significantly higher than that of the peptide hydrolysate from casein. The in vitro radical scavenging activities of PSH were significantly higher than those of the peptide hydrolysate from casein. The present findings suggest that porcine splenic peptides improve the antioxidant status in rats by enhancing hepatic catalase and GSH-Px activities, and indicate a potential mechanism of radical scavenging activity during gastrointestinal passage.

The effect of lycopene on antioxidant status in rainbow trout (Oncorhynchus mykiss) reared under high stocking density

Lycopene, the major carotenoid found in tomato, exhibits health beneficial effects by virtue of its antioxidant activity. As stocking density is known as a stress factor in fish, the effects of dietary lycopene supplementation (0, 200 or 400mgkg−1) on growth performance and antioxidant status in rainbow trout under normal (20kgm3−1) and high (100kgm3−1) stocking density were studied. Glutathione peroxidase (GSH-Px), superoxide dismutase (SOD) and catalase (CAT) activities were evaluated, as well as lipid peroxidation measured as malondialdehyde (MDA). Nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB), erythroid-derived 2-like 2 (Nrf2) and heme-oxygenase 1 (HO-1) levels were also assayed as an indicator of detoxifying/antioxidant defense mechanisms to cope with oxidative stress. Results showed that exposure to high stocking density depressed feed intake by 6.8% and body weight gain by 12.1%, increased plasma and hepatic MDA level by 88.5 and 124.3% and decreased hepatic SOD, CAT and GSH-Px activities by 22.1, 43.4 and 51.7%, respectively. In fish under crowded conditions, an expression of hepatic NF-κB was increased by 71.5%, being suppressed in Nrf2 and HO-1 by 40.6 and 42.7%, respectively. Lycopene supplementation increased linearly fish growth performance and antioxidant enzyme activity, and decreased linearly MDA concentration in both low and high stocking densities. NF-κB levels decreased hepatic Nrf2 and HO-1 levels increased linearly with lycopene supplementation at a greater extent in fish under low stocking condition. In conclusion, dietary supplementation of lycopene to fish reduces the detrimental effects of high stocking density on growth performance and modulates oxidative status via activating host defense system at cellular level. It appears that lycopene can be added up to 400mgkg−1 to rainbow trout diets to improve meat quality.

A comparative study of growth performance and antioxidant status of rabbits when fed with or without chestnut tannins under high ambient temperature

The study was conducted to determine the effects of the inclusion of a natural extract of chestnut wood (Silvafeed ENC), rich in tannins, in the diet on growth performance and antioxidant status in growing rabbits under high ambient temperature (35 °C). A total of 120 New Zealand male rabbits (average body weight 1123 ± 13.5 g, 40 d old) were divided into three groups (40 rabbits per group) and fed a basal diet or the basal diet with 5 or 10 g of ENC/kg of diet (C, ENC5 and ENC10, respectively). Rabbits had free access to diets and water in an environmentally controlled room at 35 °C and 55% relative humidity during the entire period (21 d). On d 7, 14 and 21 of the trial, body weight and feed intake were measured and blood samples collected for assay of antioxidant indices. Liver tissue samples were collected on d 21 for assay of antioxidant indices. Results showed that ENC supplementation increased (P<0.05) average daily gain (ADG) in the first week of the trial. Compared with the control group, the ENC5 reduced (P<0.05) feed conversion ratio (FCR) and the ENC10 increased (P<0.05) average daily feed intake (ADFI). From d 8 to 14 of the trial, the ENC5 increased (P<0.05) ADG and reduced (P<0.05) FCR. In the last week, the ENC10 group showed a higher (P<0.05) ADG and lower (P<0.05) FCR than the control group. Compared with the control group, ADFI was reduced (P<0.01) by ENC5 treatment. For the overall period, ENC supplementation had a positive effect (P<0.05) on ADG and FCR. The final body weight of the ENC5 group was higher (P<0.05) than the control group. Furthermore, on d 7, the inclusion of ENC increased (P<0.05) superoxide dismutase (SOD) and reduced (P<0.01) malondialdehyde (MDA). The rabbits fed ENC5 had significantly (P<0.05) lower cortisol and higher (P<0.05) total antioxidant capacity (T-AOC) and glutathione peroxidase (GSH-Px) than the control group. On d 14, addition of ENC increased T-AOC (P<0.01) and reduced MDA (P<0.01). The ENC5 group showed lower (P<0.05) cortisol and higher (P<0.05) GSH-Px than the control group. On d 21, the rabbits in ENC-treated groups had higher (P<0.01) GSH-Px activities than rabbits in the control group. The rabbits fed with the ENC10 diet had higher (P<0.05) SOD compared with the control rabbits. In contrast, the opposite was true for cortisol (P<0.05) and MDA (P<0.05). On d 21, MDA was lower (P<0.01) with dietary ENC than without ENC in liver tissue. Hepatic GSH-Px activity of rabbits fed with the ENC10 diet was higher (P<0.05) than that of the control group. ENC supplementation seemed to have a positive influence on the growth performance and antioxidant status of growing rabbits under high ambient temperature.

Epigallocatechin-3-gallate prevents lipid peroxidation and enhances antioxidant defense system via modulating hepatic nuclear transcription factors in heat-stressed quails

Epigallocatechin-3-gallate (EGCG), a polyphenol derived from green tea, exerts antioxidant effects. Oxidative stress is one of the consequences of heat stress (HS), which also depresses performance in poultry. This experiment was conducted to elucidate the action mode of EGCG in alleviation of oxidative stress in heat-stressed quail (Coturnix coturnix japonica). A total of 180 five-week-old female Japanese quails were reared either at 22°C for 24 h/d (thermoneutral, TN) or 34°C for 8 h/d (HS) for 12 wk. Birds in both environments were randomly fed 1 of 3 diets: basal diet and basal diet added with 200 or 400 mg of EGCG/kg of diet. Each of the 2×3 factorially arranged groups was replicated in 10 cages, each containing 3 quails. Performance variables [feed intake (FI) and egg production (EP)], oxidative stress biomarkers [malondialdehyde (MDA), catalase (CAT), superoxide dismutase (SOD), and glutathione peroxidase (GSH-Px)] and hepatic transcription factors [nuclear factor κ-light-chain-enhancer of activated B cells (NF-κB) and nuclear factor (erythroid-derived 2)-like 2 (Nrf2)] were analyzed using 2-way ANOVA. Exposure to HS caused reductions in FI by 9.7% and EP by 14.4%, increased hepatic MDA level by 84.8%, and decreased hepatic SOD, CAT, and GSH-Px activities by 25.8, 52.3, and 45.5%, respectively (P<0.0001 for all). The hepatic NF-κB expression was greater (156 vs. 82%) and Nrf2 expression was lower (84 vs. 118%) for quails reared under the HS environment than for those reared under the TN environment (P<0.0001 for both). In response to increasing supplemental EGCG level, there were linear increases in FI from 29.6 to 30.9 g/d and EP from 84.3 to 90.1%/d, linear decreases in hepatic MDA level from 2.82 to 1.72 nmol/g and Nrf2 expression from 77.5 to 123.3%, and linear increases in hepatic SOD (146.4 to 182.2), CAT (36.2 to 47.1), and GSH-Px (13.5 to 18.5) activities (U/mg of protein) and NF-κB expression (149.7 to 87.3%) (P<0.0001 for all). Two-way treatment interactions revealed that the degree of restorations in all response variables was more notable under the HS environment than under the TN environment as supplemental EGCG level was increased. Moreover, levels of oxidative biomarkers were strongly correlated with expressions of hepatic nuclear transcription factors. In conclusion, supplemental EGCG alleviates oxidative stress through modulating the hepatic nuclear transcription factors in heat-stressed quails.

Mobile phone radiation-induced free radical damage in the liver is inhibited by the antioxidants n-acetyl cysteine and epigallocatechin-gallate

Purpose: To investigate oxidative damage and antioxidant enzyme status in the liver of guinea pigs exposed to mobile phone-like radiofrequency radiation (RFR) and the potential protective effects of N-acetyl cysteine (NAC) and epigallocatechin-gallate (EGCG) on the oxidative damage.Materials and methods: Nine groups of guinea pigs were used to study the effects of exposure to an 1800-MHz Global System for Mobile Communications (GSM)-modulated signal (average whole body Specific Absorption Rate (SAR) of 0.38 W/kg, 10 or 20 min per day for seven days) and treatment with antioxidants.Results: Significant increases in malondialdehyde (MDA) and total nitric oxide (NOx) levels and decreases in activities of superoxide dismutase (SOD), myeloperoxidase (MPO) and glutathione peroxidase (GSH-Px) were observed in the liver of guinea pigs after RFR exposure. Only NAC treatment induces increase in hepatic GSH-Px activities, whereas EGCG treatment alone attenuated MDA level. Extent of oxidative damage was found to be proportional to the duration of exposure (P < 0.05).Conclusion: Mobile phone-like radiation induces oxidative damage and changes the activities of antioxidant enzymes in the liver. The adverse effect of RFR may be related to the duration of mobile phone use. NAC and EGCG protect the liver tissue against the RFR-induced oxidative damage and enhance antioxidant enzyme activities.

Effects of l-Canavanine and ozone on vascular reactivity in septicemic rats

Septicemia leads to oxidative stress with overproduction of reactive-oxygen species (ROS) and consumption of endogenous antioxidant enzymes. We tested a twofold hypothesis: (1) does oxidative stress (OxS) induced by sepsis acting alone or in concert with augmented inflammatory processes contributes to sepsis-related vascular dysfunction, and, (2) whether ozone (O(3)) and L-canavanine (CAV) mitigate the negative impact of the aforementioned phenomena. We investigated the relative impact of treatment with CAV and/or O(3) on vascular OxS associated vascular functional changes in septicemic rats. For this study, 60 male Sprague-Dawley rats were used and divided into six experimental groups (n = 10): control group (C), sham-operated (Sham), septicemic rats (S), S rats treated with CAV (100 mg/kg. i.p; S + CAV), S rats treated with O(3) (1.2 mg/kg, i.p.; S + O(3)) and S rats treated with both O(3) and CAV (S + O(3) + CAV). After 22 h, the mean arterial blood pressure (MAP), the aortic ring vascular reactivity to phenylephrine, abdominal aortic blood flow (AABF), serum tumor necrosis factor-alpha (TNF-alpha) and plasma nitrite/nitrate (NOx) concentration were measured. In addition, hepatic antioxidant enzyme activities sodium dismutase (SOD) and glutathione peroxidase (GSH-Px) were estimated. Septicemia caused significant elevation of serum TNF-alpha (p < 0.001) and plasma NOx (p < 0.001) and significant (p < 0.001) reduction of AABF (p < 0.001), aortic vascular response to phenylephrine (p < 0.001), MAP (p < 0.001) and hepatic SOD and GSH-Px activity (p < 0.001) compared with the C group, while treatment with O(3) and/or CAV induced significant amelioration of all those increases. Abnormalities were attenuated to a similar extent with treatment with both O(3) and CAV. These results suggested that concomitant administration of O(3) and CAV alleviated the compromised vascular reactivity in septicemic conditions and prevent its progression into septic shock compared with each alone.

Alfalfa polysaccharides improve the growth performance and antioxidant status of heat-stressed rabbits

The study was conducted to evaluate the antioxidant properties of alfalfa polysaccharides (APS) extracted from alfalfa ( Medicago sativa L.) through 1,1-Diphenyl-2-picryl-hydrazyl (DPPH) radical-scavenging assay and the effects of the inclusion (0%, 0.1%, and 0.5%) of APS in the diet on the growth performance and antioxidant status in heat-stressed rabbits. 120 New Zealand male rabbits (average body weight 1123 g, 40 d old) were divided into three groups (40 rabbits per group) and were fed with a basal diet or the basal diet with 1 g or 5 g of APS/kg of diet. Rabbits had free access to diets and water in an environmentally controlled room at 30 ± 1 °C and 55% relative humidity during the entire period (21 d). On days 7, 14 and 21 of the trial, body weight and feed intake were measured and blood samples were collected for assay of antioxidant induces. Liver tissue samples were collected on day 21 for assay of antioxidant induces. Results in vitro showed the scavenging effect of APS on DPPH radicals increased ( P < 0.05) in a dose-dependent manner. The APS exerted an inhibitory effect on DPPH radical generation, with 66.3% inhibition at 100 µg/mL and 74.5% inhibition at 250 µg/mL. Results in vivo showed that APS 0.1% supplementation increased ( P < 0.05) average daily gain (ADG) and reduced ( P < 0.05) feed conversion rate (FCR) in the first week of trial. Compared with the control group, average daily feed intake (ADFI) was significantly ( P < 0.01) reduced by APS treatment. From days 8 to 14 of the trial, ADG of the APS 0.5% group was greater ( P < 0.05) than that of the control group. Compared with the control group, FCR was significantly ( P < 0.05) reduced by APS treatment. From days 15 to 21 of the trial, ADFI of the APS 0.1% group was greater ( P < 0.05) than that of the control group. For the overall period, APS 0.5% supplementation had a significantly ( P < 0.05) positive effect on ADG. ADFI and FCR were lower ( P < 0.05) with APS than without APS. Furthermore, on day 7, the inclusion of APS reduced significantly MDA ( P < 0.01). The rabbits fed with APS 0.1% had significantly ( P < 0.01) lower cortisol and greater ( P < 0.05) T-AOC, SOD, and GSH-Px than the control group. On day 14, addition of APS increased T-AOC ( P < 0.01) and reduced MDA ( P < 0.05). The APS 0.5% group showed lower ( P < 0.05) cortisol and greater ( P < 0.05) GSH-Px than the control group. On day 21, the rabbits fed with the APS 0.5% diet had greater ( P < 0.05) GSH-Px and T-AOC compared with the control rabbits. In contrast, the opposite was true for cortisol ( P < 0.05) and MDA ( P < 0.05). On day 21, MDA was lower ( P < 0.01) with APS than without APS in the liver tissue. Hepatic GSH-Px activity of rabbits fed with the APS 0.5% diet was greater ( P < 0.05) than those of other groups. APS supplementation seemed to have a positive influence on the growth performance and antioxidant status of heat-stressed rabbits.

The effects of dietary oxidized fat and selenium source on performance, glutathione peroxidase, and glutathione reductase activity in broiler chickens

Normal or elevated selenium status of broilers, which is influenced by dietary selenium sources, improves the bird’s ability to overcome the adverse effects of reactive oxygen metabolites. The objective of this study was to evaluate the effects of feeding graded levels of peroxidized poultry fat on blood and hepatic glutathione peroxidase (GSH-Px), and hepatic glutathione reductase activity in broiler chickens fed either inorganic sodium selenite (SEL) or organic selenium enriched in the organic selenium yeast product Sel-Plex (SP). Nine starter diets, varying in levels of oxidized fat (0, 3, and 6 mEq/kg) and dietary selenium sources, were fed to 360 male chicks from hatch to 21 d of age. Sel-Plex or SEL was added to the basal diet to provide either 0 or 0.2 ppm of supplemental selenium in the diets. Blood and hepatic samples were obtained for each treatment group at 21 d of age. Neither peroxidized fat nor selenium source significantly altered the activity of hepatic glutathione reductase (P ≤ 0.05). Blood GSH-Px was influenced significantly by both fat and selenium source (P ≤ 0.05), but the fat × selenium source interaction was not significant (P ≥ 0.3). A selenium source effect on the hepatic GSH-Px activity (P ≤ 0.05) was evidenced by higher GSH-Px activity, even in the basal diet with no added peroxidized fat. An increase in GSH-Px activity was seen in the erythrocyte and hepatic samples in both the SEL and SP treatments when peroxidized fat was given at 3 mEq/kg, but in the erythrocytes and in the hepatic tissues from SEL-supplemented birds, there was an apparent inhibition of GSH-Px activity. This inhibition was not seen in the hepatic tissue samples from SP-fed birds. Because elevated GSH-Px activity is indicative of oxidative stress, it was concluded that dietary SP supplementation resulted in better selenium and redox status in broilers than did SEL. These results indicate that the dietary selenium supplied in an organic form (selenium yeast as SP) improved the selenium and redox status in broilers, leading to greater resistance to oxidative stress than when the inorganic form of selenium (SEL) was fed.

Differential Effects of Sodium Selenite and Nano-Se on Growth Performance, Tissue Se Distribution, and Glutathione Peroxidase Activity of Avian Broiler

The present research evaluated differential effects of sodium selenite and nano-Se on growth performance, tissue Se distribution, and glutathione peroxidase (GSH-Px) activity of avian broiler. Broilers were randomly segregated into 12 groups so that three replicates were available for each of the three treatments (T-1, T-2, and T-3) and control groups. The control groups were fed basal diets without Se addition. T-1, T-2, and T-3 were fed with diets containing 0.2 mg kg(-1) sodium selenite, 0.2 mg kg(-1) nano-Se, and 0.5 mg kg(-1) nano-Se, respectively. Compared with the control, Se supplementation remarkably improved daily weight gain and survival rate and decreased feed conversion ratio (P < 0.05). However, no significant difference was observed between T-1, T-2, and T-3. The tissue Se content was significantly higher (P < 0.05) in Se-supplemented groups than the control, and T-3 showed the highest. Furthermore, higher Se content was observed in liver, and there was a significant difference (P < 0.05) compared with that in muscle. As for serum and hepatic GSH-Px activities, Se supplementation remarkably improved GSH-Px activity (P < 0.05), and there was no significant difference (P > 0.05) between treatments (T-1, T-2, and T-3).

Effects of Erdosteine on Acetaminophen-induced Hepatotoxicity in Rats

We investigated the effects of erdosteine on acetaminophen (APAP)-induced hepatotoxicity in rats. Superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GSH-Px), AST (aspartate aminotransferase), and ALT (alanine transaminase) activities, and malonyldialdehyde (MDA) and nitric oxide levels as oxidant/antioxidant biochemical parameters were investigated with light microscopic evaluation in adult female Wistar Albino rats. APAP administration produced a decrease in hepatic SOD, CAT, and GSH-Px activities, and coadministration of erdosteine (150 and 300 mg/kg) resulted in increases in the activities. MDA and NO levels increased in the APAP group, and erdosteine treatments prevented these increases. Significant elevations in serum AST and ALT levels were observed in the APAP group, and when erdosteine and APAP were coadministered, their serum levels were close to those in the control group. Light microscopic evaluation of livers showed that there were remarkable centrilobular (zone III) hepatic necrosis and mild to moderate sinusoidal congestion in the APAP group, whereas in the erdosteine group, cellular necrosis was minimal and the hepatocytes maintained a better morphology when compared to the APAP group. Erdosteine prevented APAP-induced liver injury and toxic side effects probably through the antioxidant and radical scavenging effects of erdosteine.

Effect of Hesperidin Supplementation on Lipid and Antioxidant Metabolism in Ethanol-fed Rats

This study examined the effect of hesperidin supplementation with an ethanol diet on lipid and antioxidant metabolism in rats. Male Sprague-Dawley rats were divided into two groups (n=10), and were assigned to one of two dietary categories: E?, ethanol diet (50 g/L) for 8 wks; E?H₄, ethanol diet for the first 4 wks and hesperidin (0.02%, w/w) supplemented ethanol diet for the last 4 wks. The plasma and hepatic lipids, hepatic cholesterol regulating enzyme activity, hepatic antioxidant enzyme activity and lipid peroxidation were determined. Supplementation with hesperidin for the last 4 wks during the 8 wks period of the ethanol diet, significantly increased the ADH activity. In conjunction with the chronic administration of ethanol, hesperidin supplementation resulted in a significant decrease in the hepatic cholesterol and triglyceride concentrations compared to the E? group. The hepatic HMG-CoA reductase and ACAT activities were significantly lower in the hesperidin-supplemented group. When comparing hepatic antioxidant enzyme activities, SOD, GSH-Px, and G6PD activities and GSH level were significantly higher in the E?H₄ group than in the E? group. Plasma TBARS levels were significantly lower in rats fed ethanol with hesperidin compared to the rats fed only ethanol; however, the hepatic TBARS levels were not significantly different between the groups. Accordingly, the additional hesperidin supplement with an ethanol diet might be effective for improving the hepatic lipid metabolism and antioxidant defense system.

In Vivo Antioxidant Activity of Methanol Extract from Quinoa Fermented with Rhizopus oligosporus

Previously, this author reported that the fermentation of quinoa with Rhizopus oligosporeus increased antioxidant activity, and the antioxidant activity of the 80% methanol extract of the fermented quinoa (Q-tempeh) was higher than the other extracts with n-hexane and water in vitro. In this paper, to clarify a beneficial effect of the fermentation of quinoa with R. oligosporus, the antioxidant activity of 80% methanol extract of Q-tempeh was investigated in rats ex vivo and in vivo. In the ex vivo experiment, the 80% methanol extract from Q-tempeh increased both activities of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) in the liver, and accelerated the production of 12-hydroxyeicosatetraenoic acid (12-HETE) in the lung. In rats fed vitamin E-free diets with 80% methanol extract of Q-tempeh, the alpha-tocopherol concentration, thiobarbituric acid-reactive substance (TBARS) value, and activities of GSH-Px and SOD in serum showed a similar concentration to those of the control rats fed a vitamin E-supplemented diet. However, the hepatic GSH-Px and SOD activities were higher than those in the control rats. On the other hand, in rats fed a vitamin E-free diet with the 80% methanol extract of quinoa, the serum alpha-tocopherol level was lower, and both TBARS values of serum and liver were higher than those in the control rats. From these results, the 80% methanol extract of Q-tempeh was inferred to be an active superoxide scavenger and peroxide reducer in vivo.

Glutathion Peroxidase and Glucose-6-Phosphate Dehydrogenase Activities in Bovine Blood and Liver

A total of 46 cattle, including 25 as control, 16 with glycogen degeneration and 5 with severe fatty degeneration were studied. Whole blood and liver tissue specimens were used to measure glutathione peroxidase (GSH-Px) and Glucose-6-Phosphate Dehydrogenase (G6PD) activities. The present study determined the value of these parameters in diagnosing glycogen and fatty degeneration in cattle from the point of the status of antioxidation and lipid peroxidation. The results showed a significant decrease in hepatic GSH-Px activity and a significant increase in hepatic G6PD activity in cases of fatty degeneration. On the other hand, there were no significant changes in erythrocytic and hepatic GSH-Px and G6PD activities in cases of glycogen degeneration. The results indicated lipoperoxidation process in the liver tissues increased in cases of fatty degeneration. Therefore, supplying animals suffering from fatty liver with sufficient quantities of nutrient antioxidants may be valuable when treatment is considered.

Effect of rutin and tannic acid supplements on cholesterol metabolism in rats

This study was designed to test the lipid-lowering and antioxidative activities of two phenolic compounds, rutin and tannic acid. Three groups of rats were given a semisynthetic diet containing 1 g of cholesterol/kg for 5 wks. The control group only received a high cholesterol diet, whereas the other two groups received a diet including 1 g of rutin or 1 g of tannic acid/kg. The rutin and tannic acid both significantly lowered the plasma lipid and hepatic cholesterol levels compared to those in the control. The hepatic HMG-CoA reductase activity was significantly lower in the tannic acid group than in the rutin group, while the hepatic ACAT activity was significantly lower in both the rutin and tannic groups compared to the control group. The overall potential of the antioxidant system was significantly enhanced by the rutin and tannic acid supplements as the plasma and hepatic TBARS levels were lowered while the hepatic SOD and GSH-Px activities were increased in the high-cholesterol fed rats. Furthermore, these results suggest that the supplementation of rutin and tannic acid promoted the excretion of fecal sterols, thereby leading to a decreased absorption of dietary cholesterol as well as lower plasma and hepatic cholesterol.

Effects of thymoquinone on antioxidant enzyme activities, lipid peroxidation and DT-diaphorase in different tissues of mice: a possible mechanism of action.

The present investigation focused, firstly, on the effects of oral administration of thymoquinone (TQ) on antioxidant enzyme activities, lipid peroxidation and DT-diaphorase activity in hepatic, cardiac and kidney tissues of normal mice. Superoxide dismutase (SOD; E.C:1.15.1.1), catalase (CAT; E.C:1.11.1.6), glutathione peroxidase (GSH-Px; E.C:1.11.1.9), glutathione-S-transferase (GST; E.C:2.5.1.18), and DT-diaphorase (E.C:1.6.99.2) enzyme activities in each tissue type were determined. Treatment of mice with the different doses of TQ (25, 50 and 100 mg kg(-1) day(-1) orally) for 5 successive days, produced significant reductions in hepatic SOD, CAT and GSH-Px activities. In addition cardiac SOD activity was markedly inhibited with the higher doses of TQ, (namely 50 and 100 mg kg(-1)). Moreover, TQ (100 mg kg(-1)) significantly reduced hepatic and cardiac lipid peroxidation as compared with the respective control group. Conversely, TQ (50,100 mg kg(-1)) and TQ (100 mg kg(-1)) enhanced cardiac and renal DT-diaphorase activity respectively. However, the selected doses of TQ neither produced any change in GST activity nor influenced reduced glutathione content in all tissues studied. TQ was tested, secondly, as a substrate for hepatic, cardiac and renal DT-diaphorase of normal mice in the presence of NADPH. Kinetic parameters for the reduction of TQ to dihydrothymoquinone (DHTQ) indicated that DT-diaphorase of different tissues can efficiently reduce TQ to DHTQ. K(m) and V(max) values revealed that hepatic DT-diaphorase exhibited the higher values, while the lower values were associated with renal DT-diaphorase. TQ and DHTQ were tested, thirdly, as specific scavengers for superoxide anion (generated biochemically) or as general scavengers for free radicals (generated photochemically). The results revealed that TQ and DHTQ acted not only as superoxide anion scavengers but also as general free radical scavengers. The IC(50) for TQ and DHTQ in biochemical and photochemical assays were in the nanomolar and micromolar range respectively. Our data may explain at least partly the reported beneficial in vivo protective effects of TQ through the combined antioxidant properties of TQ and its metabolite DHTQ.

Lipid-lowering and antioxidative activities of 3,4-di(OH)-cinnamate and 3,4-di(OH)-hydrocinnamate in cholesterol-fed rats

Background: Polyphenols appear to have antioxidant activities and may mediate lipid lowering. Methods: Four groups of rats, a high-cholesterol control (HC), HC+lovastatin, HC+3,4-di(OH)-cinnamate, and HC+3,4-di(OH)-hydrocinnamate, were given a semi-synthetic diet. The cinnamate derivative or lovastatin (0.1 g/100 g) supplements were given for 6 weeks. Results: The plasma total cholesterol concentration was significantly lowered by the 3,4-di(OH)-cinnamate supplement compared to the control or lovastatin group. The 3,4-di(OH)-cinnamate and 3,4-di(OH)-hydrocinnamate supplements significantly lowered both the hepatic cholesterol and triglyceride levels, while lovastatin only lowered the hepatic cholesterol. The hepatic HMG–CoA reductase activities were significantly lower in the 3,4-di(OH)-cinnamate and 3,4-di(OH)-hydrocinnamate groups than in the control or lovastatin group. The ACAT activity was only significantly lower in the lovastatin group compared to the other groups. With regards the hepatic antioxidant enzyme system, the CAT activity was significantly higher in the 3,4-di(OH)-cinnamate and 3,4-di(OH)-hydrocinnamate groups compared to the control or lovastatin group. The two cinnamate derivatives resulted in an increased hepatic GSH–Px activity. Meanwhile, all the supplements significantly lowered the hepatic thiobarbituric acid reactive substances (TBARS) content. However, the 3,4-di(OH)-cinnamate and 3,4-di(OH)-hydrocinnamate supplements did not alter the neutral sterol and total fecal sterol. Conclusions: Both cinnamate derivatives were potent in lipid-lowering and altering the antioxidative enzyme. Furthermore, these results also suggest that 3,4-di(OH)-cinnamate is more effective than 3,4-di(OH)-hydrocinnamate in its lipid-lowering action.