Effects of Graptopetalumparaguayense extract on tert‐ butylhydroperoxide‐induced oxidative stress

BACKGROUND: Graptopetalum paraguayense E. Walther is used in folk medicine to lower blood pressure, protect liver function and relieve pain and infection. The effect and mechanism of its 50% ethanolic extract (GE50) were investigated in tert‐butylhydroperoxide (t‐BHP)‐induced Wistar rats. The serum was analysed for aspartate aminotransferase (AST) and alanine aminotransferase (ALT) activities while the tissue cytosols were analysed for lipid peroxidation, antioxidant level and enzyme activities. RESULTS: The liver was the primary target organ while the heart appeared to be the least responsive organ for t‐BHP treatment among the three tissues investigated. t‐BHP treatment increased serum AST and ALT activities, which are indicators of liver toxicity, while GE50 pretreatment reduced t‐BHP‐induced liver damage. t‐BHP treatment induced lipid peroxidation in the liver and brain but not in the heart. GE50 pretreatment prevented t‐BHP‐induced lipid peroxidation by maintaining superoxide dismutase (SOD) activity as well as glutathione (GSH) and vitamin C levels in the liver and vitamin E level in the brain. Although t‐BHP treatment did not induce lipid peroxidation in the heart, it caused a decrease in antioxidant level. GE50 pretreatment prevented the t‐BHP‐induced decrease in vitamin C level in the heart. CONCLUSION: GE50 pretreatment in rats protects the liver and brain from possible damage by t‐BHP‐induced lipid peroxidation. Copyright © 2007 Society of Chemical Industry     

Decalepis hamiltonii roots boost antioxidant status of rat liver and brain

BACKGROUND: Roots of Decalepis hamiltonii are traditionally consumed as pickles and juice for their health benefits. We have earlier demonstrated the antioxidant property of the root extract and identified the constituent antioxidant molecules. RESULTS: This paper reports the effect of multiple‐dose (7, 15, and 30 days) treatment of Decalepis hamiltonii aqueous root extract (DHA) (50 and 100 mg kg^?1 body weight) on the antioxidant profile of rat liver and brain. Activities of the antioxidant enzymes superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), glutathione reductase (GR), and glutathione‐S‐transferase (GST) were increased and glutathione content was elevated in both liver and brain, apart from reduction in the basal level of lipid peroxidation. DHA induced stronger antioxidant boost in brain by increasing the activities of SOD, CAT, and GPx compared to liver. CONCLUSION: As failure to grapple with oxidative stress is an important factor in the etiology of several diseases, DHA's effects on improvement of antioxidant status could provide a scientific justification for the health‐promoting properties attributed to it. Copyright © 2009 Society of Chemical Industry     

Protective effect of dietary ginger on antioxidant enzymes and oxidative damage in experimental diabetic rat tissues

The role of oxidative stress has been reported in various diabetic complications. This study was undertaken to evaluate the protective effect of ginger, a medicinal plant, on the tissue antioxidant defence system and lipid peroxidative status in streptozotocin-induced diabetic rats. An increased reactive oxygen species and insufficient antioxidant activity are associated with diabetes mellitus, which is mainly responsible for diabetic pathogenesis. The role of ginger as antioxidant markers of liver and kidney were investigated. The antioxidant effect of the ginger was compared with glibenclamide, a well-known hypoglycaemic drug. The diabetic rats exhibited lower activities of superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), and glutathione reductase (GR) and reduced glutathione (GSH) content and higher level of malondialdehyde (MDA) in hepatic and renal tissues as compared with normal rats. The activities of all parameters were found to be increased, except MDA in ginger-treated diabetic rats, in hepatic and renal tissues. Ginger supplementation, for 30 days to diabetic rats, resulted in significant dose-dependent hypoglycaemic and antioxidant activities. These findings suggest that ginger treatment exerts a therapeutic protective effect in diabetes by decreasing oxidative stress, and hepatic and renal damage.     

Effect of free or protein-associated soy isoflavones on the antioxidant status in rats

BACKGROUND: The objective of this study was to investigate the effect of chronic ingestion of free and protein‐associated soy isoflavones on the antioxidant status in male Wistar rats. Free isoflavone (iso), protein‐associated soy isoflavone (iso + prot) and soy protein (prot) extracts were administered for 30 days by gavage to the rats at a dosage of 1 mg aglycone isoflavones per 200 g body weight, adjusted daily, and the prot group was given the same concentration of soy protein received by the iso + prot group. Antioxidant capacity of plasma, thiobarbituric acid‐reactive substance (TBARS) and glutathione (GSH) levels and catalase (CAT), glutathione peroxidase (GPx) and superoxide dismutase (SOD) activities in plasma, erythrocytes and tissues and gene expression levels in liver and kidney were evaluated. RESULTS: Chronic ingestion of free but not of protein‐associated soy isoflavones nor of solely soy protein increased plasma antioxidant capacity and GPx activity in erythrocytes. Soy protein increased CAT activity and gene expression in liver. SOD activity in erythrocytes was increased by all treatments. CONCLUSION: The overall results confirm that dietary soy isoflavones have a positive effect on antioxidant status, enhancing antioxidant capacity of plasma and antioxidant enzymes in various tissues, but the effects are dependent on the form of administration and on a complex mechanism of antioxidant status balance on the organism. Copyright © 2010 Society of Chemical Industry     

Angiotensin‐I‐Converting Enzyme Inhibitory Activities and In Vivo Antihypertensive Effects of Sardine Protein Hydrolysate

In our previous study, an antihypertensive protein hydrolysate was prepared from sardine. This study aimed to investigate the composition of sardine protein hydrolysate (SPH) and it's in vivo antihypertensive effect. SPH was separated sequentially with ultrafiltration and size exclusion chromatography. Fractions with high angiotensin‐I‐converting enzyme (ACE) inhibitory activity were further analyzed with RP‐HPLC and amino acids analysis. Then, SPH was individually oral administrated to spontaneously hypertensive rats (SHR) and normotensive wistar kyoto rats (WKY) for 4 wk. After treatment, the systolic blood pressure (SBP), organ index, oxidative status, serum ACE activity, and serum angiotensin‐II (ANG‐II) of all the rats were determined. According to the separation and analysis results, 3 main fractions with high ACE‐inhibitory activity were obtained with different amino acids composition. The animal experiments results showed that SPH could significantly reduce SBP (P < 0.05 or P < 0.01) within 4 h after a single oral administration. After a chronic oral administration, a steady state of SBP in SHR rats was attained. The heart weight index and left ventricular weight index were significantly reduced (P < 0.05) in SPH‐treated SHR rats. The malonyldialdehyde (MDA) levels in organs and serum, serum ACE activity, and serum ANG‐II concentration in SPH‐treated SHR rats were significantly lowered (P < 0.05 or P < 0.01) as compared to their controls. Meanwhile there was no significant effect (P > 0.05) on those parameters in WKY rats. These results indicate that SPH can decrease blood pressure in SHR rats and not in WKY rats.     

Mechanisms for antihypertensive effect of CocoanOX, a polyphenol-rich cocoa powder, in spontaneously hypertensive rats

We investigate the mechanisms involved in the long-term antihypertensive effect of a polyphenol-rich cocoa powder, named CocoanOX® (CCX), in spontaneously hypertensive rats (SHR). We have carried out two different batches of experiments. For the first batch of experiments, forty 3 week-old male SHR were randomly divided with ad libitum intake into four groups of 10 animals, that respectively received the following drinking fluids up to the 20th week of life (treatment period): tap water (control), CCX 100 mg/kg/day, CCX 200 mg/kg/day and CCX 400 mg/kg/day. Five 20 week-old rats of each group were sacrificed by decapitation. From the 20th to 24th week of life all the remaining animals were given tap water (follow-up period), and all of them were sacrificed at the end of the follow-up period. Plasma malondialdehyde (MDA), reduced glutathione in the liver, plasma and aorta angiotensin converting enzyme (ACE) activity and plasma angiotensin II were determined in all the sacrificed SHR that were included in this batch of experiments. Plasma MDA decreased and liver reduced glutathione increased in the 20 week-old CCX treated SHR. These effects were not observed in the rats that were sacrificed after the follow-up period. CCX treatment did not modify aorta ACE activity, but the activity of ACE and the levels of angiotensin II increased in the plasma of the SHR treated with the highest dose of CCX. ACE activity returned to basal values in the SHR that were sacrificed after the follow-up period. However, angiotensin II levels were slightly higher after withdrawal of CCX.For the second batch of experiments we used aorta rings obtained from untreated SHR, and we evaluated the relaxation caused by CCX in different aorta preparations. CCX relaxed the intact aorta preparations but this cocoa did not relax the endothelium-denuded aorta rings from the untreated SHR. l-NAME, but not indomethacin, inhibited the relaxation caused by CCX in the SHR aorta rings. We postulate that the antihypertensive effect of CCX might be mediated by an improvement of endothelial release of nitric oxide and by a reduction of oxidative stress. The inhibition of ACE could be implicated in the antihypertensive effect of CCX.     

Studies on the inhibitory effect of Graptopetalum paraguayense E. Walther extracts on the angiotensin converting enzyme

This study was aimed at evaluating the kinetic properties and capacities of water (GWE), 50% ethanolic (GE50) and 95% ethanolic (GE95) extracts from Graptopetalum paraguayense for the potential to inhibit angiotensin converting enzyme (ACE). The results showed that GWE, GE50 and GE95 showed potent inhibitory effects on ACE. It was found that the ACE inhibitory activities of all the tested extracts increased with the increase of their concentrations. In addition, the ACE inhibition of the tested extracts of G. paraguayense were significantly reduced after the addition of 1.5 mM ZnCl₂, suggesting the inhibitory action of the extracts may have resulted from the chelation of the ACE zinc cofactor. The inhibition kinetics, analyzed by Lineweaver–Burk plots, revealed that G. paraguayense extracts showed a mixed-type inhibition. A comparison of the 50% inhibition concentration (IC₅₀) and K_i values showed that the ethanolic extracts, including GE50 and GE95 exhibited the more effective ACE inhibitory activity than the water extracts of G. paraguayense.     

Effect of fermentation on the antioxidant activity of red beans (Phaseolus radiatus L. var. Aurea) ethanolic extract

The antioxidant activities of 50% ethanol extracts from red bean non-fermented and fermented by Bacillus subtilis or Aspergillus oryzae were determined using Sprague–Dawley rats as a testing model. Oral administration of all the extracts decreased the malondialdehyde (MDA) level in the liver but not in the brain tissue. Bacillus subtilis fermented extract increased the levels of ascorbic acid, α-tocopherol and glutathione (GSH) and the superoxide dismutase (SOD) activity in the liver tissue, while it increased only the ascorbic acid level in the brain tissue. Aspergillus oryzae fermented extract increased the levels of GSH and the SOD activity in the liver tissue, and it also increased GSH and ascorbic acid in the brain tissue. In general, the extracts from fermented red bean were more effective than the non-fermented extract in raising the antioxidant levels in the liver tissue.     

ANTIHYPERTENSIVE CAPACITY OF DEFATTED SOFT-SHELLED TURTLE POWDER AFTER HYDROLYSIS BY GASTROINTESTINAL ENZYMES

Soft‐shelled turtle (SST) is a high‐value animal cultivated in Asia, possessing many mystical folk curative properties in traditional Chinese medicine. This study investigated the effects of enzymatic hydrolysate derived from defatted SST powder on inhibition of angiotensin I‐converting enzyme (ACE) activity and on antihypertensive effect of spontaneously hypertension rats (SHR). The SST powder showed limited inhibition of ACE (IC₅₀ = 16.7 mg/mL), while its enzymatic hydrolysate exhibited a fivefold increase in inhibition of ACE (IC₅₀ = 3.2 mg/mL). The fraction of molecular weight (Mr) less than 1000 Da obtained through ultrafiltration exhibited the best inhibition of ACE (IC₅₀ = 2.8 mg/mL). The fraction of Mr less than 1000 was then separated into six fractions by gel filtration, eluted with deionized water, and the ACE inhibitory activity from three fractions was analyzed. Fractions 4 and 5 with Mr at 560–600 Da and 440–480 Da had the strongest inhibition on ACE. Single oral administration of 500 mg/kg BW dose from enzymatic hydrolysates to SHR showed a noticeable decrease of systolic blood pressure (SBP) at the sixth and eighth hour after the administration when compared to 0 h (P < 0.05). The fractions with Mr over 5000 Da from enzymatic hydrolysate significantly lowered SBP after a single oral administration at a dose of 500 mg/kg BW in SHR. On the other hand, Mr less than 5000 and 1000 Da significantly lowered SBP after a single oral administration at a dose of 150 and 50 mg/kg BW. The results suggested that hydrolysates of defatted SST powder, produced with a gastrointestinal enzyme, showed inhibition of ACE activity and antihypertensive effect in SHR.     

Neuroprotective effect of Decalepis hamiltonii roots against ethanol-induced oxidative stress

The neuroprotective potential of the aqueous extract of the roots of Decalepis hamiltonii (D. hamiltonii root aqueous extract-DHRAE) was studied against ethanol-induced oxidative stress in the rat brain. Ethanol, single dose (5 g/kg body weight), induced oxidative stress in the rat brain which was evident from the increased lipid peroxidation and protein carbonylation, reduced glutathione, and suppressed activities of antioxidant enzymes such as superoxide dismutase, catalase, glutathione peroxidase, glutathione reductase, and glutathione-S-transferase. Pretreatment of rats with multiple doses of DHRAE, 50 and 100 mg/kg b.w., for 7 consecutive days significantly prevented the ethanol-induced oxidative stress. DHRAE, as such, boosted the antioxidant status of the rat brain. The neuroprotective potential of DHRAE can be attributed to the known antioxidant constituents or its interaction with antioxidant response elements (AREs) which needs to be ascertained.     

Effect of dietary selenium on the progression of heart failure in the ageing spontaneously hypertensive rat

Oxidative stress has been directly implicated in hypertension and myocardial remodelling, two pathologies fundamental to the development of chronic heart failure. Selenium (Se) can act directly and indirectly as an antioxidant and a lowered Se status leads to a higher risk of cardiovascular disease. This study examined the role of Se on the development of hypertension and subsequent progression to chronic heart failure in spontaneously hypertensive rats (SHR). Three dietary groups were studied: (i) Se‐free; (ii) normal Se (50 μg Se/kg food); and (iii) high Se (1000 μg Se/kg food). Systolic blood pressure and echocardiography were used to detect cardiac changes in vivo. At study end, cardiac tissues were assayed for glutathione peroxidase activity, thioredoxin reductase activity, and protein carbonyls. The major finding of this study was the high heart failure‐related mortality rate in SHRs fed an Se‐free diet (70%). Normal and high levels of dietary Se resulted in higher survival rates of 78 and 100%, respectively. Furthermore, high dietary Se was clearly associated with lower levels of cardiac oxidative damage and increased antioxidant expression, as well as a reduction in disease severity and mortality in the SHR.     

Experimental evidence for the protective effects of coffee against liver fibrosis in SD rats

BACKGROUND: Coffee is one of the most commonly consumed beverages worldwide. Accumulating clinical evidence has shown an inverse relationship between coffee and liver cirrhosis. We investigated the protective effect of coffee against liver fibrosis and underlying molecular mechanisms using a dimethylnitrosamine (DMN)‐induced liver fibrosis model. RESULTS: Coffee administration significantly prevented the deterioration of body weight, organ weight, and serum biochemistry by DMN treatment. Histopathological examination revealed that necrosis/inflammation and fibrotic septa decreased significantly in coffee‐treated rats compared to those treated with DMN and water. Coffee administration also significantly inhibited the accumulation of hydroxyproline (P < 0.001) and the production of malondialdehyde (P < 0.05), as well as stellate cell activation caused by DMN injection. Coffee protected the depletion of glutathione, superoxide dismutase, and catalase in liver tissue. In addition, coffee treatment inhibited the gene expression of inducible nitric oxide synthase, transforming growth factor (TGF)‐β, tumor necrosis factor‐α, interleukin‐1, and platelet‐derived growth factor (PDGF)‐β in liver tissues, and lowered the concentration of TGF‐β and PDGF‐β in liver. Coffee inhibited NO production by macrophages. CONCLUSION: Coffee exerts protective effects against liver fibrosis via antioxidant action and the suppression of fibrogenic cytokines, TGF‐β and PDGF‐β. Copyright © 2009 Society of Chemical Industry     

大豆低聚肽对自发性高血压大鼠血压及血浆血管紧张素的影响

目的：探究大豆低聚肽对于大鼠血压及血浆血管紧张素的影响。方法：采用酶法制备大豆低聚肽,随后进行体外血管紧张素I转换酶（angiotensin I converting enzyme,ACE）活性抑制实验及体内实验,实验设正常对照组（正常血压大鼠（WKY大鼠）饲喂高剂量大豆低聚肽）、阴性对照组（自发性高血压大鼠（SHR大鼠））、阳性对照组（SHR大鼠饲喂卡托普利）和低、中、高剂量组（SHR大鼠饲喂0.90、1.80、4.50 g/kg大豆低聚肽）,喂养30 d后,观察大鼠血压、心率、尿蛋白质量、血管紧张素II质量浓度等指标的变化。结果：大豆蛋白最佳酶解条件为：碱性蛋白酶和中性蛋白酶质量分数各0.1%、50 ℃酶解4 h,此条件下10 mg/mL大豆低聚肽ACE活性抑制率达到71.2%。经饲喂不同剂量大豆低聚肽30 d后,WKY大鼠血压变化不显著（P＞0.05）,SHR大鼠血压有下降趋势;饲喂高剂量大豆低聚肽在第4周时可以显著降低SHR大鼠血压和血管紧张素II质量浓度（P＜0.05）,但对于大鼠心率和尿蛋白质量无显著影响（P＞0.05）。结论：体外实验证明,与大豆蛋白相比,大豆低聚肽对于ACE活性的抑制效果更好;体内实验证明大豆低聚肽可以降低SHR大鼠的血压和血管紧张素II质量浓度,且对正常大鼠血压无明显影响,推测大豆低聚肽通过抑制ACE活性的方式发挥降压功效。     

Aqueous extract of Hibiscus sabdariffa L. decelerates acetaminophen‐induced acute liver damage by reducing cell death and oxidative stress in mouse experimental models

BACKGROUND: Acetaminophen (AAP)‐induced oxidative stress can cause cell death to induce liver damage. The antioxidant effect of Hibiscus sabdariffa L. (HS) was shown in previous studies. In this study the effect of HS extract (HSE) on AAP‐induced liver injury in BALB/c mice was investigated. RESULTS: In vivo, BALB/c mice were fed orally with 200, 400 or 600 mg kg⁻¹ HSE for 2 weeks and then injected with 1000 mg kg⁻¹ AAP. Pretreatment with HSE decreased lipid peroxidation and increased catalase activity and glutathione level. It also decreased AAP‐induced liver injury, accompanied by decreased expression of pJNK, Bax and tBid in the liver. Additionally, HSE protected BALB/c normal liver cells from AAP‐induced damage in vitro. CONCLUSION: It has been demonstrated that HSE can protect the mouse liver from AAP‐induced injury and that the protective mechanism might involve decreasing oxidative stress and reducing cell death. Copyright © 2009 Society of Chemical Industry     

Chlorogenic acid promotes osteoblastogenesis in human adipose tissue-derived mesenchymal stem cells

High-fat diet (HFD)-induced obesity is associated with oxidative stress. The purpose of this study was to examine the antioxidant effect of Phaeodactylum tricornutum extract in mice with diet-induced obesity. Four-week-old C57BL/6J mice were fed a normal diet or HFD with and without 0.7% P. tricornutum lipid extract corresponding to 0.2% fucoxanthin for 8 weeks. P. tricornutum significantly decreased body weight and epidydimal white adipose tissue in mice fed the HFD. Serum triglyceride, glucose, insulin, and leptin levels, as well as homeostasis model assessment for insulin resistance (HOMA-IR) values, were significantly lower in the P. tricornutum group than in the HFD group. P. tricornutum significantly decreased thiobarbituric acid reactive substances (TBARS) and increased glutathione and the activities of superoxide dismutase, catalase, and glutathione peroxidase in the liver compared with the HFD group. Thus, P. tricornutum could exert antiobesity and antioxidant effects in mice fed a HFD.     

Antihypertensive activity of milk fermented by Enterococcus faecalis strains isolated from raw milk

A total of 231 microorganisms were isolated from raw cow milk samples and the angiotensin-converting enzyme-inhibitory (ACEI) activity of the resultant fermented milk produced with the isolated microorganisms was assayed. Forty-six of these microorganisms were selected on the basis of high ACEI activity. Four Enterococcus faecalis strains stood out as producers of fermented milk with potent ACEI activity (IC₅₀ (the protein concentration that inhibits 50% of ACE activity): 34–59 μg mL⁻¹). Single doses (5 mL kg⁻¹) of the whey fraction obtained from these fermented milk samples were administered to spontaneously hypertensive rats (SHR) and to normotensive Wistar-Kyoto (WKY) rats in order to investigate their possible antihypertensive activity. Highly significant decreases in the systolic blood pressure (SBP) and in the diastolic blood pressure (DBP) were observed when the fermented milk was administered to SHR. Nevertheless, the fermented milk did not modify the SBP and the DBP of the WKY rats. Raw cow milk is an excellent source of wild lactic acid bacteria able to produce fermented milk with antihypertensive activity and antihypertensive activity of milk fermented by Enterococcus faecalis strains was associated with peptides different from Ile-Pro-Pro and Val-Pro-Pro.     

Hepatoprotective effects of sea buckthorn (Hippophae rhamnoides L.) against carbon tetrachloride induced liver injury in rats

BACKGROUND: Liver injuries induced by carbon tetrachloride are the best‐characterized system of xenobiotic‐induced hepatotoxicity and commonly used model for the screening of hepatoprotective activities of drugs. The present study evaluates the hepatoprotective activity of sea buckthorn (Hippophae rhamnoides L.), family Elaeagnaceae, on carbon tetrachloride (CCl₄)‐induced liver injury in male albino rats. The study was performed on Sprague–Dawley male albino rats weighing about 180–200 g. The animals were pretreated with three different doses of leaf extract (50, 100 and 200 mg kg^?1 body weight) for 5 days. Hepatotoxicity was induced by single oral administration of 1.5 mL CCl₄ kg^?1 body weight on the fifth day. The animals were then sacrificed and assessed for various biochemical parameters. RESULTS: Administration of CCl₄ significantly enhanced glutamate oxaloacetate transferase (GOT), glutamate pyruvate transferase (GPT), alkaline phosphatase (ALP) and bilirubin, and decreased total protein levels in the serum. Treatment with CCl₄ also significantly decreased reduced glutathione (GSH), and decreased glutathione peroxidase and superoxide dismutase activity. CCl₄ treatment also caused a significant increase in hepatic lipid peroxidation as assessed by malondialdehyde (MDA) levels in the tissue. Pretreatment of leaf extract at a concentration of 100 and 200 mg kg^?1 body weight significantly (P < 0.05) protected the animals from CCl₄‐induced liver injury. The extract significantly restricted the CCl₄‐induced increase of GOT, GPT, ALP and bilirubin and better maintained protein levels in the serum. Further, it also enhanced GSH and decreased MDA levels. CONCLUSION: The results show that sea buckthorn leaf extract has significant hepatoprotective effects which might be due to its antioxidant activity and can be developed as a nutraceutical or food supplement against liver diseases. Copyright © 2008 Society of Chemical Industry     

Effect of date seeds on oxidative damage and antioxidant status in vivo

BACKGROUND: Date seeds have been shown to contain high amounts of antioxidants. However, in vivo studies on date seeds are lacking. Therefore the purpose of this study was to determine the effect of date seeds on oxidative damage and antioxidant status in vivo. Male Wistar rats were fed a basal diet containing 0, 70 or 140 g kg^?1 date seeds for 30 days. All three diets were isonitrogenous and isocaloric. Indication of oxidative damage was assessed in the liver and serum, and antioxidant status was assessed in the liver. Serum biochemical parameters, including indicators of tissue cellular damage and complete blood count with differential, were also determined. RESULTS: The results showed that date seeds significantly (P < 0.05) reduced liver and serum malondialdehyde (a lipid peroxidative damage product) and serum lactate dehydrogenase and creatine kinase. Liver antioxidants (vitamin E, vitamin C, glutathione, superoxide dismutase, glutathione peroxidase and catalase), complete blood count with differential and other serum biochemical parameters assessed were not significantly altered by date seeds. CONCLUSION: The results obtained suggest a protective effect of date seeds against in vivo oxidative damage, possibly through the action of their bioactive antioxidants. Copyright © 2011 Society of Chemical Industry     

Effect of supplementation with Cu and Zn on antioxidant enzyme activity in the rat tissues

The activities of antioxidant enzymes—copper, zinc- and manganese-superoxide dismutase (CuZnSOD and MnSOD), catalase (CAT), glutathione peroxidase (GSH-Px), glutathione S-transferase (GST) and glutathione reductase (GR)—were examined in the liver, heart, small intestine and brain, after supplementation with chelated forms of Cu and Zn. In the supplemented animals increased activity of CuZnSOD were found in the liver and heart. Activity of MnSOD and GSH-Px in the heart and GSH-Px in small intestine was decreased. After 43 days of Cu and Zn supplementation no changes in enzymes activity in the rats brain were found. The increased CuZnSOD activity in liver and heart after supplementation may be due to increased levels of the accumulation of excess Cu and Zn in these tissues. Decreased activity of other antioxidant enzymes could be the consequence of establishing a new antioxidant homeostasis, as Zn and Cu may act as antioxidants.