Acid Reactive Substances Formation Research Articles

Physicochemical Properties and Oxidative Stability of an Emulsion Prepared from (-)-Epigallocatechin-3-Gallate Modified Chicken Wooden Breast Myofibrillar Protein.

The deterioration of wooden breast myofibrillar protein (WBMP) causes a decline in its processing performance, and the protein becomes easier to oxidize. Previous studies have revealed that the use of (-)-epigallocatechin-3-gallate (EGCG) may improve the physicochemical properties and oxidative stability of proteins in aqueous solutions. The effects of varying concentrations (0.01%, 0.02%, 0.03%, and 0.04% w/v) of EGCG on the physicochemical properties of a WBMP emulsion (1.2% WBMP/10% oil) and the inhibition of lipid and protein oxidation were studied. The results revealed that a moderate dose of EGCG (0.03%) could significantly (p < 0.05) improve the emulsion activity index (4.66 ± 0.41 m2/g) and emulsion stability index (91.95 ± 4.23%), as well as reduce the particle size of the WBMP emulsion. According to the micrographs and cream index, 0.03% EGCG retarded the phase separation by stopping the aggregation of droplets and proteins, thus significantly improving the stability of WBMP emulsions. During storage at 50 °C for 96 h, 0.03% EGCG inhibited lipid oxidation (lipid hydroperoxide and 2-thiobarbituric acid-reactive substance formation) and protein oxidation (carbonyl formation and sulfhydryl loss). In contrast, lower and higher EGCG concentrations (0.01%, 0.02%, and 0.04%) demonstrated shortcomings (such as weak antioxidant capacity or protein over-aggregation) in improving the quality and oxidation stability of the emulsion. In conclusion, a moderate dose of EGCG (0.03%) can be used to improve the quality and shelf life of WBMP emulsions.

Protection of mice against carbon tetrachloride-induced acute liver injury by endogenous and exogenous estrogens

Gender is a crucial factor determining susceptibility to drug-induced liver injury (DILI) in humans and experimental animals. However, no general concept of sex differences in DILI has been established, as metabolic events specific to one DILI model are difficult to apply to other DILI models. Herein, we examined sex differences in carbon tetrachloride (CCl4)-induced hepatotoxicity, a widely employed DILI model. Male and female CD-1 mice were intraperitoneally administered CCl4. Additionally, some male mice were administered genistein or another isoflavone to evaluate the effects of exogenous estrogens. Dose-dependent alanine aminotransferase leakage was observed at a CCl4 range of 0.5–10 mmol/kg, with male-dominant sex differences mainly observed at lower doses. No sex differences in hepatic glutathione levels or thiobarbituric acid-reactive substance formation were detected. CCl4 induced hepatic inflammatory genes, interleukin (IL)-6 and tumor necrosis factor (TNF)-α, predominantly in female mice, which might be involved in DILI resistance, observed in female mice. Treatment of male mice with phytoestrogens, especially genistein, attenuated CCl4-induced hepatotoxicity. Moreover, genistein inhibited IL-6 and TNF-α expression, suggesting possible hepatoprotection via immunosuppression. In conclusion, female mice are resistant to CCl4-induced hepatotoxicity, and male mice were afforded protection by genistein, probably via mechanisms based on anti-estrogenic, antioxidant and/or anti-inflammatory effects.

Impact of tea polyphenols on the stability of oil-in-water emulsions coated by whey proteins

The ability of tea polyphenols (0, 0.01, 0.02 or 0.04 w/v %) to inhibit lipid and protein oxidation in walnut oil-in-water (O/W) emulsions was examined, as well as to alter their stability to aggregation and creaming. The lipid droplets in these emulsions were coated by whey proteins. The physical stability of the emulsions during storage (50 °C, 96 h) was improved by addition of 0.01% tea polyphenols, but reduced when higher levels were added. Low levels (0.01%) of tea polyphenols inhibited lipid oxidation (lipid hydroperoxide and 2-thiobarbituric acid-reactive substance formation) and protein oxidation (carbonyl and Schiff base formation, sulfhydryl and intrinsic fluorescence loss, and molecular weight changes). However, high levels (0.04%) of tea polyphenols were less effective at inhibiting lipid oxidation, and actually promoted protein oxidation. Tea polyphenols are natural antioxidants that can enhance the quality and shelf life of emulsified polyunsaturated lipids when used at an appropriate concentration.

Antioxidant and cryoprotective effects of Amur sturgeon skin gelatin hydrolysate in unwashed fish mince

Antioxidant and cryoprotective effects of Amur sturgeon skin gelatin hydrolysates prepared using different commercial proteases in unwashed fish mince were investigated. Gelatin hydrolysates prepared using either Alcalase or Flavourzyme, were effective in preventing lipid oxidation as evidenced by the lower thiobarbituric acid-reactive substances formation. Gelatin hydrolysates were able to retard protein oxidation as indicated by the retarded protein carbonyl formation and lower loss in sulfhydryl content. In the presence of gelatin hydrolysates, unwashed mince had higher transition temperature of myosin and higher enthalpy of myosin and actin as determined by differential scanning calorimetry. Based on low field proton nuclear magnetic resonance analysis, gelatin hydrolysates prevented the displacement of water molecules between the different compartments, thus stabilizing the water associated with myofibrils in unwashed mince induced by repeated freeze–thawing. Oligopeptides in gelatin hydrolysates more likely contributed to the cryoprotective effect. Thus, gelatin hydrolysate could act as both antioxidant and cryoprotectant in unwashed fish mince.

Antioxidant and anti-inflammatory potential of the aqueous extract and polysaccharide fraction from brown marine macroalgae Padina sp. from Gulf of Mannar of Peninsular India

Objective: To evaluate the antioxidant and anti-inflammatory potential of the aqueous extract and polysaccharide fraction from two brown marine macroalga, Padina gymnospora (P. gymnospora) and Padina tetrastomatica (P. tetrastomatica) harvested from Gulf of Mannar of peninsular India. Methods: The antioxidant activity was evaluated using different in vitro systems, viz., 1,1- diphenyl-2-picrylhydrazyl (DPPH), 2, 2′-azino-bis-3ethylbenzothiozoline-6-sulfonic acid diammonium salt (ABTS), H2O2/ HO. radical scavenging, Fe2+ ion chelating ability, and reducing potential. Folin–Ciocalteu method was used to determine the total phenolic content, and the results were expressed as mg of gallic acid equivalents (GE). Thiobarbituric acid-reactive substance formation inhibition assay was employed to assess the ability of the samples to inhibit lipid oxidation in a model system. COXII and LOXV inhibition assays were employed to assess the anti-inflammatory potential of aqueous extract and polysaccharide fraction. Results: The aqueous extract fraction of P. tetrastomatica realized high total phenolic content (288 mg GE/g), and its activity towards scavenging short-lived radicals (OH. and H2O2) (27.8% and 68.3%, respectively; 0.6 mg/mL) are higher than those registered for Padina gymnospora. Aqueous extract and polysaccharide fractions of P. gymnospora showed higher anti-inflammatory activities against LOXV (56% and 53%, respectively) and COXII (30% and 35%, respectively; 1 mg/mL) enzymes. The correlation studies confirmed that polysaccharides present with the Padina sp. are responsible for their anti-inflammatory potential. IR spectral data of polysaccharide fraction revealed the presence of polysaccharide in alginate for

Markers of lipid peroxidation and α‐tocopherol levels in the blood and neoplastic tissue of dogs with malignant mammary gland tumors

Excess reactive oxygen species due to oxidative stress and the ensuing lipid peroxidation are believed to be involved in mammary gland tumor (MGT) pathogenesis. The purpose of this study was to evaluate the extent of lipid peroxidation as evidenced by thiobarbituric acid-reactive substances (TBARS) formation, and the concentration of α-tocopherol as an inhibitor of lipid peroxidation, in blood and neoplastic tissue of dogs with malignant MGT. The correlation between inflammatory cell infiltration score and TBARS or α-tocopherol in MGT was also evaluated. Sixteen intact female dogs with malignant MGT and 12 clinically healthy and age/weight-matched controls were included in the study. In all dogs, serum TBARS, α-tocopherol, total cholesterol, and triglycerides were measured. Tissue TBARS and α-tocopherol levels were determined in 1 cm(3) sized tissue samples collected from MGT and adjacent, ipsilateral, normal mammary gland tissue from the 16 affected dogs. The degree of inflammatory cell tumor infiltration was evaluated histologically. There were no statistically significant differences in serum levels of TBARS, α-tocopherol, total cholesterol, and triglycerides between dogs with and without malignant MGT. TBARS were significantly higher, whereas α-tocopherol was lower in neoplastic tissue when compared with normal mammary gland tissue. There was no correlation between TBARS or α-tocopherol concentration and the inflammatory cell infiltration score in neoplastic tissue. The increased level of TBARS suggests oxidative stress induction in canine malignant MGT. The origin of this phenomenon is not clear, as a potential oxidative burst could not be attributed to inflammatory cells infiltrating the tumors.

Antioxidant activity of ginseng cultivated under mountainous forest with different growing years

Ginseng cultivated and grown naturally under mountainous forest is formally called “Lin-Xia-Shan-Shen” (LXSS) and grown in manual condition is called garden ginseng (GG) according to Chinese pharmacopoeia (2010 edition). Usually the growing condition of LXSS is similar to wild ginseng and mostly used in Chinese folks in ancient times. The antioxidant properties of LXSS with different growing years were evaluated by their inhibitions of thiobarbituric acid-reactive substance (TBA-RS) formation in liver homogenate and 2, 2-diphenyl-1-picrylhydrazyl (DPPH)-radical scavenging activity comparing with those of GG. The inhibitions of different polar extracts (n-butanol and water) of LXSS and GG on TBA-RS formation were also evaluated. The results showed that the antioxidant effects of LXSS were higher than those of GG and the TBARS formation inhibition of LXSS with longer growing years were stronger than those with shorter growing years, while the DPPH-radical scavenging activity of LXSS did not show significant difference with the change of the growing year. The results indicated that the inhibitory effect of TBA-RS formation and the DPPH-radical scavenging of LXSS were correlated with the contents of ginsenosides. In adddition, the starch contents of LXSS and GG were determined by micro-amount method with spectrophotometer. It showed that the starch content in GG was higher than that of LXSS whose starch decreased gradually with the growing year.

Hepatoprotective action of dietary bluefin tuna skin proteins on CCl4-intoxicated mice

We have shown that dietary bluefin tuna skin (TUS) protects against carbon tetrachloride (CCl4)-induced hepatic damage in mice. The CCl4-induced necrotic area was decreased in mice fed a TUS-containing diet. Consistent with the decreased necrotic area, dietary TUS markedly lowered the elevated serum aspartate aminotransferase (AST) and alanine aminotransferase (ALT) activities and the thiobarbituric acid-reactive substance (TBARS) formation induced by CCl4 injection. TUS diets also decreased phosphorylation of inhibitory kappa B-α and blocked the translocation of nuclear factor-kappa B to the nucleus. TUS is composed mainly (80.7 %) of type I collagen, and our results revealed that dietary tuna collagen peptides (TUCP) attenuated the increased hepatic necrotic area, serum AST and ALT activities, and liver TBARS levels induced by CCl4, similar to TUS, thus enabling us to attribute the hepatoprotective action of TUS in CCl4-intoxicated mice to tuna collagen. Therefore, TUS and TUCP may be potential food resources that are capable of alleviating hepatitis symptoms.

Threshold dose of liver tumor promoting effect of β-naphthoflavone in rats

To determine the threshold dose of β-Naphthoflavone (BNF) that induces hepatocellular tumor promoting effects, reactive oxygen species (ROS) generation and thiobarbituric acid-reactive substance (TBARS) formation, and drug-metabolizing enzymes that protect against ROS generation, two-stage liver carcinogenesis model was used. Partial hepatectomized rats (n = 11 to 12) were fed diets containing 0, 0.03, 0.06, 0.125 or 0.25% BNF for 6 weeks after an intraperitoneal injection of N-diethylnitrosamine (DEN) to initiate hepatocarcinogenesis. Histopathologically, glutathione S-transferase placental form (GST-P)-positive foci significantly increased in rats given 0.25% BNF. No marked changes in ROS production and TBARS contents were observed between the BNF treated and DEN alone groups. Real-time RT-PCR showed that the expression of Cyp1a1, Cyp1a2, Cyp1b1 and Nqo1 significantly increased in the groups given 0.03% BNF or more, but Ugt1a6, Akr7a3 and Gstm1 significantly increased in the groups given 0.125% BNF or more. Gpx2 and Yc2 significantly increased in the groups given 0.06% BNF or more and 0.25% BNF, respectively. Inflammation-related genes such as Ccl2, Mmp12, Serpine1 and Cox-2 significantly increased in the 0.25% BNF group. In immunohistochemistry, the number of cyclooxygenase-2 (COX-2)-positive cells increased in rats given 0.25% BNF. These results suggest that 0.25% BNF is the threshold dose for liver tumor promotion, and the fact that inflammation-related genes and COX-2 protein increased in the 0.25% BNF group strongly suggests that inflammation is involved in the liver tumor promoting effect of BNF in rats.

Platelet activation, oxidative stress and overexpression of inducible nitric oxide synthase in moderate heart failure

1. Chronic heart failure (CHF) is a common disabling disorder associated with thromboembolic events, the genesis of which is not yet fully understood. Nitric oxide (NO), derived from the vascular endothelium and platelets, has an important role in the physiological regulation of blood flow. It is generated from the amino acid L-arginine via NO synthase (NOS). 2. The main objective of the present study was to investigate NO production and its relationship with platelet aggregation, oxidative stress, inflammation and related amino acids in patients with moderate CHF. The expression and activity of NOS isoforms were analysed by western blotting and conversion of L-[(3)H]-arginine to L-[(3)H]-citrulline, respectively, in CHF patients (n = 12) and healthy controls (n = 15). Collagen- and ADP-induced platelet aggregation, oxidative stress (thiobarbituric acid-reactive substances (TBARS) formation and superoxide dismutase (SOD) activity) and plasma levels of amino acids and inflammatory markers (fibrinogen and C-reactive protein (CRP)) were also determined. 3. Both collagen- and ADP-induced platelet aggregation were increased in CHF patients compared with controls. Platelets from CHF patients did not show any changes in NOS activity in the presence of overexpression of inducible NOS. Systemic and intraplatelet TBARS production was elevated, whereas SOD activity was decreased in CHF patients. l-arginine plasma concentrations were lower in CHF patients than in controls. Systemic levels of CRP and fibrinogen were increased in CHF patients. 4. The results show that, in patients with moderate CHF, there is platelet activation and reduced intraplatelet NO bioavailability due to oxidative stress, which suggests a role for platelets in the prothrombotic state.

Comparative evaluation of manganese peroxidase- and Mn(III)-initiated peroxidation of C18 unsaturated fatty acids by different methods

The peroxidation of C18 unsaturated fatty acids by fungal manganese peroxidase (MnP)/Mn(II) and by chelated Mn(III) was studied with application of three different methods: by monitoring oxygen consumption, by measuring conjugated dienes and by thiobarbituric acid-reactive substances (TBARS) formation. All tested polyunsaturated fatty acids (PUFAs) were oxidized by MnP in the presence of Mn(II) ions but the rate of their oxidation was not directly related to degree of their unsaturation. As it has been shown by monitoring oxygen consumption and conjugated dienes formation the linoleic acid was the most easily oxidizable fatty acid for MnP/Mn(II) and chelated Mn(III). However, when the lipid peroxidation (LPO) activity was monitored by TBARS formation the linolenic acid gave the highest results. High accumulation of TBARS was also recorded during peroxidation of linoleic acid initiated by MnP/Mn(II). Action of Mn(III)-tartrate on the PUFAs mimics action of MnP in the presence of Mn(II) indicating that Mn(III) ions are involved in LPO initiation. Although in our experiments Mn(III) tartrate gave faster than MnP/Mn(II) initial oxidation of the unsaturated fatty acids with consumption of O 2 and formation of conjugated dienes the process was not productive and did not support further development of LPO. The higher effectiveness of MnP/Mn(II)-initiated LPO system depends on the turnover of manganese provided by MnP. It is proposed that the oxygen consumption assay is the best express method for evaluation of MnP- and Mn(III)-initiated peroxidation of C18 unsaturated fatty acids.

Inhibition of liver X receptor-α-dependent hepatic steatosis by isoliquiritigenin, a licorice antioxidant flavonoid, as mediated by JNK1 inhibition

Isoliquiritigenin (ILQ), a flavonoid obtained from Glycyrrhizae species, has an antioxidant effect. This study investigated the potential of ILQ for inhibiting liver X receptor-α (LXRα)-mediated lipogenesis and steatosis in hepatocytes and its underlying molecular basis. Treatment with ILQ antagonized the ability of an LXRα agonist (T0901317) to activate sterol regulatory element binding protein-1c (SREBP-1c), thereby repressing transcription of fatty acid synthase, acetyl-CoA carboxylase, ATP-binding cassette transporter-A1, and stearoyl-CoA desaturase-1. ILQ treatment inhibited activating phosphorylation of JNK1 elicited by palmitate or TNFα. JNK1, but not JNK2, increased LXRα phosphorylation at serine residues, promoting LXRα activation. The ability of ILQ to inhibit JNK1 downstream of ASK1–MKK7 led to the repression of T0901317-inducible LXRα and SREBP-1c activation. In mice fed a high-fat diet, ILQ treatment inhibited hepatic steatosis, as shown by a decrease in fat accumulation and repression of lipogenic genes. The results of blood biochemistry and histopathology confirmed attenuation of high-fat diet-induced liver injury by ILQ. Moreover, ILQ inhibited oxidative stress, as indicated by decreases in thiobarbituric acid-reactive substance formation, iNOS and COX2 induction, and nitrotyrosinylation. Our results demonstrate that ILQ has the ability to repress LXRα-dependent hepatic steatosis through JNK1 inhibition and protect hepatocytes from oxidative injury inflicted by fat accumulation.

Inhibition of SREBP-1c-mediated hepatic steatosis and oxidative stress by sauchinone, an AMPK-activating lignan in Saururus chinensis

Sauchinone, as an AMP-activated kinase (AMPK)-activating lignan in Saururus chinensis, has been shown to prevent iron-induced oxidative stress and liver injury. Sterol regulatory element binding protein-1c (SREBP-1c) plays a key role in hepatic steatosis, which promotes oxidative stress in obese subjects. Previously, we identified the role of AMPK in liver X receptor-α (LXRα)-mediated SREBP-1c-dependent lipogenesis. Because sauchinone as an antioxidant has the ability to activate AMPK, this study investigated its effects on SREBP-1c-dependent lipogenesis in hepatocytes and in high-fat diet (HFD)-induced hepatic steatosis and oxidative injury. Sauchinone prevented the ability of an LXRα agonist (T0901317) to activate SREBP-1c, repressing transcription of the fatty acid synthase, acetyl-CoA carboxylase, stearoyl-CoA desaturase-1, ATP-binding cassette transporter A1, and LXRα genes. Consistent with this, an HFD in mice caused fat accumulation in the liver with SREBP-1c induction, which was attenuated by sauchinone treatment. Also, sauchinone had the ability to inhibit oxidative stress as shown by decreases in thiobarbituric acid-reactive substance formation, nitrotyrosinylation, and 4-hydroxynonenal production. Moreover, it prevented not only the liver injury, but also the AMPK inhibition elicited by HFD feeding. These results demonstrate that sauchinone has the capability to inhibit LXRα-mediated SREBP-1c induction and SREBP-1c-dependent hepatic steatosis, thereby protecting hepatocytes from oxidative stress induced by fat accumulation.

Salicylic acid-induced hepatotoxicity triggered by oxidative stress

Salicylic acid is a widely used nonsteroidal anti-inflammatory drug (NSAID). But it is known to cause serious liver damage occasionally. Mitochondrial dysfunction and oxidative stress are predicted to be the major factors of salicylic acid-induced liver injury. We investigated the influence of salicylic acid on ATP contents, oxygen consumption and lipid peroxidation in the presence of the same concentration of salicylic acid. Leakage of lactate dehydrogenase (LDH) was significantly higher in the presence of 5 mM salicylic acid than in its absence. Salicylic acid-induced thiobarbituric acid-reactive substance (TBARS) formation and spontaneous chemiluminescence (CL) in rat hepatocytes, whereas antioxidants, such as promethazine (PMZ) and N,N-diphenylphenylenediamine (DPPD), suppressed both TBARS formation and LDH leakage. TBARS formation in rat liver microsomes was suppressed by diethyldithiocarbamate (a specific inhibitor of cytochrome P450 (CYP)2E1) and diclofenac (a specific inhibitor of CYP2C11). These results suggest that salicylic acid-induced lipid peroxidation was related to oxidative metabolism mediated by CYP2E1 and CYP2C11. On the other hand, 5 mM salicylic acid induced a drastic decrease of ATP contents in rat isolated hepatocytes. Furthermore, mitochondrial respiration control ratio (RC ratio), calculated by State 3/State 4 also decreased with the increase of salicylic acid concentration. These findings suggest that salicylic acid would trigger mitochondrial dysfunction and cause ATP decrease, leading to lethal liver cell injury by lipid peroxidation, although this hypothesis remains to be elucidated in vivo.

Acetylcholinesterase Activity, Lipid Peroxidation, and Bioaccumulation in Silver Catfish (Rhamdia quelen) Exposed to Cadmium

Cadmium is a metal with no biological function in superior organisms and it is very toxic even at very low concentrations. Thus the objective of this study was to verify some toxicological parameters in silver catfish (Rhamdia quelen) exposed to cadmium. In this study, silver catfish was exposed to 0 (control), 0.236, and 0.414 mg L(-1) cadmium for 7 and 14 days, followed by the same periods of recovery. The effects of cadmium on acetylcholinesterase (AChE) activity and metal accumulation in brain and muscle were verified. Thiobarbituric acid-reactive substance (TBARS) formation was evaluated in brain. An increase in TBARS levels was verified after exposure and recovery periods and AChE activity in brain was reduced after 14 days of exposure. These parameters did not return to control values after the recovery period. In muscle AChE was altered during both exposure periods. Alterations in AChE activity may be a good indicator of cadmium contamination in R. quelen.

Antioxidant Activity of Some Polyphenolic Extracts Obtained from Plants with Antitumoral Potential on Linoleic Acid Emulsion

Polyphenols consist in a wide range of biological molecules present in plants and they have a variety of biological and chemical activities in vitro and in vivo. The most important classes of polyphenols are flavonoids and phenolic acids. Plant polyphenols are especially known for their important antioxidant activity; for instance, lipid peroxidation is implicated in the pathogenesis of cancer, atherosclerosis and toxic cell injuries. In this study, air dried aerial parts of European Mistletoe (Viscum album), European Birthwort (Aristolochia clematitis), Greater Celandine (Chelidonium majus) and Stag’s-horn Clubmoss (Lycopodium clavatum) were powdered and extracted with 60% ethanol (v/v). The total polyphenols content of the ethanolic extracts was estimated by a spectrophotometric method. The ethanolic extracts were investigated for antioxidant activity in linoleic acid/water emulsion system. The progression of the oxidation processes was monitored at 80°C for 7 days by measuring conjugated dienes, hydroperoxides and thiobarbituric acid reactive substances (TBARS) formation. The antioxidant activity of the sample extracts was expressed as inhibition percentage, comparatively to controls containing no antioxidant. The obtained results revealed that the vegetal extracts inhibited the formation of conjugated dienes, lipid hydroperoxides and thiobarbituric acid reactive substances (TBARS); the dynamics of lipid peroxidation inhibition is different from one plant to another

ANTIOXIDANT ACTIVITY OF ENGLISH WALNUT (JUGLANS REGIA L.)

ABSTRACT Phenolic contents of different fractions (contents of whole nut, skin and kernel) of English walnut (Juglans regia L.) were determined and their antioxidative capacities investigated using a number of in vitro model systems. Phenolic compounds extracted from walnut skin into 95% ethanol contained the highest amount of total phenolics and exhibited the highest antioxidative capacity as evaluated by the trolox equivalent antioxidant capacity assay. Extracts of walnut phenolics showed a high ferrous ion chelating ability and effectively scavenged 2,2′‐diphenyl‐1‐picrylhydrazyl radicals, the latter considerably stronger for the skin with 50% inhibition concentration of 3.4 µg extract per mL. Further, inhibition of 2‐thiobarbituric acid reactive substances formation in a bulk corn oil model system was also significant (P < 0.05) for all three phenolic extracts and for pure gallic acid at 10 ppm gallic acid equivalents final assay concentration after four days of storage at 60C.PRACTICAL APPLICATIONSWalnut is a healthful nut that contains alpha‐linolenic acid in its lipid fraction, and its skin is rich in polyphenolics with strong antioxidant properties, as demonstrated in this study. Thus, walnut with skin and skin of walnuts serve as good free radical scavengers and could be effective in reducing oxidative stress among other beneficial health effects, which could be exploited for product development.

Protective Effects of Amburoside A, a Phenol Glucoside from Amburana cearensis, against CCl4-Induced Hepatotoxicity in Rats

The aim of this study was to investigate the possible beneficial effects of amburoside A, AMB [4-(O-beta- D-glycopyranosyl)benzyl protocatechoate], against carbon tetrachloride (CCl (4)) toxicity in rats. AMB is a phenol glucoside from the Brazilian medicinal plant Amburana cearensis, popularly used for the treatment of respiratory tract affections. Acute AMB (25 and 50 mg/kg, I. P. or P. O.) treatments of CCl (4)-intoxicated rats significantly inhibited the increase in serum aspartate aminotransferase (AST) and alanine aminotransferase (ALT) levels, as compared to the group treated with CCl (4) only. Histological studies showed less centrolobular necrosis and inflammatory cell infiltrates in the liver of animals treated with AMB plus CCl (4), when compared to the group treated with CCl (4) alone. In hepatic tissues, AMB at both doses inhibited CCl (4)-induced thiobarbituric acid-reactive substances (TBARS) formation, indicating a blockade of CCl (4)-induced lipid peroxidation. AMB also reversed the decrement in glutathione contents of hepatic tissues in CCl (4)-intoxicated rats. Furthermore, it restored catalase activity to normal values, which was significantly increased after CCl (4) treatment. Our results indicate that CCl (4)-induced oxidative damage in hepatic tissues is reversed by AMB treatment. The protective effect of AMB is probably due to the phenolic nature of this glucoside.

Hepatoprotective role of captopril on paraquat induced hepatotoxicity

Paraquat (PQ) is a highly toxic herbicide that is used in most of the countries without restriction. The cytotoxic effect of PQ is mediated by radicals, which are the products of PQ reduction in cells. The anti-oxidative action of captopril, an angiotensin-converting enzyme inhibitor, appears to be through its ability to scavenge reactive oxygen species. In this study, the heptoprotective effect of captopril against PQ-induced hepatotoxicity was evaluated using primary cultured rat hepatocytes. Hepatocytes were isolated from male Wistar rats using a two-step collagenase perfusion, following incubation in the presence of captopril at 0.1, 0.2, 0.4 and 0.8 mM with or without PQ (5 mM). Hepatoprotective effects of captopril were studied indicating glutathione level intensity, thiobarbituric acid reactive substances (TBARs) formation, lactate dehydrogenase (LDH) leakage and cell viability every 70 min for 210 min. Captopril at 0.2 mM concentration maintained the LDH leakage, glutathione level and cell viability in the presence of 5 mM PQ. In spite of a significant elevation in TBARs formation in the PQ group, captopril did not show any significant protection. In conclusion, our data reveals that incubation of freshly isolated rat hepa-tocytes with captopril (0.2 mM) significantly protected the hepatocytes against the cytotoxicity of PQ (P < 0.05).

The effects of an iron-catalyzed oxidation system on lipids and proteins of dark muscle fish

The effects of a hydroxyl radical-generating system induced by iron catalyzed oxidation (Fe 2+/H 2O 2) on lipids and proteins of sardine, Atlantic bonito, anchovy and bluefish were investigated. Thiobarbituric acid-reactive substances (TBARs, mg malonaldehyde/kg fish muscle) formation was used to evaluate oxidative damage of the lipid in dark muscle fish due to iron catalyzed oxidation. The amount of TBARs was observed to increase significantly in sardine and anchovy as the incubation time increased, while Atlantic bonito and bluefish reached their maximum values of TBARs within the first 3 h of incubation, and after that did not change ( p < 0.05). Carbonyl contents (nmol carbonyl/mg protein) of all fish samples measured as an index of protein oxidation were affected differently by the iron-catalyzed oxidation system during incubation. However, significant increases in the carbonyl groups were detected in sardine, Atlantic bonito and bluefish, but not in anchovy as a result of the long incubation time (5 h) ( p < 0.05). When comparing to increases Atlantic bonito showed the maximum increase protein carbonyl. The electrophoretic patterns in the presence and absence of β-mercaptoethanol showed that a loss of proteins generally occurred in all fish at the end of incubation, and the greatest alteration in protein bands was observed in anchovy during Fe 2+-catalyzed oxidation. The bands above 50 kDa disappeared within the first 1 h of incubation. The loss of protein (both high and low molecular weight) may involve disulfide and non-disulfide covalent linking during the iron catalyzed incubation. These data suggest that an increase in TBARs and fragmentation, and a loss of proteins exposed to iron-catalyzed oxidation may explain the oxidative damage of lipids and proteins which causes quality loss and limits the storage life of dark muscle fish.