Paula Rossini Augusti

Astaxanthin prevents changes in the activities of thioredoxin reductase and paraoxonase in hypercholesterolemic rabbits

This study explored the effects of the antioxidant astaxanthin on paraoxonase and thioredoxin reductase activities as well as on other oxidative stress parameters and on the lipid profile in hypercholesterolemic rabbits. Rabbits were fed a standard or a hypercholesterolemic diet alone or supplemented with 50, 100 and 500 mg/100 g of astaxanthin for 60 days. Antioxidant enzymes activities, lipid profile and oxidative stress markers were evaluated in the serum. The hypercholesterolemic diet increased lipids, including unsaturated fatty acids level, whereas it decreased saturated fatty acids level. These changes were accompanied by increased levels of oxidized low-density lipoprotein and oxidized low-density lipoprotein antibodies, as well as lipid and protein oxidation. Astaxanthin (100 and 500 mg/100 g) prevented hypercholesterolemia-induced protein oxidation, whereas 500 mg/100 g of astaxanthin decreased protein oxidation per se. The activities of superoxide dismutase and thioredoxin reductase were enhanced, whereas paraoxonase activity was inhibited in hypercholesterolemic rabbits. All astaxanthin doses prevented changes in thioredoxin reductase and paraoxonase activities. This effect was not related to a direct effect of astaxanthin on these enzymes, because in vitro astaxanthin enhanced thioredoxin reductase and had no effect on paraoxonase activity. Astaxanthin could be helpful in cardiovascular diseases by restoring thioredoxin reductase and paraoxonase activities.

Astaxanthin reduces oxidative stress, but not aortic damage in atherosclerotic rabbits.

We evaluated whether carotenoid astaxanthin (ASX) could prevent oxidative and atherosclerotic damage in rabbits. Rabbits received regular chow (control) or an atherogenic diet (1% cholesterol) alone or supplemented with 50, 100, and 500 mg% ASX for 60 days (n = 5-9 per group). The atherogenic diet increased the serum cholesterol levels and the ratio of the intima/media area in the aortic arch. These changes were not prevented by ASX. Atherosclerotic rabbits showed increased aortic lipid peroxidation and nonprotein thiol group (NPSH) levels along with inhibition of glutathione peroxidase (GSH-Px). All ASX doses attenuated lipid peroxidation and the increase in NPSH but not the inhibition of GSH-Px. Aortic superoxide dismutase (SOD), catalase (CAT), and thioredoxin reductase (TrxR) activities were enhanced in atherosclerotic rabbits. Although all ASX doses prevented the increase in SOD activity, only 100 and 500 mg% ASX prevented the increase in CAT activity. Furthermore, these same doses partially prevented the increase in TrxR activity, while 50 mg% ASX completely prevented the effects of the atherogenic diet on this enzyme. However, ASX did not attenuate the hypercholesterolemia or the atherosclerotic lesions caused by the atherogenic diet at any of the doses evaluated. Our results indicate that although ASX did not prevent hypercholesterolemia or atherosclerotic lesions, it could play a beneficial role by preventing lipid peroxidation and changes in antioxidant enzyme activities.

The antiatherogenic effect of bixin in hypercholesterolemic rabbits is associated to the improvement of lipid profile and to its antioxidant and anti-inflammatory effects

Hypercholesterolemia and oxidative stress have been implicated in the pathophysiology of atherosclerosis and coronary artery disease. We investigated whether the carotenoid bixin (BIX) may reduce oxidative damage, inflammatory response, and the atherosclerotic lesion induced by hypercholesterolemia in rabbits. Rabbits received regular chow (control) or a hypercholesterolemic diet (0.5xa0% cholesterol) alone or supplemented with BIX (10, 30 or 100xa0mg/kg body weight, b.w.) or simvastatin (15xa0mg/kg b.w.) for 60xa0days. Treatment with BIX or simvastatin reduced the atherosclerotic lesions in cholesterol-fed rabbits (up to 55 and 96xa0% reduction, respectively). This protective effect of BIX was accompanied by decrease in the levels of tumor necrosis factor alpha by 15xa0%, interleukin 6 by 19xa0%, lipid peroxidation by 60xa0%, non-high-density lipoprotein cholesterol (non-HDL-C) by 37xa0%, and triglycerides by 41xa0%. BIX increased by 160xa0% the HDL-C levels and decreased by 67xa0% the atherogenic index of hypercholesterolemic rabbits. In atherosclerotic rabbits, the non-protein thiol groups content and the activity of the antioxidant enzymes superoxide dismutase, catalase, glutathione reductase, and thioredoxin reductase were increased in the aortic tissue, whereas paraoxonase activity was reduced in the serum. All these changes were completely prevented by BIX or simvastatin treatment. These results demonstrate that BIX reduces the extent of atherosclerotic lesions and this effect was associated with the decrease in oxidative stress, inflammatory response, and improvement of dyslipidemia, which were most effectively controlled after treatment with 10–30xa0mg BIX/kg b.w. BIX consumption may, therefore, be an adjuvant to prevent atherosclerosis reducing risk factors for coronary diseases.

Imbalance in superoxide dismutase/thioredoxin reductase activities in hypercholesterolemic subjects: relationship with low density lipoprotein oxidation

BackgroundThere is a relationship among hypercholesterolemia, oxidative stress and inflammation in the atherogenesis. Thus, the objective of the present study was to assess paraoxonase (PON1), superoxide dismutase (SOD) and thioredoxin reductase (TrxR-1) activities and their relationship with lipids, oxidative stress and inflammation in subjects with different low density lipoprotein-cholesterol (LDL) levels.MethodsSerum lipids, highly sensitive C-reactive protein (hs-CRP), lipid and protein oxidation, oxidized LDL (LDLox) and LDLox autoantibodies (LDLoxAB) levels and enzymes activities were measured in a total of 116 subjects that were divided into the following groups according to their LDL levels: low-LDL group (LDLu2009<u2009100u2009mg/dL, nu2009=u200923), intermediate-LDL group (LDL 100–160u2009mg/dL, nu2009=u200950) and high-LDL group (LDLu2009>u2009160u2009mg/dL, nu2009=u200943).ResultsThe LDLox and hs-CRP levels increased in the high-LDL group (2.7- and 3.7- fold, respectively), whereas the intermediate and high-LDL groups had higher LDLoxAB (2.2- and 3.1-fold) when compared to low-LDL group (pu2009<u20090.05). Similarly, SOD activity, the atherogenic index (AI) and protein oxidation were also higher in the intermediate (1.3-, 1.3- and 1.2-fold) and high-LDL (1.6-, 2.3- and 1.6-fold) groups when compared to the low-LDL group (pu2009<u20090.05). Lipid oxidation and SOD/TrxR-1 ratio increased only in the high-LDL group (1.3- and 1.6-fold) when compared to the low-LDL group (pu2009<u20090.05). The SOD/TrxR-1 ratio was positively correlated to TBARS (ru2009=u20090.23, pu2009<u20090.05), LDLox (ru2009=u20090.18, pu2009<u20090.05), LDLoxAB (ru2009=u20090.21, pu2009<u20090.05), LDL (ru2009=u20090.19, pu2009<u20090.05) and AI (ru2009=u20090.22, pu2009<u20090.05). PON1 and TrxR-1 activities were similar among groups.ConclusionsSome oxidative events initiate when LDL levels are clinically acceptable. Moreover, hypercholesterolemic patients have an imbalance in SOD and TrxR-1 activities that is positively associated to LDL oxidation.

Hydroethanolic extracts from different genotypes of açaí (Euterpe oleracea) presented antioxidant potential and protected human neuron-like cells (SH-SY5Y)

Fruit breeding programs have resulted in bioactive compounds increase and health effects. Thus, this study aimed to evaluate the antioxidant activity and neuroprotective effects of the hydroethanolic extracts from six açaí (Euterpe oleracea) genotypes using ABTS, deoxyribose, and glutathione oxidation assays, as well as, SH-SY5Y cells insulted with H2O2. L22P13 genotype showed the highest total content of anthocyanins, while L06P13 showed a high content of total carotenoids. However, the genotypes showed no difference in the antioxidant activity by ABTS and deoxyribose assays. The hydroethanolic extracts from different genotypes of açaí showed a protective effect (13-62%) on SH-SY5Y cells insulted by H2O2 at a concentration of 50μg/mL by DCFH-DA assay. Except L04P16, no genotypes showed cytotoxicity in the SRB assay. These results indicate that açaí genotypes have antioxidant effect against reactive species generated in SH-SY5Y cells, suggesting a neuroprotective effect of the hydroethanolic extracts from these fruits.

Wheat Bran and Cadmium in Human Health

Abstract Cadmium (Cd) is an important food contaminant that has a long half-life and high toxicity. Although cereals are among the foods that contribute most to dietary Cd exposure, some cereal constituents, especially those associated with bran, can decrease Cd bioavailability. This chapter focuses on the interaction between dietary Cd and wheat bran. To understand the mechanisms involved in the interaction between bran constituents and dietary minerals, we first review the effects of dietary fiber, phytates, and protein on metal bioavailability. We then discuss possible sources of Cd exposure as well as the toxicological aspects of dietary exposure to Cd. Finally, we review the specific interaction between wheat bran and Cd exposure, including the risk of wheat bran contamination with Cd and information from inxa0vitro and inxa0vivo studies regarding the constituents of wheat that may bind Cd and reduce its gastrointestinal absorption and accumulation.

Prooxidant activity of norbixin in model of acute gastric ulcer induced by ethanol in rats

Free radicals and oxidative stress play a central role in gastric injuries caused by ethanol (EtOH). Antioxidant strategies to counteract EtOH toxicity are highly desirable. Norbixin (NBIX) is a carotenoid with antioxidant potential largely used in the food industry. This study evaluated the NBIX effects in a model of gastric ulcer induced by EtOH in rats. Male Wistar rats received NBIX doses of 0, 10, and 25 mg/kg by gavage 1 h after EtOH administration (0 or 75% solution, 1 mL/200 g of animal). The animals were euthanized 1 h after the NBIX administration, and their stomachs were removed for macroscopic and histopathological analyses, quantification of nonprotein sulfhydryl (NPSH) groups, lipid peroxidation (LPO) levels, and catalase (CAT) activity determination. NBIX increased LPO in gastric mucosa and caused CAT inhibition and NPSH depletion in EtOH-treated animals. Results showed that NBIX did not protect gastric tissue against EtOH damage, and this could be associated to a prooxidant effect.

Acute Exposure to Low Lead Levels and its Implications on the Activity and Expression of Cytosolic Thioredoxin Reductase in the Kidney

Renal thioredoxin reductase‐1 (TrxR‐1) activity is stimulated at lead doses lower than that necessary to inhibit δ‐aminolevulinate dehydratase activity (δ‐ALA‐D), which is a classical early biomarker of lead effects. Thus, we hypothesized that the activity of TrxR‐1 could be a more sensitive early indicator of lead effects than is δ‐ALA‐D. To evaluate this hypothesis, we assessed the blood and renal TrxR‐1 activity and its gene expression along with biomarkers of oxidative damage, antioxidant enzyme activities and biomarkers of lead exposure in rats acutely exposed to lead. A histopathological analysis was performed to verify renal damage. The increase in renal TrxR‐1 activity paralleled the increase in the blood and renal lead levels at 6, 24 and 48 hr after the exposure to 25 mg/kg lead acetate (p < 0.05), whereas its expression was increased 24 and 48 hr after exposure. These effects were not accompanied by oxidative or tissue damage in the kidneys. Blood TrxR‐1 activity was not affected by lead exposure (up to 25 mg/kg). Erythrocyte δ‐ALA‐D activity was inhibited 6 hr after the exposure to 25 mg/kg lead acetate (p < 0.05) but recovered thereafter. Renal δ‐ALA‐D activity decreased 24 and 48 hr after the exposure to 25 mg/kg lead acetate. There were no changes in any parameters at lead acetate doses <25 mg/kg. Our results indicate that blood TrxR‐1 activity is not a suitable indicator of lead effects. In contrast, the increase in renal TrxR‐1 expression and activity is implicated in the early events of lead exposure, most likely as a protective cellular mechanism against lead toxicity.

Microcystin-LR exposure induces oxidative damage in Caenorhabditis elegans: Protective effect of lutein extracted from marigold flowers

Microcystin-LR (MIC-LR) is a hepatotoxin, with toxicity mechanisms linked to oxidative stress. Besides, neurotoxic effects of MIC-LR have recently been described. Herein, we evaluated the effects of environmentally important concentrations of MIC-LR (1, 10, 100, 250, and 500xa0μg/L) on oxidative stress markers and the survival rate of the nematode Caenorhabditis elegans (C. elegans). In addition, a possible protective effect of the carotenoid lutein (LUT) extracted from marigold flowers against MIC-LR toxicity was investigated. Higher concentrations (250 and 500xa0μg/L) of MIC-LR induced the generation of reactive oxygen species (ROS) and resulted in a survival loss in C elegans. Meanwhile, all MIC-LR concentrations caused an increase in the superoxide dismutase (SOD) expression, while catalase (CAT) expression was only affected at 500xa0μg/L. The carotenoid LUT prevented the ROS generation, impairment in the CAT expression, and the survival loss induced by MIC-LR in C.xa0elegans. Our results confirm the toxicity of MIC-LR even in a liver-lacking invertebrate and the involvement of oxidative events in this response. Additionally, LUT appears to be able to mitigate the MIC-LR toxic effects.

The Hepatoprotective Effect of Jaboticaba Peel Powder in a Rat Model of Type 2 Diabetes Mellitus Involves the Modulation of Thiol/Disulfide Redox State through the Upregulation of Glutathione Synthesis

Jaboticaba peel powder (JPP) is rich in bioactive compounds, mainly soluble and insoluble polyphenols with great antioxidant properties. The aim of this study is to evaluate the effects of JPP supplementation on the oxidative stress and hepatic damage in a rat model of type 2 diabetes mellitus (T2DM). Diabetic rats received vehicle or JPP at 2.7 (JPP-I), 5.4 (JPP-II), or 10.8 (JPP-III) g/L in drinking water during 8 weeks. JPP-III attenuated hyperglycaemia and dyslipidemia increased by 86% the liver content of nonprotein thiol groups and by 90% the GSH/GSSG ratio by activating glutathione synthesis. Accordingly, JPP supplementation prevented the loss of activity of the sulfhydryl-dependent enzyme δ-aminolaevulinic acid dehydratase and attenuated hepatic injury assessed by the reduction of serum aspartate aminotransferase activity and liver hypertrophy. Our results support that JPP supplementation to T2DM rats decreases hepatic damage most likely by increasing glutathione synthesis and modulating the thiol/disulfide redox balance.