Hydroperoxide Levels Research Articles

The potential toxic effects of hexavalent chromium on oxidative stress biomarkers and fatty acids profile in soft tissues of Venus verrucosa.

Hexavalent chromium (chromium (VI)), a highly toxic heavy metal, is a common pollutant of aquatic ecosystems. The present study aimed to elucidate the potential toxic effects of chromium (VI) on oxidative stress biomarkers and fatty acids profile in the gills and digestive gland of Venus verrucosa, an ecologically and economically important bivalve species. Three doses of chromium (VI) (1, 10 and 100μg.L-1) were chosen for V. verrucosa exposure during 7 days under controlled conditions. A significant increase in the levels of malondialdehyde, lipid hydroperoxides and hydrogen peroxide was observed in the gills and digestive gland of chromium (VI)-exposed V. verrucosa as compared to the control group. Furthermore, an induction of enzymatic antioxidant activities (superoxide dismutase, glutathione peroxidase and glutathione S-transferase) and an enhancement of non-enzymatic antioxidant levels (non-protein thiols, glutathione and vitamin C) were marked. An alteration of fatty acids composition was also noted following chromium (VI) exposure. The obtained results highlighted the importance of assessing oxidative damage biomarkers and fatty acids profile in the study of chromium (VI)-induced toxicity in V. verrucosa.

Biomarkers of the oxidative stress and neurotoxicity in tissues of the bullfrog, Lithobates catesbeianus to assess exposure to metals

Lithobates catesbeianus tadpoles were exposed to 1μgL-1 of zinc (Zn), copper (Cu) and cadmium (Cd) alone or combined (1:1 and 1:1:1) for 2 and 16 days. Results showed a significant increase in the superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx) and glutathione S-transferase (GST) activities in the liver, kidney and muscle (except for GPx) in the groups exposed to metal either alone or co-exposed after 2 days compared to the control. After 16 days, SOD, CAT and GST activities decreased significantly in the liver and kidney and GPx activity increased in the liver. Reduced glutathione (GSH) increased in the liver and kidney following combined exposure and decreased after 2 days of metal exposure in the muscle. There were significant increases in lipid hydroperoxide (LPO) levels in the liver, kidney and muscle (2 and 16 days), with the highest levels after metal co-exposure. Cholinesterase (ChE) activity increased significantly in the brain after 2 days of exposure but decreased in the brain (16 days) and muscle (2 days) after exposure to metals, alone and combined. The current study highlighted that the antioxidant system of L. catesbeianus was sensitive to metals and specially to the co-exposure of the three metals, despite presenting differences in the response among tissues. In addition, tadpoles were sensitive at both periods of exposure, but in different modes with stress response (activation, up-regulation) at 2 days and oppression (down-regulation) at 16 days.

Эффективность реамберина в коррекции процессов перекисного окисления липидов в плазме крови больных эпилепсией детей

The antioxidant activity of reamberin was studied in children with epilepsy: 10 patients with epilepsy received intravenous reamberin (Research and Technological Pharmaceutical Firm POLYSAN, Saint Petersburg, Russia) 200 ml of 1,5 % infusion solution at a rate of 40-80 drops/min (2-4 ml/min) once daily for 5 days; 15 patients with epilepsy received only valporic acid (a control group). The efficacy of the medication was evaluated by the levels of lipid hydroperoxides, conjugated dienes, and malondialdehyde and by the activity of the main components of the antioxidant system (ceruloplasmin, vitamin E, catalase) in the blood of epileptic children. The administration of reamberin to patients with epilepsy significantly reduced the plasma levels of lipid hydroperoxides by 15 %, conjugated dienes by 15 %, and malondialdehyde by 24 % compared to the patients in the control group. An analysis of the effect of succinate-containing medications on the activity of the antioxidant system components revealed that the blood concentrations of ceruloplasmin and catalase were 37 % and 24 %, respectively, higher than those in the control group. Thus, the inclusion of reamberin into the treatment of children with epilepsy should be considered pathogenically justified, clinically reasonable, and promising.

Spirulina Lipids Alleviate Oxidative Stress and Inflammation in Mice Fed a High-Fat and High-Sucrose Diet.

High-fat and high-sucrose diet (HFHSD)-induced obesity leads to oxidative stress and chronic inflammatory status. However, little is known about the beneficial effects of total lipids extracted from Spirulina. Hence, in the present study, Spirulina lipids were extracted with chloroform/methanol (SLC) or ethanol (SLE) and then their effects on oxidative stress and inflammation in the mice fed a HFHSD were investigated. The results show that the major lipid classes and fatty acid profiles of SLC and SLE were almost similar, but the gamma-linolenic acid (GLA) and carotenoid contents in SLE was a little higher than that in SLC. Dietary 4% SLC or SLE for 12 weeks effectively decreased the hepatic lipid hydroperoxide levels as well as increased the activities and mRNA levels of antioxidant enzymes in the mice fed a HFHSD. In addition, supplementation with SLC and SLE also markedly decreased the levels of serum pro-inflammatory cytokines and the mRNA expression of pro-inflammatory cytokines in the liver and epididymal white adipose tissue of mice fed a HFHSD, and the effects of SLC and SLE were comparable. These findings confirm for the first time that dietary Spirulina lipids could alleviate HFHSD-induced oxidative stress and inflammation.

Expression of Heterologous OsDHAR Gene Improves Glutathione (GSH)-Dependent Antioxidant System and Maintenance of Cellular Redox Status in Synechococcus elongatus PCC 7942.

An excess of reactive oxygen species (ROS) can cause severe oxidative damage to cellular components in photosynthetic cells. Antioxidant systems, such as the glutathione (GSH) pools, regulate redox status in cells to guard against such damage. Dehydroascorbate reductase (DHAR, EC 1.8.5.1) catalyzes the glutathione-dependent reduction of oxidized ascorbate (dehydroascorbate) and contains a redox active site and glutathione binding-site. The DHAR gene is important in biological and abiotic stress responses involving reduction of the oxidative damage caused by ROS. In this study, transgenic Synechococcus elongatus PCC 7942 (TA) was constructed by cloning the Oryza sativa L. japonica DHAR (OsDHAR) gene controlled by an isopropyl β-D-1-thiogalactopyranoside (IPTG)-inducible promoter (Ptrc) into the cyanobacterium to study the functional activities of OsDHAR under oxidative stress caused by hydrogen peroxide exposure. OsDHAR expression increased the growth of S. elongatus PCC 7942 under oxidative stress by reducing the levels of hydroperoxides and malondialdehyde (MDA) and mitigating the loss of chlorophyll. DHAR and glutathione S-transferase activity were higher than in the wild-type S. elongatus PCC 7942 (WT). Additionally, overexpression of OsDHAR in S. elongatus PCC 7942 greatly increased the glutathione (GSH)/glutathione disulfide (GSSG) ratio in the presence or absence of hydrogen peroxide. These results strongly suggest that DHAR attenuates deleterious oxidative effects via the glutathione (GSH)-dependent antioxidant system in cyanobacterial cells. The expression of heterologous OsDHAR in S. elongatus PCC 7942 protected cells from oxidative damage through a GSH-dependent antioxidant system via GSH-dependent reactions at the redox active site and GSH binding site residues during oxidative stress.

Eicosapentaenoic acid (EPA) has optimal chain length and degree of unsaturation to inhibit oxidation of small dense LDL and membrane cholesterol domains as compared to related fatty acids in vitro

BackgroundOxidation of small dense low-density lipoprotein (sdLDL) and membranes is causally related to atherosclerosis. The omega-3 fatty acid (FA) eicosapentaenoic acid (EPA, 20:5, ω-3) significantly reduced oxidized LDL in patients with hypertriglyceridemia by unknown mechanisms. We compared EPA effects to related FAs of varying chain length and unsaturation on oxidation of sdLDL and model membranes, and on cholesterol crystal domains. We compared EPA to the FAs: stearic (SA, 18:0), oleic (OA, 18:1, ω-9), linoleic (LA, 18:2, ω-6), alpha-linolenic (ALA, 18:3, ω-3), eicosanoic (EA, 20:0), eicosatrienoic (ETE, 20:3, ω-3), arachidonic (AA, 20:4, ω-6), docosapentaenoic (DPA, 22:5, ω-3), and docosahexaenoic (DHA, 22:6, ω-3). MethodsHuman sdLDL or model membranes of cholesterol and 1,2-Dilinoleoyl-sn-glycero-3-phosphocholine [18:2(cis)PC or DLPC] were preincubated with FAs followed by copper-induced oxidation. Malondialdehyde (MDA) or lipid hydroperoxides (LOOH) levels measured oxidation; small-angle X-ray diffraction assessed cholesterol domain formation. ResultsAfter 40 min, EPA reduced MDA levels 70% compared to vehicle (p < 0.001). Lesser inhibition was observed with DHA, DPA, ETE, and ALA (33%, 34%, 32%, and 16%, respectively; all p < 0.001 versus vehicle). Similar relative FA effects were observed in model membranes where EPA more substantially inhibited cholesterol crystal domain formation. ConclusionWe observed relationships between hydrocarbon length and unsaturation with antioxidant activity and membrane cholesterol domain formation. EPA had the most favorable molecular structure, likely contributing to membrane stability, improved lipoprotein clearance, and reduced inflammation. General significanceInsight is provided into FA hydrocarbon length and unsaturation relationships with antioxidant activity in lipoproteins and membranes, and cholesterol crystal domains formation.

Neuroprotective and hepatoprotective effect of whole red rice forms against oxidative stress in streptozotocin induced diabetic rats

Whole red rice ( Oryza sativa L.), consumed as staple food in many countries worldwide, is rich in phytochemicals, mainly antioxidants having health potency. The present study evaluated the neuro- and hepatoprotective efficacy of raw and parboiled whole red rice against streptozotocin (STZ) induced oxidative stress, and antioxidant metabolism both in diabetic and normal non-diabetic rats. Wistar rats were rendered diabetic by a single intraperitoneal ( i.p.) injection of streptozotocin (45 mg/kg body wt.), supplemented with raw and parboiled whole red rice for six weeks . Results revealed a drastic increase in oxidative stress markers, such as lipid peroxidation, nitric oxide (NO) level, hydroperoxide (HP) level; antioxidant enzymes superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), glutathione reductase (GR), thioredoxin reductases (TR), glutathione S-transferase ( GST), acetylcholinesterase (AChE) activity, and decrease in endogenous antioxidant, glutathione (GSH) in diabetic rat. On the other hand, addition of raw and parboiled whole red rice in the diet counteracted the STZ induced oxidative stress in diabetic groups and improved the neuro and hepatic antioxidant system. Both, parboiled and raw red rice forms, exercised similar impacts in diabetic as well as in normal rats suggesting improved antioxidant defence mechanism. Results have shown that the whole red rice possess antidiabetic potential with the antioxidant improving ability, and could be utilized as dietary supplements in diabetes management.

Modification of the Ferrous Oxidation‐Xylenol Orange Method for Determination of Peroxide Value in Highly Pigmented Sea Cucumber Viscera Lipid

AbstractA ferrous oxidation‐xylenol orange (FOX) method was modified to measure the levels of hydroperoxides in highly pigmented sea cucumber (Cucumaria frondosa) viscera lipid. With the FOX method, oil hydroperoxides oxidize Fe(II) to Fe(III) ions, which in turn bind to xylenol orange (XO) to form a complex that has a maximum absorbance at 560 nm. When applied to lipid extracts containing high levels of carotenoid pigments, the carotenoids interfere in the absorbance measurement because the XO‐complex and carotenoids absorb at the same wavelength. To avoid this, an approach was developed where carotenoids were removed from the solution containing the XO‐complex before absorbance measurements were made. This was accomplished by aqueous extraction of the reaction solution, leaving an organic layer containing the carotenoid pigment. The absorbance of the aqueous layer was subsequently measured at 560 nm allowing for determination of the lipid hydroperoxide content (mmol kg−1) using a cumene hydroperoxide calibration curve. The method was validated using oxidized, unpigmented fish oils. The modified FOX method described herein was linear, accurate, and precise, and was validated over a hydroperoxide concentration range of 5–35 meq kg−1 lipid. This modified FOX method for hydroperoxide determination of highly pigmented lipids is a valuable alternative to the methods presently available for determination of peroxide values.

Salicylic acid and aspirin stimulate growth of Chlamydomonas and inhibit lipoxygenase and chloroplast desaturase pathways

Chemical stimulants, used to enhance biomass yield, are highly desirable for the commercialisation of algal products for a wide range of applications in the food, pharma and biofuels sectors. In the present study, phenolic compounds, varying in substituents and positional isomers on the arene ring have been evaluated to determine structure-activity relationship and growth. The phenols, catechol, 4-methylcatechol and 2, 4-dimethyl phenol were generally inhibitory to growth as were the compounds containing an aldehyde function. By contrast, the phenolic acids, salicylic acid, aspirin and 4-hydroxybenzoate markedly stimulated cell proliferation enhancing cell numbers by 20–45% at mid-log phase. The order of growth stimulation was ortho > para > meta with respect to the position of the OH group. Both SA and aspirin reduced 16:3 in chloroplast galactolipids. In addition, both compounds inhibited lipoxygenase activity and lowered the levels of lipid hydroperoxides and malondialdehydes in the cells. The present study has demonstrated the possibility of using SA or aspirin to promote algal growth through the manipulation of lipid metabolising enzymes.

Stress response and lipid composition in shrimpLitopenaeus vannameifed diets enriched with squid or scallop viscera meal

We substituted 10% of fishmeal with scallop (Argopecten ventricosus) or squid (Dosidiscus gigas) by-product meal in a feed for shrimp (Litopenaeus vannamei) growth assay that lasted 60 days and then shrimps were submitted to handling stress. Shrimp fed the control diet had smaller weight gain and lower recovery after stress. Prostaglandins in gills were affected by diet and stress, with significant differences in shrimp fed the control diet before and after the stress. Hydroperoxides were increased after stress, while isoprostanoids were higher in shrimp fed the control diet. The gene expression of Glutathione peroxidase and Catalase was increased on the stressed shrimp fed the scallop diet, with no differences among diets for Superoxide dismutase or Cyclooxygenase. Arachidonic acid in the phospholipid fraction of muscle was the only fatty acid affected by stress and diet. Cholesterol oxidation products were significantly higher in shrimp fed the scallop diet compared to shrimp fed the control diet before applying the stress. A PCA analysis grouped in one-factor growth variables, as well as Superoxide dismutase, esterified astaxanthin and isoprostane, while another factor was determined by stress, prostaglandin and hydroperoxide levels in gills. The partial substitution of fishmeal with scallop of squid by-product meals affected growth and stress differently, indicating shrimp that grew up more were not necessarily more tolerant to handling stress, which can have a strong repercussion in aquaculture, particularly during density control, recording of growth and harvest.

Decreased malondialdehyde levels in fish (Astyanax altiparanae) exposed to diesel: Evidence of metabolism by aldehyde dehydrogenase in the liver and excretion in water.

Increased malondialdehyde (MDA) levels are commonly considered an indicator of lipid peroxidation derived from oxidative stress insults promoted by exposure of fish to pollutants. However, a decrease in MDA levels after xenobiotic exposure has been also reported, an effect that is mostly attributed to enhanced antioxidant defenses. In this study, we assessed whether pollutant-mediated MDA decrease would be associated with antioxidant enhancement or with its metabolism by aldehyde dehydrogenase (ALDH) in the liver and gills of lambari (Astyanax altiparanae) exposed to diesel oil (0.001, 0.01, and 0.1mL/L). MDA levels were decreased in the liver of lambari exposed to diesel. The activities of the antioxidant enzymes, catalase (CAT) and glutathione peroxidase (GPx), were unchanged in the liver, while that of glucose-6-phosphate dehydrogenase (G6PDH) was decreased. In contrast, levels of total glutathione (tGSH) and the activity of glutathione S-transferase (GST) were increased in the liver, which partly support antioxidant protection against lipid peroxidation. More importantly, ALDH activity increased in a concentration-dependent manner, being negatively correlated with MDA levels, indicating MDA metabolism by ALDH. In the gills, diesel exposure increased MDA and lipid hydroperoxide levels, and promoted increases in antioxidant defenses, indicating oxidative stress. Curiously, ALDH activity was undetectable in the gills, supporting the possibility of direct MDA excretion in the water by the gills. Analyses of MDA in the water revealed increased levels of MDA in the aquaria in which the fish were exposed to diesel, compared to control aquaria. A second experiment was carried out in which the fish were intraperitoneally injected with MDA (10mg/kg) and analyzed after 1, 6, and 12h. MDA injection caused a time-dependent decrease in hepatic MDA levels, did not alter ALDH, CAT, GPx, and GST activities, and decreased G6PDH activity and tGSH levels. In the gills, MDA injection caused a slight increase in MDA levels after 1h, but did not alter GPx, G6PDH, and GST activities. MDA injection also enhanced CAT activity and tGSH levels in the gills. MDA concentration in water increased progressively after 1, 6, and 12h, supporting the hypothesis of direct MDA excretion as an alternative route for MDA elimination in fish. Our results suggest that the decreased MDA levels after exposure of lambari to diesel oil pollutant probably reflects an association between enhanced antioxidant protection, MDA metabolism, and MDA excretion in water.

Serum Lipid Oxidative Stress Products as Risk Factors Are the Candidate Predictive Biomarkers for Human Abdominal Aortic Aneurysms.

This research was designed to determine the association of serum lipid peroxidation products with disease severity in patients with abdominal aortic aneurysm (AAA). In total, 76 pairs of AAA cases as well as matched controls were enrolled in our research using propensity score matching (PSM). And their malondialdehyde (MDA), lipid hydroperoxide (LPO), and glutathione peroxidase (GSH-Px) levels were also detected through enzyme-linked immunosorbent assay (ELISA). Additionally, the relative clinical data of enrolled participants were extracted. The serum biomarker concentrations were measured in 76 patients with AAAs (diameter between 30 and 54 mm, n = 54; diameter ≥55 mm, n = 22) and 76 control patients from observational cohort study. After PSM adjustment for clinical variables, including age, gender, heart ratio, body mass index, smoking, hypertension, diabetes mellitus, coronary heart disease, and stroke, the serum MDA and LPO among AAA cases were remarkably increased compared with those from the normal patients. Inversely, serum GSH-Px was significantly decreased in patients with AAA compared to the control group. Besides, the serum levels of MDA and LPO were independently associated with AAA risk. Typically, there was significantly positive correlation between MDA level and LPO level (R = 0.358) but negative correlation of MDA level with GSH-Px (R = -0.203) level in patients with AAA. Meanwhile, the area under the receiver operating characteristic curve was 0.965 when MDA was used to diagnose AAA, and the optimal threshold value was 0.242 nmol/mL. Moreover, serum MDA level was significantly increased in cases with rupture AAA compared to those in selective AAA cases. Logistic regression analysis suggested that a higher serum MDA level indicated an elevated risk of AAA rupture (odds ratio = 2.536; 95% CI: 1.037-6.203; P =0.041). Our present findings suggest that serum peroxidation contents were evidently changed among AAA cases. Serum MDA and LPO concentrations could be used to predict disease severity in patients with AAA. Moreover, serum MDA may serve as the candidate biomarker for diagnosis of AAA and accurate identification of increased risks of AAA rupture.

Antidiabetic effect of olive leaf extract on streptozotocin-induced diabetes mellitus in experimental animals.

Background: recently, a relationship between diabetic complications and oxidative stress has been emphasized. There have been some studies showing the effect of olive leaf on hyperglycemia and diabetic complications due to its antioxidant properties. In many studies the effect of olive leaf on plasma total antioxidant level has been measured by different methods. Our study represents the first time it has been measured by a new method of total thiol disulfide homeostasis. Aim: chronic exposure to hyperglycemia and hyperlipidemia contributes to the pathogenesis of diabetic complications through oxidative stress mediators. Thiol is one of the most important antioxidant barriers in humans, and thiol disulfide homeostasis is a new oxidative stress marker. We aimed to investigate the effect of olive leaf extract (OLE) obtained from fresh leaves of Olea europaea, var oleaster on diabetic complications through their hypoglycemic and antioxidant effect in diabetic rats. Methods: twenty-eight Wistar albino rats aged 12-13 weeks were used in the study. The rats were divided into a control group (C), a diabetic control group (DC), a diabetic group treated with 200 mg/kg OLE (D+200), and a diabetic group treated with 400 mg/kg OLE (D+400), having 7 rats in each group. The treatment groups received OLE by the gavage method for 21 days. At the end of the study, all rats were sacrificed by cervical dislocation. Blood samples collected from the heart were centrifuged and glucose, total cholesterol, triglyceride, urea, uric acid, creatinine, alanine aminotransferase (ALT), aspartate aminotransferase (AST), lipid hydroperoxide (LOOH) level, and thiol-disulfide homeostasis were determined. The hemoglobin A1c (HbA1c) analysis was performed on complete blood. In addition, a tail flick test and hot plate modeling were performed to indicate pain perception loss. Results: it was observed that OLE had no effect on serum glucose and HbA1c levels. On the contrary, OLE reduced the levels of total cholesterol (p < 0.01), urea (p < 0.01) and hot plate latency (p < 0.01) in a significant manner. Also, OLE showed a tendency to reduce LOOH levels and to increase thiol levels in a dose-dependent manner (p > 0.05). Conclusion: OLE supplementation for 21 days, at the amounts used, cannot protect against hyperglycemia but may be protective against hypercholesterolemia and tissue damage as caused by diabetes mellitus in rats.

The effect of nitrogen monoxide donors on the indexes of cadmium-induced oxidative stress in different rat tissues

Oxidative stress is considered to be the main mechanism of cadmium ions toxic effect on the cells and is caused by cadmium, as a non-transition metal, indirectly. Oxidative damage to cells due to the action of cadmium ions is tissue-specific and is associated with the antioxidant system inhibition, free heme accumulation and essential metals substitution in metalloproteins. Nitrogen monoxide (NO) exhibits high affinity for heme and proteins and peptides sulfhydryl groups, known to be the main molecular targets for cadmium ions. Taking all the above-mentioned into account, the aim of this work was to study the effect of NO radicals donors on the prooxidant-antioxidant state of mammalian tissues under oxidative stress caused by cadmium chloride administration in vivo. Male Wistar rats weighing 160–200 g were used in the study. CdCl2 was administered subcutaneously at a dose of 14 mg/kg body weight. The direct donor of the NO radical sodium nitroprusside (SNP, 1 mg/kg mass) and the substrate of the NO synthase reaction L-arginine (600 mg/kg mass) were administered intraperitoneally. In order to study the corrective action, donors of the NO radical were injected 0.5 h before the cadmium salt. The objects of investigation were blood plasma and liver, kidneys and spleen homogenates of rats. The cadmium chloride treatment caused a number of prooxidant-antioxidant balance disorders, most of which were revealed a day after injection. The accumulation of lipid peroxidation products was found in rat serum, liver, and spleen. The enhancement of prooxidant processes in these tissues may originate from cadmium ions and hemolysis products entry. In the antioxidant system, significant changes were observed under cadmium action only in the liver: an increase in the reduced glutathione content and SOD activity and a decrease in catalase activity. The precursor of nitric oxide L-arginine did not change the basal level of prooxidant-antioxidant parameters, and in most cases did not affect their dynamics in the organs studied after cadmium chloride administration. A direct NO donor, sodium nitroprusside, acted in liver and spleen mostly as a prooxidant. In liver, the injection of only nitroprusside, as well as the combined administration of SNP and CdCl2, led to free radical processes activation just in two hours. In spleen, the combined treatment by SNP and cadmium salt also caused an earlier development of oxidative stress, as witnessed by an increase in lipid hydroperoxides level and a decrease in reduced glutathione content. Therefore, the injection of a direct NO donor, sodium nitroprusside, and a substrate of NO synthase, L-arginine, in selected doses has insignificant corrective action on cadmium-induced oxidative stress in the liver, kidneys and spleen. However, in blood both donors of NO effectively prevented the accumulation of lipid peroxidation products under CdCl2 treatment; in addition, L-arginine significantly reduced the lactate dehydrogenase release, which may indicate blood cells and blood vessels protection from the damage caused by cadmium ions.

Combined treatment with ultrasound-targeted microbubble destruction technique and NM-aFGF-loaded PEG-nanoliposomes protects against diabetic cardiomyopathy-induced oxidative stress by activating the AKT/GSK-3β1/Nrf-2 pathway

The present study sought to investigate the effect of non-mitogenic acidic fibroblast growth factor (NM-aFGF) loaded PEGylated nanoliposomes (NM-aFGF-PEG-lips) combined with the ultrasound-targeted microbubble destruction (UTMD) technique on modulating diabetic cardiomyopathy (DCM)and the mechanism involved. Animal studies showed that the diabetes mellitus (DM) group exhibited typical myocardial structural and functional changes of DCM. The indexes from the transthoracic echocardiography showed that the left ventricular function in the NM-aFGF-PEG-lips + UTMD group was significantly improved compared with the DM group. Histopathological observation further confirmed that the cardiomyocyte structural abnormalities and mitochondria ultrastructural changes were also significantly improved in the NM-aFGF-PEG-lips + UTMD group compared with DM group. The cardiac volume fraction (CVF) and apoptosis index in the NM-aFGF-PEG-lips + UTMD group decreased to 10.31 ± 0.76% and 2.16 ± 0.34, respectively, compared with those in the DM group (CVF = 21.4 ± 2.32, apoptosis index = 11.51 ± 1.24%). Moreover, we also found significantly increased superoxide dismutase (SOD) activity and glutathione peroxidase (GSH-Px) activity as well as clearly decreased lipid hydroperoxide levels and malondialdehyde (MDA) activity in the NM-aFGF-PEG-lips + UTMD group compared with those in the DM group (p < .05). Western blot analysis further revealed the highest level of NM-aFGF, p-AKT, p-GSK-3β1, Nrf-2, SOD2 and NQO1 in the NM-aFGF-PEG-lips + UTMD group. This study confirmed using PEGylated nanoliposomes combined with the UTMD technique can effectively deliver NM-aFGF to the cardiac tissue of diabetic rats. The NM-aFGF can then inhibit myocardial oxidative stress damage due to DM by activating the AKT/GSK/Nrf-2 signaling pathway, which ultimately improved the myocardial structural and functional lesions in diabetic rats.

Aging and low-intensity exercise change oxidative biomarkers in brain regions and radiographic measures of femur of Wistar rats.

We investigated changes in oxidative biomarkers in brain regions such as brainstem, cerebellum, and cerebral cortex of 3-, 6-, 18-, 24-, and 30-month-old rats. We also assessed the effects of low-intensity exercise on these biomarkers in these regions of 6-, 18-, and 24-month-old rats that started exercise on a treadmill at 3, 15, and 21 months of age, respectively. Radiographic images of the femur were taken for all rats. A total of 25 rats (age: twelve 6-, ten 18-, ten 24-, and three 30-month-old rats) were used. Lipid hydroperoxide levels increased in cerebellum at 18 months. Total antioxidant activity exhibited lowest values in brainstem at 3 months. Superoxide dismutase activity did not exhibit significant changes during aging. Total thiol content exhibited lowest values in brain regions of 24- and 30-month-old rats. Exercise reduced total thiol content in brainstem at 6 months, but no change occurred in other regions and other ages. Femur increased its length and width and cortical thickness with advancing age. No change occurred in medullary width. Radiolucency increased and sclerosis was found in cortical and medullary bone with advancing age. Exercise reduced radiolucency and medullary sclerosis. Therefore, aging differentially changed oxidative biomarkers in different brain regions and radiographic measures of the femur. Low-intensity exercise only ameliorated some radiographic measurements of femur. Since the present study possessed limitations (small number of rats per group), a beneficial effect of regular low-intensity exercise on oxidative markers in brain cannot be ruled out.

Burdock (Arctium lappa L.) root attenuates preneoplastic lesion development in a diet and thioacetamide-induced model of steatohepatitis-associated hepatocarcinogenesis.

Nonalcoholic steatohepatitis (NASH) is considered growing risk factor for hepatocellular carcinoma development in high-income countries. Diet- and chemically induced rodent models have been applied for the translational study of NASH-associated hepatocarcinogenesis due to their morphological and molecular similarities to the corresponding human disease. Arctium lappa L. (burdock) root tea has been extensively consumed in Traditional Chinese Medicine due to its potential therapeutic properties. Indeed, the bioactive compounds of A. lappa root, as the polyphenols, have already showed antioxidant and anti-inflammatory properties in different in vivo and in vitro bioassays. In this study, we investigated whether burdock root ethanolic extract (BRE) administration attenuates NASH-associated hepatocarcinogenesis. Eight-week-old male Wistar rats received choline-deficient high-fat diet for 8 weeks and multiple thioacetamide doses for 4 weeks in order to induce NASH and preneoplastic glutathione-S-transferase pi (GST-P)+ preneoplastic foci. Subsequently, rats were treated with BRE (100 or 200 mg/kg body weight) or vehicle by oral gavage for 2 weeks. BRE displayed high levels of chlorogenic and caffeic acids and BRE administration reduced total fatty acid and lipid hydroperoxide levels, while increasing the activities of antioxidant superoxide dismutase and catalase enzymes in the liver. Furthermore, burdock intervention diminished the size of GST-P+ remodeling preneoplastic lesions (PNLs) and displayed a trend on reducing hepatocyte proliferation (Ki-67) inside them. These findings suggest that short-term exposure to BRE alleviated remodeling PNL development in NASH-associated hepatocarcinogenesis.

The influence of harmful physical factors and industrial dust on changes in some biochemical and functional indicators of the cardiovascular system and respiratory system in workers engaged in underground mining of ore

Introduction. The health of workers is determined by both social and individual, as well as production factors, including noise, vibration and dust, characteristic of technological processes in mining enterprises. Industrial noise above 90 dBA and dust in the form of suspended and fine particles causes dysfunction of the cardiovascular system and respiratory organs.The aim of the study is to assess the impact of harmful physical factors and industrial dust on changes in some biochemical and functional indicators of the cardiovascular system and respiratory system of employees of the enterprise for underground mining of ore.Materials and methods. The assessment of working conditions of workers engaged in underground mining and processing of chrome ores, the analysis of industrial dust on the dimension and quantitative content of fine particles PM10 and PM2. 5, the study of biochemical parameters of lipid metabolism, oxidant and antioxidant systems, indicators of respiratory function. Results. Harmful working conditions (class 3.1–3.4) in terms of noise and vibration were revealed at the workplaces of employees of the main specialties observation group. In the air of the working zone, the highest content of fine particles PM2.5 (2.68±0.54 mg/m3) and PM10 (4.64±0.93 mg/m3) was established at the site of drilling operations and cleaning of the bottom-hole space. Deviations of biochemical parameters characterizing intensification of free radical processes and antioxidant protection, imbalance of lipid spectrum parameters, and violation of functional parameters of external respiration were revealed. A high degree of connection with the working conditions of the frequency of increased levels of lipid hydroperoxide and antioxidant activity (EF=60.71–65.84%) was established.Conclusions. In high noise level (more than 94 dBA), general and local vibration (more than 116 and 127 dB respectively) and the content of fine particles PM2. 5 (more of 2.14 mg/m3) and PM10 (over of 3.71 mg/m3) at underground mining of chrome ore workers have identified abnormalities in the form of increase 1.6 times the level of lipid hydroperoxides and total antioxidant activity, reducing to 1.2 times the level of high density lipoprotein, improving 1.2–1.3 times of low-density lipoproteins, triglycerides, and atherogenic index in blood serum, peak expiratory flow. A high degree of professional conditioning have the frequency of increasing the level of lipid hydroperoxide in blood serum and antioxidant activity of blood plasma.

Antioxidant and Anti-hyperlipidemic Effects of Bark Extract of Pinus eldarica in Dexamethasone-induced Dyslipidemic Rats

Background & Objective: Although Pinus eldarica is considered as a pine with many valuable phytochemical constituents, little is known about the pharmacological effects of its bark extract. Therefore, the present study aimed to evaluate in vivo antioxidant activity and also the possible beneficial effects of the bark extract of P. eldarica on dexamethasone-induced dyslipidemia in rats. Materials & Methods: Total phenolic content was determined using Folin-Ciocalteu method. The in vivo antioxidant assays included the measurement of hydroperoxides level and ferric reducing antioxidant power (FRAP) value in plasma samples of rats receiving intraperitoneal injections (IP) injections of plant extract (100, 200 and 400 mg/kg) for 28 days. For induction of dyslipidemia, dexamethasone (10 mg/kg) was subcutaneously administered during 8 days. Different doses of extract were given orally plus dexamethasone in three groups of animals. Serum lipids, blood glucose and malondialdehyde (MDA) levels and liver histopathology were assessed. Results: High total phenolic content was determined as 375±1.2 mg gallic acid equivalent/ g of dried bark extract. The extract significantly decreased plasma hydroperoxides level at all doses and increased FRAP value at the dose of 400 mg/kg during in vivo antioxidant analysis. P. eldarica led to a significant reduction in serum levels of blood glucose, total cholesterol, triglyceride and MDA and improved liver histopathological changes at the doses of 200 and 400 mg/kg in dyslipidemic rats. Conclusion: These findings suggest the potential antioxidant, antihyperlipidemic and antihyperglycemic activities for the bark extract of P. eldarica which may be due to the high amounts of phenolic compounds.

Chromium and human low-density lipoprotein oxidation

Chromium is a catalytic metal able to foster oxidant damage, albeit its capacity to induce human LDL oxidation is to date unkown. Thus, we have investigated whether trivalent and hexavalent chromium, namely Cr(III) and Cr(VI), can induce human LDL oxidation. Cr(III) as CrCl3 is incapable of inducing LDL oxidation at pH 7.4 or 4.5. However, Cr(III), specifically at physiological pH of 7.4 and in the presence of phosphates, causes an absorbance increase at 234 resembling a spectrophotometric kinetics of LDL oxidation with a lag- and propagation-like phase. In this regard, it is conceivable that peculiar Cr(III) forms such as Cr(III) hydroxide and, especially, Cr(III) polynuclear hydroxocomplexes formed at pH 7.4 interact with phosphates generating species with an intrinsic absorbance at 234 nm, which increases over time resembling a spectrophotometric kinetics of LDL oxidation. Cr(VI), as K2Cr2O7, can instead induce substantial human LDL oxidation at acidic pH such as 4.5, which is typical of the intracellular lysosomal compartment. LDL oxidation is related to binding of Cr(VI) to LDL particles with quenching of the LDL tryptophan fluorescence, and it is inhibited by the metal chelators EDTA and deferoxamine, as well as by the chain-breaking antioxidants butylated hydroxytoluene and probucol. Moreover, Cr(VI)-induced LDL oxidation is inhibited by mannitol conceivably by binding Cr(V) formed from LDL-dependent Cr(VI) reduction and not by scavenging hydroxyl radicals (OH); indeed, the OH scavengers sodium formate and ethanol are ineffective against Cr(VI)-induced LDL oxidation. Notably, heightened LDL lipid hydroperoxide levels and decreased LDL tryptophan fluorescence occur in Cr plating workers, indicating Cr-induced human LDL oxidation in vivo. The biochemical, pathophysiological and clinical implications of these novel findings on chromium and human LDL oxidation are discussed.