Lipid Hydroperoxide Levels Research Articles

Lipid Profile and Aquaporin Expression under Oxidative Stress in Breast Cancer Cells of Different Malignancies.

Breast cancer is the major cause of tumor-associated mortality in women worldwide, with prognosis depending on the early discovery of the disease and on the type of breast cancer diagnosed. Among many factors, lipids could contribute to breast cancer malignancy by participating in cellular processes. Also, aquaporins are membrane channels found aberrantly expressed in cancer tissues that were correlated with tumor aggressiveness, progression, and metastasis. However, the differences in lipid profile and aquaporin expression between cell types of different malignant potential have never been investigated. Here, we selected three breast cancer cell lines representing the three major breast cancer types (hormone positive, HER2NEU positive, and triple negative) and analyzed their lipid profile and steady state lipid hydroperoxide levels to correlate with cell sensitivity to H2O2. Additionally, the expression profiles of AQP1, AQP3, and AQP5 and the Nrf2 transcription factor were evaluated, before and after oxidative challenge. We found that the lipid profile was dependent on the cell type, with the HER2-positive cells having the lowest level PUFA, whereas the triple negative showed the highest. However, in triple-negative cancer cells, a lower level of the Nrf2 may be responsible for a higher sensitivity to H2O2 challenge. Interestingly, HER2-positive cells showed the highest increase in intracellular ROS after oxidative challenge, concomitant with a significantly higher level of AQP1, AQP3, and AQP5 expression compared to the other cell types, with AQP3 always being the most expressed isoform. The AQP3 gene expression was stimulated by H2O2 treatment in hormone-positive and HER2NEU cells, together with Nrf2 expression, but was downregulated in triple-negative cells that showed instead upregulation of AQP1 and AQP5. The lipid profile and AQP gene expression after oxidative challenge of these particularly aggressive cell types may represent metabolic reprogramming of cancer cells and reflect a role in adaptation to stress and therapy resistance.

Spinal Manipulation Therapy Improves Tactile Allodynia and Peripheral Nerve Functionality and Modulates Blood Oxidative Stress Markers in Rats Exposed to Knee-Joint Immobilization

ObjectiveThe purpose of our study was to evaluate the effect of manually assisted lumbar spinal manipulation therapy on tactile allodynia, peripheral nerve functional recovery, and oxidative markers in rats exposed to knee immobilization-inducing hypersensitivity. MethodsTactile allodynia and sciatic, tibial, and peroneal functional indices were assessed before the knee joint immobilization, 24 hours after the knee cast removal, and 24 hours after 3 weeks of lumbar therapy with the Activator Adjusting Instrument, model 4 (AAI 4). Subsequently, the blood was collected from each rat, and oxidative markers such as lipid hydroperoxide levels; nitric oxide metabolites; and superoxide dismutase, catalase, and glutathione peroxidase activities were assessed. ResultsThe AAI 4 improved the immobilization-induced allodynia and recovered the peripheral nerve functional indices impaired after knee immobilization. Immobilized rats treated with AAI 4 therapy presented a lack of significant changes in lipid hydroperoxides and nitric oxide metabolites in the plasma contrasting with rats that were kept freely in their cages, with no therapy applied, which presented elevated lipid hydroperoxides levels. Also, the antioxidant catalase enzymatic activity decreased in the blood of rats immobilized and treated with AAI 4. ConclusionThese results suggest that manually assisted lumbar spinal manipulation therapy modulates systemic oxidative stress, which possibly contributes to the analgesia and recovery of peripheral nerve functionality.

Astragalin reduces lipopolysaccharide-induced acute lung injury in rats via induction of heme oxygenase-1.

Astragalin, a bioactive component of medicinal plants such as Rosa agrestis, has anti-inflammatory and antioxidant features. Induction of heme oxygenase (HO)-1 is an effective strategy to reduce excessive generated oxidants during the pathogenesis of acute lung injury (ALI). The aim of the present study is to investigate that whether the anti-inflammatory and antioxidant features of astragalin is HO-1 dependent in lipopolysaccharide (LPS)-induced ALI. Sprague-Dawley rats were used in animal study. Intratracheal LPS was performed to induce experimental ALI model. Astragalin was administrated 1h after LPS challenge. Human lung epithelial cells were used in cell study. Samples from rats were harvested at 24h post LPS challenge. Astragalin treatment inhibited LPS-induced inflammatory cells infiltration in the lung and pulmonary edema. Astragalin treatment markedly enhanced the activity of HO-1 compared with vehicle-treated group at 24h post LPS challenge. Levels of lipid hydroperoxide, a marker for oxidative stress, were decreased in astragalin-treated animals compared with vehicle-treated group. However, the protective effect of astragalin on LPS-induced ALI was abolished in an inhibitor of HO-1-treated animals. Moreover, the astragalin-induced the upregulation of HO-1 in human lung epithelial cells was inhibited when nuclear factor erythroid-2-related factor 2 (Nrf2) was silenced by small interfering RNA. Astragalin reduces LPS-induced ALI via activation of Nrf2/HO-1 pathway.

Betula etnensis Raf. (Betulaceae) Extract Induced HO-1 Expression and Ferroptosis Cell Death in Human Colon Cancer Cells.

Betula etnensis Raf. (Birch Etna) belonging to the Betulaceae family grows on the eastern slope of Etna. Many bioactive compounds present in Betula species are considered promising anticancer agents. In this study, we evaluated the effects of B. etnensis Raf. bark methanolic extract on a human colon cancer cell line (CaCo2). In order to elucidate the mechanisms of action of the extract, cellular redox status, cell cycle, and heme oxygenase-1 (HO-1) expression in ferroptosis induction were evaluated. Cell viability and proliferation were tested by tetrazolium (MTT) assayand cell cycle analysis, while cell death was evaluated by annexin V test and lactic dehydrogenase (LDH) release. Cellular redox status was assessed by measuring thiol groups (RSH) content, reactive oxygen species (ROS) production, lipid hydroperoxide (LOOH) levels and (γ-glutamylcysteine synthetase) γ-GCS and HO-1 expressions. The extract significantly reduced cell viability of CaCo2, inducing necrotic cell death in a concentration-depending manner. In addition, an increase in ROS levels and a decrease of RSH content without modulation in γ-GCS expression were detected, with an augmentation in LOOH levels and drastic increase in HO-1 expression. These results suggest that the B. etnensis Raf. extract promotes an oxidative cellular microenvironment resulting in CaCo2 cell death by ferroptosis mediated by HO-1 hyper-expression.

Effect of glycyrrhizin on nicotine-induced behavioral disturbance of planarian, Dugesia japonica

Nicotine is a component of tobacco products and is one of the most commonly abused substances that leads to addiction. Therefore, the present study was performed to investigate the behavioral pattern and toxicity by nicotine exposure in planarians. Basically, planarians were exposed to different concentration of nicotine for 5 min. To investigate detoxification effect, planarians were exposed to nicotine for 5 min, and treated glycyrrhizin for 5 min, then motility and seizure-like behavior were observed for 5 min. As a result, the motility of nicotine-exposed planarians decreased approximately more than 50% compared to freshwater control. However, the motility of glycyrrhizin-exposed planarians recovered than nicotineexposed planarians. In the assessment of seizure-like behavioral pattern, planarians exposed to nicotine showed head-bop or c-like type rather than screw-like or snake-like patterns. However, planarians exposed to glycyrrhizin showed no seizure-like behavior. To examine the oxidative stress response, planarians were cultured in fresh water containing 1 mM nicotine for 1 day. Planarians were homogenized and extracted to assay the contents of reactive oxygen species (ROS), lipid hydroperoxides (LH), glutathione (GSH), catalase (CAT), and superoxide dismutase (SOD). The result showed that a significantly higher level of ROS, LH indicated in planarians exposed to nicotine, on the other hand, glycyrrhizin-exposed planarians were significantly decreased ROS, LH levels. In conclusion, the motility decreased when planarians were exposed to nicotine, in a dose-dependent manner, whereas seizurelike behavior increased. Nicotine induced behavioral disturbances and cell toxicity in planarians were recovered by glycyrrhizin, suggesting a candidate substance for nicotine addiction treatment.

Influence of chromium citrate on oxidative stress in the tissues of muscle and kidney of rats with experimentally induced diabetes

Chromium is one of the important trace elements that is essential for carbohydrate, protein and lipid metabolism. Chromium improves glucose metabolism and reduces insulin resistance due to increased insulin sensitivity. Therefore, it is important to consider the use of chromium citrate as a nutritional supplement with potential hypoglycemic and hypolipidemic effects. In this research work, we investigated the activity of the antioxidant system and the level of lipid hydroperoxides in the tissues of skeletal muscles and kidneys of experimental diabetic rats and for rats which received in their daily diet chromium citrate in the amounts 0.1 and 0.2 μg/mL of water. We induced the experimental model of diabetes by intraperitoneal injection of alloxan in the amount 150 mg/kg of body weight of the animals. We monitored glucose levels by measuring daily glucose levels with a portable glucose meter. For research, we selected animals with a glucose level > 11.1 mmol/L. We monitored the body weight of rats. On the 40th day of the study, we withdrew the animals from the experiment by decapitation. We selected the tissue for research, namely skeletal muscles and kidneys. In samples of the tissue homogenates, we measured the activity of antioxidant enzymes and the content of lipid peroxide oxidation products. As a result of our research, we found that the products of lipid peroxide oxidation and glutathione peroxidase activity increased in skeletal muscle of animals with diabetes mellitus. The activity of glutathione reductase, catalase, superoxide dismutase, and the content of reduced glutathione decreased at the same time. In the kidneys of diabetic rats, the activity of glutathione peroxidase, glutathione reductase, catalase and content of lipid hydroperoxides increased but the activity of superoxide dismutase and the content of reduced glutathione decreased. The addition of chromium citrate to the diet of animals in amounts 0.1 and 0.2 μg/mL led to the suppression of oxidative stress. The activity of catalase, glutathione peroxidase and the content of lipid hydroperoxides, TBA-positive substances decreased. Also, the activity of superoxide dismutase increased with the addition of chromium citrate. These results indicate normalization of antioxidant defense in the skeletal muscle and kidneys of experimental rats with experimental diabetes given chromium citrate in the amount 0.1 mg/mL of water.

The effects of delta-9-tetrahydrocannabinol on Krüppel-like factor-4 expression, redox homeostasis, and inflammation in the kidney of diabetic rat.

Diabetes mellitus is a complex, multifactorial disorder that is attributed to pancreatic β cell dysfunction. Pancreatic β cell dysfunction results in declining utilization of glucose by peripheral tissues as kidney and it leads to nephropathy. Excessive production and accumulation of free radicals and incapable antioxidant defense system lead to impaired redox status. Macromolecular damage may occur due to impaired redox status and also immune imbalance. Δ9-Tetrahydrocannabinol (THC) is the main active ingredient in cannabis. THC acts as an immunomodulator and an antioxidant agent. Our aim was to evaluate the effects of THC in the diabetic kidney. We analyzed macromolecular damage biomarkers as protein carbonyl (PCO), lipid hydroperoxide (LHP), malondialdehyde (MDA), 8-hydroxy-2'-deoxyguanosine (8-OHdG), and antioxidant defense system biomarkers as thiol fractions (T-SH, NP-SH, P-SH) and Cu/Zn-superoxide dismutase activity for the antioxidative effects of THC. Furthermore, mRNA expression of Krüppel-like factor-4, secreted immunopositive cell number changes of interleukin-6, nuclear factor κβ (NF-κβ), and peroxisome proliferator-activated receptor-γ and tumor necrosis factor α (TNF-α) levels were analyzed for the immunomodulatory activity of THC. Diabetic rats showed significantly increased levels of PCO, LHP, MDA, and 8-OHdG when compared with controls (P < 0.05 for each parameter). THC significantly reduced the elevated levels of PCO and 8-OHdG (P < 0.05 for both parameters) and also LHP and MDA levels were insignificantly reduced by THC. Also, thiol fractions insignificantly increased in THC administered diabetic kidney when compared with diabetic rats. The NF-κβ cell number significantly decreased in the diabetic rats treated with THC compared with the diabetic group. According to our data, THC has ameliorative effects on the impaired redox status of diabetic kidney and also it acts as an immunomodulator. Therefore, THC might be used as a therapeutic agent for diabetic kidneys but its usage in the healthy kidney may show adverse effects.

Expression of Antioxidant Enzymes in Patients with Uterine Polyp, Myoma, Hyperplasia, and Adenocarcinoma.

We previously found that compared to patients with benign uterine diseases (polyps, myomas), patients with premalignant (hyperplasia simplex and complex) and malignant (adenocarcinoma) lesions had enhanced lipid peroxidation and altered uterine antioxidant enzyme (AOE) activities. To further elucidate the mechanism of the observed changes, we examined protein and mRNA levels of copper-zinc superoxide dismutase (CuZnSOD), catalase (CAT), glutathione peroxidase (GPx), glutathione reductase (GR), and transcription factor Nrf2. We also examined correlations of AOE expression with AOE activity, lipid hydroperoxides (LOOH) level, and level of Nrf2. Our results showed decreased CuZnSOD, CAT, and Nrf2 levels, and increased GPx and GR levels in hyperplasias, while in patients with adenocarcinoma, the level of CAT was decreased and GR was increased, compared to benign groups. Similar changes in mRNA levels were also detected, indicating predominantly translational control of the AOE expression. The positive correlation of enzyme expression/activity was recorded for CuZnSOD, GPx, and GR, but only among groups with benign diseases. Only GR and GPx expressions were positively correlated with LOOH. Nrf2 protein was positively correlated with mRNA levels of CuZnSOD and GR. Observed results indicate involvement of diverse redox mechanisms in etiopathogenesis of different gynecological diseases, and may improve redox-based approaches in current clinical practice.

Assessment of Oxidative Stress in Patients with Sudden Hearing Loss: A Non-randomized Prospective Clinical Study.

The etiology of sudden hearing loss (SHL) has not been fully elucidated. Previous studies claimed that different etiological factors may play a role in the pathogenesis of SHL. The aim of the present study is to investigate the presence of oxidative stress (OS) in SHL cases using thiol-disulfide balance. In addition, total oxidant status (TOS), total antioxidant status (TAS), oxidative stress index (OSI) and lipid hydroperoxide levels (LOOH) were investigated. A total of 30 cases (15 female, 15 male, mean age 48.9 ± 8.1years, age range: 36-68years) were included in the study. Thiol and disulfide amounts, thiol/disulfide ratios, TOS, TAS, OSI and LOOH scores of the case group and control group were compared. Native thiol (SH) and total thiol (SH + SH) values were significantly lower in the SHL group than in the control group (p = 0.028 and p = 0.044, respectively). The LOOH value, TOS value and OSI value were significantly higher in the SHL group than in the control group (all p values < 0.05). The TAS value was significantly lower in the SHL group than in the control group (p = 0.0001). The present study has presented that the thiol-disulfide balance was impaired in SHL cases. OS may play a role in the development of SHL.

The Effect of Standardised Flower Extracts of Sorbus aucuparia L. on Proinflammatory Enzymes, Multiple Oxidants, and Oxidative/Nitrative Damage of Human Plasma Components In Vitro.

Polyphenol-rich plant extracts might alleviate the negative impact of oxidative stress and inflammation, but careful phytochemical standardisation and evaluation of various mechanisms are required to fully understand their effects. In this context, flower extracts of Sorbus aucuparia L.—a traditional medicinal plant—were investigated in the present work. The LC-MS/MS profiling of the extracts, obtained by fractionated extraction, led to the identification of 66 constituents, mostly flavonols (quercetin and sexangularetin glycosides with dominating isoquercitrin), pseudodepsides of quinic and shikimic acids (prevailing isomers of chlorogenic acid and cynarin), and flavanols (catechins and proanthocyanidins). Minor extract components of possible chemotaxonomic value were flavalignans (cinchonain I isomers) and phenylamides (spermidine derivatives). As assessed by HPLC-PDA and UV-spectrophotometric studies, the extracts were polyphenol-abundant, with the contents up to 597.6 mg/g dry weight (dw), 333.9 mg/g dw, 382.0 mg/g dw, and 169.0 mg/g dw of total phenolics, flavonoids, proanthocyanidins, and caffeoylquinic acids, respectively. Their biological in vitro effects were phenolic-dependent and the strongest for diethyl ether, ethyl acetate, and n-butanol fractions of the methanol-water (7 : 3, v/v) extract. The extracts showed significant, concentration-dependent ability to scavenge in vivo-relevant radical/oxidant agents (O2∙−, OH∙, H2O2, ONOO–, NO∙, and HClO) with the strongest effects towards OH∙, ONOO–, HClO, and O2∙− (compared to ascorbic acid). Moreover, the extracts efficiently inhibited lipoxygenase and hyaluronidase (compared to indomethacin) but were inactive towards xanthine oxidase. At in vivo-relevant levels (1-5 μg/mL), they also effectively protected human plasma components (proteins and lipids) against ONOO–-induced oxidative damage (reduced the levels of 3-nitrotyrosine, lipid hydroperoxides, and thiobarbituric acid-reactive substances) and normalised/enhanced the total nonenzymatic antioxidant capacity of plasma. In cytotoxicity tests, the extracts did not affect the viability of human PBMCs and might be regarded as safe. The results support the application of the extracts in the treatment of oxidative stress-related pathologies cross-linked with inflammatory changes.

Muscular apoptosis but not oxidative stress increases with old age in a long-lived diver, the Weddell seal.

Seals experience repeated bouts of ischemia-reperfusion while diving, potentially exposing their tissues to increased oxidant generation and thus oxidative damage and accelerated aging. We contrasted markers of oxidative damage with antioxidant profiles across age and sex for propulsive (longissismus dorsi) and maneuvering (pectoralis) muscles of Weddell seals to determine whether previously observed morphological senescence is associated with oxidative stress. In longissismus dorsi, old (age 17-26 years) seals exhibited a nearly 2-fold increase in apoptosis over young (age 9-16 years) seals. There was no evidence of age-associated changes in lipid peroxidation or enzymatic antioxidant profiles. In pectoralis, 4-hydroxynonenal-Lys (4-HNE-Lys) levels increased 1.5-fold in old versus young seals, but lipid hydroperoxide levels and apoptotic index did not vary with age. Glutathione peroxidase activity was 1.5-fold higher in pectoralis of old versus young animals, but no other antioxidants changed with age in this muscle. With respect to sex, no differences in lipid hydroperoxides or apoptosis were observed in either muscle. Males had higher HSP70 expression (1.4-fold) and glutathione peroxidase activity (1.3-fold) than females in longissismus dorsi, although glutathione reductase activity was 1.4-fold higher in females. No antioxidants varied with sex in pectoralis. These results show that apoptosis is not associated with oxidative stress in aged Weddell seal muscles. Additionally, the data suggest that adult seals utilize sex-specific antioxidant strategies in longissismus dorsi but not pectoralis to protect skeletal muscles from oxidative damage.

The effects of N-acetylcysteine on cisplatin induced cardiotoxicity.

Recent studies reported that oxidative stress is an important mechanism that contributes to cisplatin induced cardiotoxicity. In the present study, the effects of N-acetylcysteine (NAC), which is an antioxidant, on cisplatin induced cardiotoxicity were investigated in a rat model. Thirty two rats were separated into 4 equal groups: Control, NAC-250, CP (cisplatin), CP+NAC. Rats in the experimental groups were treated with a single dose of cisplatin intraperitoneally (ip) (10 mg/kg) and NAC (ip, 250 mg/kg) for 3 consecutive days. At the end of the experiment, cardiotoxicity was determined from plasma CK-MB, LDH, cTnI and cardiac myosin light chain-1 (CMLC-1) levels. In the tissue samples, total oxidant capacity (TOC), total antioxidant capacity (TAC), lipid hydroperoxide (ROOH) and thiol levels were measured. The hearts were also analyzed histopathologically. It was determined that cisplatin increased the tissue TOC, ROOH levels and decreased TAC and thiol levels. NAC administration after cisplatin treatment was observed to have ameliorated histological and functional changes in heart. In conclusion, the results of this experimental study suggested that oxidative stress had a serious effect on cisplatin cardiotoxicity, and NAC could be used as a therapeutic agent in addition to standard cisplatin treatment protocols (Tab. 3, Fig. 1, Ref. 35).

The effect of hyperglycemic peak induced by oral glucose tolerance test on the oxidant and antioxidant levels

Background/aim The possibility of adverse effects of the oral glucose tolerance test (OGTT) carried out for the screening of gestational diabetes among pregnant women and fetuses is a frequently discussed topic. The purpose of this study was to investigate the effects of the hyperglycemia peak during OGTT on the levels of oxidants and antioxidants in the body.Materials and methods Eighty individuals who applied to the Outpatient Clinic with suspected diabetes and OGTT indication were included in the study. Glucose, total oxidant capacity status (TOS), total antioxidant capacity (TAS), superoxide dismutase (SOD), and lipid hydroperoxide (LOOH) levels were tested on blood samples collected from these individuals at 0, 60, and 120 min during the OGTT carried out with 75 g of glucose. Oxidative stress index (OSI) was calculated as the ratio of TOS to TAS.Results While the oxidative parameters TOS and LOOH were significantly increased at 60. min of OGTT, only LOOH was significantly increased at 120. min of OGTT. Significant decreases in antioxidative parameters (TAS, SOD) were observed at 60. and 120. min of the OGTT and OSI was significantly increased at 60. and 120. min of the OGTT.Conclusion Oxidative stress parameters were increased and antioxidative parameters were decreased during the OGTT. However, more extended studies are required to determine the effects of the increased oxidative stress on pregnant women and fetuses.

СРАВНИТЕЛЬНАЯ ЭФФЕКТИВНОСТЬ ЯНТАРНОЙ КИСЛОТЫ И РЕАМБЕРИНА ПРИ ОКИСЛИТЕЛЬНОМ СТРЕССЕ В ЭКСПЕРИМЕНТЕ

The search and development of methods for correction of oxidative stress in conditions of exposure to adverse environmental factors is an actual problem of modern medicine. In experimental conditions the possibility to correct free radical lipid oxidation of rats’ organism membranes was studied with the introduction of the succinic acid and of the succinate containing medication called Reamberin (Polysan, St. Petersburg). The animals were divided into 4 groups and each of them had 20 rats: the group with intact animals which were held in standard conditions of vivarium; the control group in which rats were exposed to ultraviolet radiation during three minutes daily; the experimental group in which before ultraviolet radiation animals had a daily intraabdominal intake of the succinic acid in a dose of 100 mg/kg; the experimental group in which before ultraviolet radiation animals had a daily intraabdominal intake of Reamberin in a dose of 100 mg/kg (20 ml/kg). It was found out that in the blood of experimental animals a daily ultraviolet radiation during three minutes contributes to the increase of lipid hydroperoxides level (by 48-53%), of diene conjugate (by 43-48%), and of malonic dialdehyde (by 48-61%) against the decrease of antioxidant system activity in the blood of intact animals. The introduction of the succinic acid to rats contributes to the significant decrease in the blood of lipid hydroperoxides by 15-16%, of diene conjugates by 9-16%, and of malonic dialdehyde by 15% in comparison with the rats of the control group. The introduction of the succinate containing Reamberin to rats in the conditions of oxidative stress contributes to the significant decrease of lipid hydroperoxides in the blood by 27-28%, of diene conjugates by 23-28%, and of malonic dialdehyde by 26-29% in comparison with the rats of the control group. While analyzing the effect of the succinate containing drugs on the activity of the components of antioxidant system it was shown that the level of ceruloplasmin in the blood of animals was significantly higher by 25-32%, of vitamin E by 28-33% in comparison with the rats of the control group. So, the application of the succinate containing antioxidants in the conditions of ultraviolet radiation under experiment leads to the stabilization of the processes of peroxidation against the increase of antioxidant system activity. The intraabdominal introduction in laboratory animals of Reamberin in a dose of 100 mg/kg of succinate prevents the accumulation of lipoperoxidation products and increases the activity of main components of the antioxidant system in rats’ blood plasma, which indirectly exceeds similar effect of succinic acid in a dose of 100 mg/kg in the conditions of oxidative stress.

Hydraulic fracturing fluid biocide, tributyl tetradecyl phosphonium chloride, causes mitochondrial dysfunction that is enhanced by sodium chloride in Chironomus riparius

Tributyl tetradecyl phosphonium chloride (TTPC) is a biocide used in hydraulic fracturing fluid to minimize bacterial contamination. This study used the larvae of the freshwater insect Chironomus riparius to investigate the toxicity of TTPC, NaCl, and TTPC+NaCl. LC50s (mg/L) at 24 hours for TTPC, NaCl, and TTPC+NaCl were 0.57, >10,000, and 0.32, respectively, indicating a synergistic effect for TTPC+NaCl. ATP production was significantly increased in response to TTPC alone as compared to controls, but decreased significantly when TTPC was combined with NaCl, indicating severe damage to mitochondria. Superoxide dismutase (SOD) activity and lipid hydroperoxides (LPO) levels both increased in response to TTPC treatment, however, only LPO activity increased when TTPC was combined with NaCl. Red laser stimulation failed to enhance ATP production in response to increasing concentrations of TTPC and TTPC+NaCl. Taken together, these results indicate that hydraulic fracturing fluids entering freshwater ecosystems may put macroinvertebrates at risk.

Relationship of fruit and vegetable intake to dietary antioxidant capacity and markers of oxidative stress: A sex-related study.

Oxidative stress contributes to the development of chronic diseases. Fruits and vegetables contain several phytonutrients (carotenoids, polyphenols) that exert antioxidant effects. The aim of this study was to investigate sex differences in fruit and vegetable intake, and the relationship to plasma levels of carotenoids as well as to total antioxidant capacity (pTAC). We studied also sex differences in the relationship between fruit and vegetables intake and plasma levels of lipid hydroperoxides, as well as of oxidized low-density lipoprotein (ox-LDL). This study included 83 healthy adults (35 men and 48 women, mean age 40 ± 10 y). Dietary intake of carotenoids and total antioxidant capacity (dTAC) were evaluated on the basis of a 15-d food frequency questionnaire. Plasma levels of β-carotene, lutein, and pTAC were studied. Moreover, levels of plasma lipid hydroperoxides and ox-LDL were evaluated using the ferrous oxidation-xylenol orange 2 (FOX2) assay and a monoclonal antibody-based enzyme-linked immunosorbent assay procedure, respectively. Dietary habits were sex-related with a higher intake of fruits and vegetables (P < 0.05) and β-carotene (P < 0.001) in women than in men. Mean values of plasma lutein and β-carotene were higher in women than in men. Mean values of ox-LDL and lipid hydroperoxides were higher in men than in women (P < 0.05). Significant negative correlations were established between the individual values of ox-LDL and the levels of lutein versus β-carotene and versus pTAC values in plasma in both groups. Individuals belonging to the tertile with the highest daily intake of fruits and vegetables or the highest daily dTAC showed the lowest levels of plasma ox-LDL. In each category, sex-related differences were observed with men showing higher levels of ox-LDL than women. Moreover, lower levels of plasma β-carotene were observed in men in each tertile of daily intake of fruits and vegetables compared with females. Based on the data obtained, we confirm that high fruit and vegetable consumption exerts a positive effect on antioxidant defenses and decreases oxidative damage of plasma lipoproteins for both sexes. The results suggest that the protective effect can be found to a higher extent in women than in men. Sex-based differences are apparent in many chronic diseases. Thus, a higher consumption of antioxidant-rich fruits and vegetables should be recommended in efforts to prevent diseases in which sex-related differences in oxidative stress play a considerable role.

Lipid damage is the best marker of oxidative injury during the cardiac remodeling process induced by tobacco smoke

BackgroundOxidative stress is one potential mechanism that explain the direct effects of smoking on cardiac remodeling process. However, no study has compared different myocardial products of macromolecule oxidation after tobacco smoke exposure. Thus, the aim of this study was to investigate the lipid hydroperoxide (LH) levels, protein carbonyl concentrations and DNA damage in cardiac tissue of rats exposed to tobacco smoke.MethodsMale Wistar rats were divided into two groups: group C (control, n = 14) composed of animals not exposed to cigarette smoke; group ETS (exposed to tobacco smoke, n = 14) composed by animals exposed to cigarette smoke. The animals were exposed to 2 month of ETS and morphological, biochemical and functional analyses were performed.ResultsCardiac cotinine levels were elevated in the ETS group. In addition, the myocyte cross-sectional area was higher in the ETS group. (C = 266.6 ± 23.2 μm2 and ETS = 347.5 ± 15.1 μm2, p < 0.001). Cardiac LH was higher in the ETS group than in group C (C = 196.4 ± 51.5 nmol/g and ETS = 331.9 ± 52.9 nmol/g, p < 0.001). However, there were no between-group differences in cardiac protein carbonyl concentration or DNA damage.ConclusionsTherefore, our results suggest that, in this model, lipid damage is a good marker of oxidative damage during the cardiac remodeling process induced by 2 months of exposure to tobacco smoke.

Hydrolytic enzymes mediated lipid-DNA catabolism and altered gene expression of antioxidants under combined application of lead and simulated acid rain in Fenugreek (Trigonella foenum graecum L.) seedlings.

Understanding ill effects of simultaneous existence of various abiotic stresses, commonly observed due to various anthropogenic activities and global climate change these days, over plants growth, metabolic activity and yield responses are important for continued agricultural productivity and food security. In the present study, seedlings of Fenugreek (Trigonella foenum graecum L.) were subjected to lead (Pb, 1200 ppm) and/or simulated acid rain (SAR, pH 3.5) for 30 days, and were then analysed. The results revealed reduced growth, and total lipid and DNA contents, while enhanced Pb accumulation, biological concentration factor, biological accumulation coefficient, translocation factor, lipase activity, and levels of free fatty acid, conjugated diene, lipid hydroperoxide, DNA oxidation and DNase activity under Pb and/or SAR exposure. Additionally, activities and gene expression levels of antioxidants (superoxide dismutase, catalase, guaiacol peroxidase and ascorbate peroxidase) were enhanced in response to applied treatments. The results also suggested that inhibitions/ accelerations determined under joint addition of Pb and SAR were comparatively more profound than those measured under their single application. Additionally, root was more sensitive to Pb treatment, compared to both leaf and shoot. Hence, under simultaneous presence of two or more number of abiotic stresses, the strategy opted by plants for survival is chiefly governed by the interaction between prevailing stressors, which is then conceived by plants as a new state of stress.

Effects of a glyphosate-based herbicide on survival and oxidative status of a non-target herbivore, the Colorado potato beetle (Leptinotarsa decemlineata)

Glyphosate is the globally most used herbicide against a wide range of weeds. Glyphosate has been considered safe to animals as it mainly targets physiological pathways in plants. However, recent toxicological studies have revealed that glyphosate can cause various toxic effects also on animals. In this study, we investigated the direct toxic effects of a glyphosate-based herbicide (GBH, Roundup® Bio) on 1) survival and 2) oxidative status of a non-target herbivore by using Colorado potato beetles (Leptinotarsa decemlineata), originating from Poland and USA, as model species. Larvae were randomly divided into three groups: 1) high concentration (100% Roundup Bio, 360 g/l), 2) low concentration (1.5% Roundup Bio) and 3) control group (water). Larvae were exposed to Roundup for different time periods: 2 h, 24 h, 48 h, 72 h and 96 h. Larval survival decreased in the group treated with high concentration of GBH compared to controls, whereas the low concentration group did not differ from the control group. GBH treatment had no association with oxidative status biomarkers (i.e. catalase, superoxide dismutase, glutathione-S-transferase, glutathione and glutathione related enzymes), but increased lipid hydroperoxide levels after 2 h exposure, suggesting increased oxidative damage soon after the exposure. Larvae of different origin also differed in their oxidative status, indicating population-dependent differences in antioxidant defence system. Environmentally relevant concentrations of GBH are not likely to affect larval survival, but high concentrations can reduce survival and increase oxidative damage of non-target herbivores. Also, populations of different origin and pesticide usage history can differ in their tolerance to GBH.

Oxidative Status in Different Areas of the Cerebral Cortex of Wistar Rats during Focal Ischemia and Its Modulation with Carnosine.

Oxidative status was assessed in different areas of the cerebral cortex of male Wistar rats under normal condition and during permanent 24-h focal ischemia. In intact animals, the level of lipid hydroperoxides in the frontal lobes of both hemispheres was by 36% higher than in other cortical areas, while total antioxidant activity was by 25% higher than in other areas. During ischemia, changes in oxidative status were localized only in the ischemic focus and penumbra zone and did not involve other cortical areas. We demonstrated for the first time a neuroprotective effect of therapeutic administration of carnosine in low doses (50 mg/kg) on parameters of the oxidative status under conditions of focal ischemia comparable to its effect of high doses (500 mg/kg) as well as its local effect in the penumbra zone. A dose-dependent effect of carnosine on antioxidant activity in the penumbra zone during ischemia was also demonstrated. These findings confirm effectiveness of not only preventive carnosine administration, but also its application in the postischemic period of the stroke.