Decreased Total Antioxidant Capacity Levels Research Articles

Hydroxychloroquine attenuated motor impairment and oxidative stress in a rat 6-hydroxydopamine model of Parkinson’s disease

Purpose Parkinson’s disease (PD) is associated with the destruction of dopaminergic neurons in the substantia nigra (SN). Hydroxychloroquine (HCQ) has the capability to cross the blood–brain barrier and promote a neuroprotective potential. This study evaluated the effects of HCQ on the 6-hydroxydopamine (6-OHDA)-induced PD model in rats. Methods Wistar rats were randomly divided into sham, PD, PD + levodopa and PD + HCQ groups. The PD model was induced by a stereotactic administration of 6-OHDA into the left SN pars compacta (SNpc) and confirmed by rotation and the Murprogo’s tests. HCQ (100 mg/kg, p.o.) and levodopa (12 mg/kg, p.o.) were administered once a day for 21 days. Three weeks after surgery, the behavioral tests were performed. Brain lipid peroxidation index (MDA), glutathione peroxidase activity (GPx), total antioxidant capacity (TAC) levels and α-synuclein protein expression in the SN were also measured. Results The behavioral tests demonstrated that induction of PD increased the muscle rigidity and the number of rotations, which were reversed by HCQ treatment. Also, induction of PD was associated with an increase in α-synuclein protein levels and MDA and decreased TAC levels and GPx activity. However, HCQ decreased α-synuclein and MDA levels while increased TAC levels and GPx activity. In addition, histopathological data showed that HCQ protects dopaminergic neurons against 6-OHDA-induced toxicity. Conclusion According to the results, HCQ has a beneficial effect in improving PD-related pathophysiology, in part, by mitigating oxidative stress and protecting the dopaminergic neurons in the SN.

Effects of vanillic acid on Aβ1-40-induced oxidative stress and learning and memory deficit in male rats

Alzheimer's disease (AD) is a neurodegenerative disease, in which the accumulation of β-amyloid (Aβ) peptide in the extracellular space causes a progressive reduction in cognitive performance. Aβ stimulates active oxygen species generation leading to oxidative stress and neural cell death. Vanillic Acid (VA) is the oxidant form of vanillin widely found in vanilla beans. VA has many properties, such as suppressing apoptosis and eliminating the harmful effects of oxidative stress in animal models. The VA effects on impaired learning and memory in Aβ rats were assessed. Forty adults male Wistar rats were assigned to the following five groups in random: the control, sham (received saline (vehicle) via intracerebroventricular (ICV) injection), Aβ (received Aβ1–40 via ICV injection), VA (50 mg/kg by oral gavage once a day through four weeks), and Aβ + VA (50 mg/kg) groups. Open field test, novel object recognition (NOR) test, Morris water maze (MWM) test, and passive avoidance learning (PAL) task were performed, and finally, we determined the malondialdehyde (MDA), total antioxidant capacity (TAC) and total oxidant status (TOS) levels. Aβ decreased the cognitive memory in NOR, spatial memory in MWM, and passive avoidance memory in PAL tests. In contrast, VA improved learning and memory in the treated group. Aβ significantly increased MDA and TOS and decreased TAC levels, whereas VA treatment significantly reversed TAC, TOS and MDA levels. In conclusion, VA decreased the Aβ effects on learning and memory by suppressing oxidative stress and can be regarded as a neuroprotective substance in AD.

The Protective Effects of Vitamins A and E on Titanium Dioxide Nanoparticles (nTiO2)-Induced Oxidative Stress in the Spleen Tissues of Male Wistar Rats.

Titanium dioxide nanoparticles (nTiO2) can accumulate in different tissues and damage them with oxidative stress induction. Different components with antioxidant capacity can protect the tissues. So in this study, the protective effects of vitamin A and E on the nTiO2-induced oxidative stress in rats' spleen tissues were examined. Thirty-six male Wistar rats were randomly divided into 6 groups: Control 1 (received water), nTiO2, nTiO2 + vitamin E, nTiO2 + vitamin A, nTiO2 + vitamin A and E, and Control 2 (received olive oil). To investigate the status of oxidative stress, total antioxidant capacity (TAC), total oxidant status (TOS), and lipid peroxidation (LPO) were determined in spleen tissue as well as the activities of antioxidant enzymes, including glutathione peroxidase (GPx) and superoxide dismutase (SOD). Also, the gene expression of GPx, SOD, and nuclear factor-E2-related factor-2 (Nrf-2) were determined by qRT-PCR. To evaluate the spleen histopathological changes, H&E staining was carried out. nTiO2 significantly increased TOS and LPO levels, whereas it decreased TAC level, GPx and SOD activities, and gene expression of GPx, SOD, and Nrf-2 in spleen tissues of rats compared with controls (p < 0.05). In vitamin-treated rats, the levels of TOS and LPO significantly decreased, and the level of TAC, the activities of GPx and SOD, and the gene expression of GPx, SOD, and Nrf-2 increased compared to nTiO2 group (p < 0.05). These parameters are maintained near to normal levels. Histological findings confirmed the protective effects of these vitamins on tissue damage caused by nTiO2. Vitamin A and E can protect the spleen tissues from nTiO2-induced oxidative stress.

Swimming Exercise Ameliorates the Chronic Immobilization Stress-Induced Alterations in Spleen and Splenic T-cell population in Adult Male Albino Rats: Histological and Immunohistochemical study

Background: Stress is an integral part of modern life results in long-term alterations of the immune system. Exercise may have effects on immune functioning.Aim of the Work: To study chronic stress-induced alterations on serum corticosterone levels, splenic antioxidants, splenic morphology, and splenic T cell population, also to investigate the influence of swimming-exercise to counteract these alterations.Methods: Forty-rats were equally divided into four groups: control group, exercised group (EX-group), immobilization stressed group (IS-group) and exercised & immobilization stressed group (EX&IS-group). Assessment of serum corticosterone, splenic malondialdehyde (MDA), splenic total antioxidant capacity (TAC), as well as histological and immunohistochemical approaches were done.Results: EX-group had similar results if compared to control group apart from significantly increased TAC and decreased MDA levels. IS-group had significantly increased corticosterone and MDA with significantly decreased TAC levels, significantly decreased white pulp number and size, loss of the prominent marginal zone and expansion of red pulp with decreased cellularity if compared to control and EX-groups. While, exercise in EX&IS-group significantly decreased corticosterone and splenic MDA with significantly increased TAC levels, preserved the normal architecture with significant increased number and size of the lymphatic follicles and increased cellularity compared to the IS-group. Immunohistochemicaly, IS-group had significantly decreased CD3+ and CD4+ cells with a significantly increased CD8+ and apoptotic cells. Meanwhile, exercise prevent the effects of stress in EX&IS-group which had significantly increased CD3+ and CD4+ cells and significantly decreased CD8+ and apoptotic cells compared to the IS-group.Conclusion: Swimming exercise showed significant counteraction against the effect of chronic stress on serum corticosterone levels, splenic antioxidants, spleen microarchitecture changes and its cellular phenotypes, and also suppression of apoptosis of splenocytes. Exercise conditioned the animals to tolerate the various effects of stress, in turn, it could be hypothesized that active lifestyle is likely to be beneficial to immune function in stress exposure.

Blood total antioxidant status is associated with cortical glucose uptake and factors related to accelerated aging.

Identifying cerebral vulnerability in late life is of paramount importance to prevent pathological trajectories of aging before the onset of symptoms. Considerable evidence suggests that impaired antioxidant mechanisms are a fingerprint of aging-related conditions, but there is a lack of human research linking total antioxidant capacity (TAC) measured in peripheral blood to in vivo brain changes and other factors featuring accelerated aging. To address this issue, we have assessed in cognitively normal elderly subjects (N = 100) correlations between serum TAC, using the oxygen radical absorbance capacity assay, surface-based cortical thickness, surface-based 18F-fluorodeoxyglucose positron emission tomography cortical uptake, and different factors associated with accelerated aging [i.e., serum homocysteine (HCY), self-reported memory problems, and self-reported patterns of physical activity]. While no relationship was observed between serum TAC and variations in cortical thickness, decreased TAC level was significantly associated with lower FDG uptake in temporal lobes bilaterally. Remarkably, decreased TAC level was linked to increased HCY concentrations, moresubjective memorycomplaints, and lower frequency of physical activity. Overall, our results suggest that decreased serum TAC level may be helpful to detect vulnerable trajectories of aging.

Antioxidative properties of Thymus vulgaris on liver rats induced by paclitaxel

Background: Thymus vulgaris (Thym) is a species of flowering plant in the mint family Lamiaceae with potent antioxidant, and it has been beneficial effects during short-term administration. Paclitaxel sold under the brand name Tax (Tax) is chemotherapy drug which capable to produce free radicals. Objective: This study was designed to evaluate the effects of Thym against toxic effects of Tax to the liver of rats. Materials and Methods: Sixty-four male rats were assigned to eight groups: Control normal and Tax control groups (20 mg/kg); Thym groups (4.5, 9, 18 mg/kg), and Tax + Thym-treated groups (4.5, 9, 18 mg/kg). Treatments were administered intraperitoneally daily for 2 weeks. Griess technique was assessed for determined serum nitrite oxide (NO) level. Aspartate aminotransferase, ALANINE aminotransferase, and alkaline phosphatase concentrations were determined for liver functional disturbances. In addition, liver malondialdehyde (MDA), total antioxidant capacity (TAC), the diameter of hepatocytes, and the central hepatic vein (CHV) were investigated. Results: Tax administration significantly improved liver MDA and NO level, the mean diameter of CHV and hepatocyte, liver enzymes, and decreased TAC level compared to the normal control group (P

The Impact of Endometritis on Specific Oxidative Stress Parameters in Cows

This study was aimed to investigate the presence of uterine infection and the relationship between the severity of uterine infection and some oxidative stress parameters in cows in early postpartum period. Sixty six cows that were in the period between the 30th and 32rd days of postpartum were included in the study. Endometrial inflammation was scored according to the condition of the uterus at rectal and ultrasonographic examinations and the character and amount of uterine discharge from endometritis I through III, the latest being the most severe. Endometrial samples were taken from the clinically healthy animals by cytobrush method, and then stained with Giemsa for presence of polymorphonuclear leukocytes (PMN). Cows with a PMN percentage less than 18% were considered to be healthy (control, n=20). All cows were sampled for blood. Nitric oxide (NO) levels in Group I (Endometritis I; n=20), Group II (Endometritis II; n=16), Group III (Endometritis III; n=10) and the control group were determined to be 23.0±0.63 nmol/mL, 32.23±0.97 nmol/mL, 36.56±0.48 nmol/mL, and 11.10±0.29 nmol/mL, respectively. The differences among the groups were found to be statistically significant. Malondialdehyde (MDA) level was highest in Group III (6.38±0.13 μmol/L), and its level significantly decreased with the reduced severity of endometritis. The comparison of the groups for total antioxidant capacity (TAC) and total oxidant capacity (TOC) demonstrated that endometritis caused a decrease in TAC levels (P&lt;0.05), but did not affect TOC levels. Endometritis increased serum NO and MDA levels, and decreased TAC levels, but had no effect on TOC levels. In conclusion, NO and MDA, as well as TAC can be used as a biochemical marker for estimation of the severity of endometritis in cows.

Toxicological evaluation of submerged liquid culture from Phanerochaete chrysosporium mycelium on human blood cells: cytotoxicity, genotoxicity and oxidative damage

Mushrooms produce a variety of bioactive antioxidant secondary metabolites including ectins, polysaccharides, pigments, phenolic compounds, sterols and terpenes. Extracellular and intracellular compounds produced by submerged liquid fermentation are important industrially and economically. Phanerochaete chrysosporium (PC) is the model white-rot fungus that easy cultivation on lignocellulose-containing substrates. PC can be used as a bioprotein source. Aims of this study were to determine the in vitro antioxidant, cytotoxic and genotoxic effects of hot water extract obtained from PC on human peripheral blood monunuclear cells (hPBMCs). Cytotoxicity was determined by lactate dehydrogenase (LDH) leakeage assay and neutral red (NR). Total antioxidant capacity (TAC) and total oxidant status (TOS) were detected to determine the oxidative damage. Genotoxicity was characterized by micronuclei and chromosome aberrations assays for specify DNA damage. PC (5-75 µg/ml) significantly increased antioxidant capacity and these doses did not cause any significant alterations to cytotoxicity on hPBMCs. The elavated doses of PC (5-250 µg/ml) did not cause increase in genotoxic. Whereas, 250 and 500 µg/ml doses of PC statistically increased TOS levels, NR uptake, LDH release, CA/cell frequency and MN formation however decreased TAC levels. This study is the first time on cytotoxicity, genotoxicity and oxidative damage of PC on hPBMCs. In conclusion, the consumption of PC can be safe for humans, but it has also exposure period and dose-dependent effects on inducing oxidative damage and toxicity on hPBMCs.

Cytotoxic activity of the aqueous extract of Micromeria fruticosa (L.) Druce subsp. serpyllifolia on human U-87 MG cell lines

Micromeria fruticosa (L.) Druce subsp. serpyllifolia, which is widely used in folk medicine as a medicinal herbal tea, is grown in different areas of Turkey and the Mediterranean region. The present study was conducted to evaluate the aqueous extract of Micromeria fruticosa subsp. serpyllifolia for its antioxidant and antiproliferative activity on a human glioblastoma multiforme cell line (U-87 MG), which has not been reported before. Here, the extract was added to cultures at 8 different concentrations (0-200 ?g/mL). Cell viability and cell membrane damage was determined using the MTT and LDH assays for 48 h, respectively. To examine the oxidative effects, total antioxidant capacity (TAC) and total oxidant status (TOS) levels were measured. The extract displayed considerable antiproliferative activities at the high concentrations of 175 and 200 ?g/mL. Furthermore, the extract caused a significant increase in the release of the lactate dehydrogenase (LDH) enzyme in a concentration-dependent manner; 200 ?g/mL of extract enhanced the release of LDH. Treatments with extract at higher doses increased TOS levels and decreased TAC levels in human U-87 MG cells. Our study suggests that the aqueous extract of Micromeria fruticosa ssp. serpyllifolia was capable of inducing growth inhibition of cancer cells. These results encourage further research to assess the value of the extract in modern phytotherapy.

Cytotoxicity and genotoxicity of iron oxide nanoparticles: An in vitro biosafety study

With the development of nanotechnology and the wide use of iron oxide nanoparticles, it has become necessary to assess the potential adverse biological effects of magnetite. This study investigated the cytotoxicity, genotoxicity and oxidative damage of different concentrations of magnetite (0 to 1000 mg/L) in human whole blood cultures. After supplementation of magnetite, the blood samples were incubated for 72 h. Cell viability was assessed by the 3-(4,5-dimethyl-thiazol-2-yl) 2,5-diphenyltetrazolium bromide (MTT) and lactate dehydrogenase (LDH) release assays. The total antioxidant capacity (TAC) and total oxidant status (TOS) were determined to evaluate the dose-dependent effects of magnetite on the oxidant/antioxidant balance and to evaluate the potential oxidative injury due to increased oxidative stress. Genotoxicity was estimated by by the sister chromatid exchange (SCE), micronuclei (MN) and chromosome aberration (CA) assays and determination of 8-oxo-2-deoxyguanosine (8-OH-dG) levels. The results of MTT and LDH assays showed that the higher concentrations of magnetite (100, 150, 300, 500 and 1000 mg/L) decreased cell viability. Concentrations of magnetite higher than 10 mg/L increased TOS levels and decreased TAC levels in human blood cells. Increasing concentrations of magnetite caused significant increases in MN, SCE and CA rates and 8-OH-dG levels. The obtained results showed that magnetite exerted dose-dependent effects on oxidative damage, genotoxicity and cytotoxicity in human blood cells.

Determination of in vitro and in vivo protective effects of Ghrelin against oxidative stress: Experimental Study

Antioxidant properties of ghrelin have been recently reported in animal models and cell culture experiments. This study was set to examine the possible in vitro and in vivo anti-oxidative effects of ghrelin in rat and HepG2 cell culture. In this study, thirty six male Wistar Rats were randomly allocated into six experimental groups of six; Intraperitoneally, group 1 (Control) received 1 ml PBS, group 2 received 0.1 mM/kg tert-Butylhydroperoxide (tBOOH), groups 3 and 4 received 0.1 mM/kg t-BOOH and then received 10 and 50 µg/kg ghrelin, respectively. Groups 5 and 6 received 10 and 50 µg/kg ghrelin, respectively. Rats were anesthetized 24 h after last injection and blood samples were taken by cardiac puncture. Carbonylated proteins, nitric oxide (NO) and total antioxidant capacity (TAC) levels were measured in sera. HepG2 cells were plateaued at a density of 1.5 x 10 5 per well in eight plates. After treatment with ghrelin (0, 10, 25 and 50 nM) for 30 min, cells were treated with TBOOH (100 or 200 µM) for 24 h to analyze cell proliferation by MTT assay at 570 nm. Evidence of oxidative stress including increased carbonylated proteins and NO levels and decreased TAC level were observed after tBOOH injection. In rats with oxidative stress, subsequent treatment with ghrelin decreased NO and carbonylated proteins level and increased TAC level. The cell viability was decreased after t-BOOH treatment in dose dependent manner; in contrast, ghrelin in all used concentrations caused an elevation in cell viability after 24 h incubation time. These data taken together indicate that ghrelin reduces oxidative stress, but its exact mechanism is yet to be investigated.

MTHFR C677T and eNOS G894T variants in preeclamptic women: Contribution to lipid peroxidation and oxidative stress

ObjectivesWe aimed to investigate the association between methylenetetrahydrofolate reductase (MTHFR) C677T and endothelial nitric oxide synthase (eNOS) G894T polymorphisms with lipid peroxidation, total antioxidant capacity (TAC) and the risk of preeclampsia in preeclamptic women. Design and MethodsWe screened a sample of 198 unrelated women with mild and severe forms of preeclampsia and 101 unrelated women with normal pregnancy with the eNOS and MTHFR variants using PCR-RFLP method. Also, the serum malondialdehyde (MDA) and TAC levels were determined using HPLC and commercial kits, respectively. ResultsThe frequency of combined genotypes of MTHFR CT and TT (CT+TT) and T allele tended to be higher in severe preeclamptic women compared to controls. There was no significant difference for eNOS G894T genotype and allele frequencies between patients and controls. A significantly higher level of triglycerides was observed in the presence of combined genotypes of MTHFR CT and TT and also eNOS GT and TT (GT+TT) in preeclamptic women compared to controls with the same genotype. Also, the presence of MTHFR TT genotype in severe preeclamptic women was significantly associated with the increased serum MDA level compared to CC genotype. In severe preeclamptic women the presence of CT and combined genotypes of CT and TT was significantly associated with the decreased TAC level compared to CC genotype. Also, a higher MDA level was observed in mild preeclamptic women with eNOS TT genotype compared to those with GG genotype but the difference was not significant. ConclusionThe present study indicates that MTHFR C677T polymorphism through affecting on TG level, lipid peroxidation and oxidative stress might be involved in the pathogenesis of severe preeclampsia.

The relationship between oxidative stress, smoking and the clinical severity of psoriasis

Recent studies suggested that increased oxidant products and decreased antioxidant system functions may be involved in the pathogenesis of psoriasis. In this study, we investigated total oxidative status, Paraoxonase (PON)1/arylesterase enzyme activities and severity of the disease in smoker and non-smoker psoriatic patients. Fifty-four patients with plaque type psoriasis (28 smokers and 26 non-smokers) and 62 healthy volunteers (16 smokers and 46 non-smokers) were enrolled in the study. Serum total oxidant status (TOS), total antioxidant capacity (TAC) and arylesterase levels were measured, and oxidative stress index (OSI) was calculated in all participants. Psoriasis Area and Severity Index scores were significantly higher in smoker patients than in non-smoker patients (P = 0.014). Both smoker and non-smoker patients had significantly increased TOS levels and OSI values and decreased TAC levels than healthy subjects (all P values = 0.000). The TAC and TOS levels, OSI values and arylesterase activities were similar between smoker and non-smoker patients. The levels of triglyceride (TG), total cholesterol (TC), low-density lipoprotein (LDL) and high-density lipoprotein (HDL) were not significantly different between smoker and non-smoker psoriasis patients. When compared with non-smoking controls, only smoking psoriasis patients had significantly higher TG (P = 0.005), lower HDL (P = 0.022) and lower arylesterase levels (P = 0.015). There were no significant correlations with Psoriasis Area and Severity Index (PASI) scores and TAC, TOS, OSI, TG, TC, HDL and LDL levels in all psoriasis patients. Oxidative stress is increased in psoriasis patients regardless of their smoking status. The decreased arylesterase activity in smoker psoriasis patients suggested that smoking may be a considerable risk factor that increases the severity of psoriasis by increasing oxidative stress in these patients.

Hepatoprotective potential of astaxanthin against 2,3,7,8-tetrachlorodibenzo-p-dioxin in cultured rat hepatocytes

The purpose of this study was to evaluate the effect of carotenoid astaxanthin (ASTA) on cultured primary rat hepatocytes treated with 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) on the cell viability (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide, MTT), lactate dehydrogenase (LDH) activity, 8-oxo-2-deoxyguanosine (8-OH-dG), total antioxidant capacity (TAC), and total oxidative stress (TOS) levels, and liver micronucleus rates. ASTA (2.5, 5, and 10 µM) was added to cultures alone or simultaneously with TCDD (5 and 10 µM) for 48 h. The results of MTT and LDH assays showed that both doses of TCDD caused significant decrease in cell viability. Also, TCDD significantly increased TOS and decreased TAC level in rat hepatocytes. On the basis of increasing doses, the dioxin caused significant increase in micronucleated hepatocytes) and 8-OH-dG level as compared to control culture. The presence of ASTA with TCDD minimized its effects on primary hepatocytes cultures and DNA damages.

PP078. Total antioxidant capacity in patients with pregnancy induced hypertension: Its relation to maternal and/or perinatal complications

Pregnancy-induced hypertension (PIH) is a major cause of maternal and perinatal mortality and morbidity, particularly in under-resourced countries, like Mexico. Studies on PIH have shown increased oxidative stress products such as malondialdehyde and decrease of total antioxidant capacity (TAC). In this research we measured one marker of oxidative stress (OS) the TAC in patients with PIH and we associated it with the development of maternal and/or fetal complications. Determine whether the plasma level of total antioxidant capacity (as a marker of oxidative stress) influences the development of maternal and/or perinatal complications in patients with PIH. A observational, analytical, clinical study was conducted in patients with gestational hypertension (GH), mild preeclampsia (MP), severe preeclampsia (SP) and normal pregnancy (NP) > or = 28weeks gestational age. Serum samples were collected and stored at -70°C until use for the determination of total antioxidant capacity. It was associated with the development of maternal and/or perinatal complications. TAC level in normotensive patients (NP) was mean of 2679 +/- 2014mEq/L while in hypertensive patients (GH, MP, SP) was on mean of 1502 +/-1340mEq/L (p<0.05), in the GH group was 1620 +/-1042mEq/L, in the MP group was 1977 +/-1865mEq/L, in the SP was 819 +/-305meq/L The mean TAC level in the 29 patients who had maternal and/or perinatal complications was 1521mEq/L, while in the 38 patients who showed no maternal and/or perinatal complications the mean was 2355mEq/L (p<0.05). Of the 29 patients who had complications 15 (52%) had greatly diminished TAC levels (less than 1000mEq/L), 9 (31%) had between 1000 and 2500mEq/L and only 5 (17%)>2500mEq/L. 72% (28/39) of PIH group had one or more maternal and/or perinatal complications, while only 1 patient (3.6%) of 28 patients with NP had one or more maternal and/or perinatal complications (p<0.05). Patients with decreased TAC level had a higher percentage of maternal and/or perinatal complications. Patients with PIH classified as mild preeclampsia, showing reduced TAC level should be in close observation as they have the risk of developing life-threatening complications since management is usually as outpatient.

Eicosapentaenoic acid protects against 2,3,7,8-tetrachlorodibenzo-p-dioxin-induced hepatic toxicity in cultured rat hepatocytes

2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) is a persistent and ubiquitous environmental contaminant. The health impact of TCDD exposure is of great concern to the general public. Recent reports have implied that eicosapentaenoic acid (EPA) might be a potential chemopreventive agent and influence hepatotoxicity. The aim of the current study was to explore the effectiveness of EPA in alleviating the toxicity of TCDD on primary cultured rat hepatocytes. EPA (5, 10 and 20μM) was added to cultures alone or simultaneously with TCDD (5 and 10μM). Rat hepatocytes were treated with TCDD and EPA for 48h, and then cytotoxicity was detected by [3-(4,5-dimethyl-thiazol-2-yl) 2,5-diphenyltetrazolium bromide] (MTT) assay and lactate dehydrogenase (LDH) release, while total antioxidant capacity (TAC) and total oxidative stress (TOS) levels were determined to evaluate the oxidative injury. The DNA damage was also analyzed by liver micronucleus assay (LMN) and 8-oxo-2-deoxyguanosine (8-OH-dG). The results of MTT and LDH assays showed that TCDD but not EPA decreased cell viability. TCDD also increased TOS level and significantly decreased TAC level in rat hepatocytes in a clear dose dependent manner. On the basis of increasing doses, the dioxin caused significant increases of micronucleated hepatocytes (MNHEPs) and 8-OH-dG as compared to control culture. Whereas, in cultures treated with EPA alone, TOS level did not change and the level of TAC significantly increased. The presence of EPA with TCDD minimized the toxic effects of the dioxin on primary hepatocytes cultures. Noteworthy, EPA has a protective effect against TCDD-mediated DNA damages.

Propolis protects against 2,3,7,8-tetrachlorodibenzo-p-dioxin-induced toxicity in rat hepatocytes

The present experiment was undertaken to determine the effectiveness of propolis in alleviating the toxicity of TCDD on cultured primary rat hepatocytes. Propolis (25, 50 and 100μM) was added to plain culture or simultaneously with TCDD (5 and 10μM). The hepatocytes were treated with TCDD and propolis for 48h. Then cell viability was detected by [3-(4,5-dimethyl-thiazol-2-yl) 2,5-diphenyltetrazolium bromide] (MTT) assay and lactate dehydrogenase (LDH) release, while total antioxidant capacity (TAC) and total oxidative stress (TOS) levels were determined to evaluate the oxidative injury. The DNA damage was also analyzed by liver micronucleus assay (LMN) and 8-oxo-2-deoxyguanosine (8-OH-dG). The results of MTT and LDH assays showed that TCDD decreased cell viability. TCDD also increased TOS level and decreased TAC level in rat hepatocytes. On the basis of increasing doses, the TCDD caused significant increases of micronucleated hepatocytes (MNHEPs) and 8-OH-dG levels as compared to control culture. In cultures treated with propolis alone, cell viability and TOS level were not affected, while the level of TAC was significantly increased in dose-dependent fashion. The presence of propolis with TCDD modulated its toxic effects on primary hepatocytes cultures. Noteworthy, propolis has a protective effect against TCDD-mediated DNA damages.

Olive (Olea europaea L.) leaf extract counteracts genotoxicity and oxidative stress of permethrin in human lymphocytes

The aim of this study was to investigate the protective effects of olive leaf extract (OLE) on genotoxicity and oxidative damage in cultured human blood cells treated with permethrin (PM) in the presence of a rat liver S9 mix containing cytochrome P 450 enzymes. Anti-genotoxic activities of OLE were studied using sister chromatid exchange (SCE) and chromosome aberration (CA) tests and furthermore total antioxidant capacity (TAC) and total oxidative status (TOS) were examined to determine the oxidative damage. Our results clearly revealed that treatment with PM (200 mg/l) alone increased SCE and CA rates and TOS level, decreased TAC level in cultured human blood cells. The OLE alone at the all tested doses did not induce any significant changes in the genotoxicity endpoint. However OLE leads to increases of plasma TAC level in vitro. OLE starts showing this positive effect at 100 mg/l. The combined treatment showed significant improvements in cytogenetic and biochemical parameters tested. Moreover, this improvement was more pronounced in the group received the high dose of the OLE. It could be concluded that the ethanol extract of OLE induced its genoprotective effect via the increase in the antioxidant capacity, inhibition of oxidative stress and scavenging of free radicals.

The Association of Oxidant Status and Antioxidant Capacity in Children With Acute and Chronic ITP

This study was undertaken to investigate oxidant and antioxidant systems in patients with immune thrombocytopenic purpura (ITP). With this purpose, we measured the levels of serum malondialdehyde (MDA), total antioxidant capacity (TAC), total oxidant status (TOS), and other oxidative stress parameters. Fifty-two pediatric patients with ITP (25 acute, 27 chronic) and 21 healthy children were included in the study. Patients with acute ITP were studied, before and after, methylprednisolone treatment. Hemoglobin, hematocrit, platelet count, and TAC were statistically significantly lower in patients with acute ITP before treatment than those in the control group (P<0.05). In addition, in this group, MDA, TOS levels, and OSI (oxidative stress index) were found to be higher than those in the control group. In chronic ITP group, although hemoglobin hematocrit, platelet counts, and TAC levels were statistically significantly lower than those in the control groups,the mean platelet volume, MDA, TOS, and OSI were found to be statistically significantly higher (P<0.05). Platelet count and mean platelet volume values were statistically significantly lower in patients with acute ITP before treatment than after treatment (P<0.05). We also found a positive correlation between thrombocyte count and TAC, in patients with acute ITP before treatment (r: 0.601, P<0.001) and acute ITP after treatment (r: 0.601, P<0.001) and chronic ITP (r: 0.601, P<0.001). A negative correlation was found between thrombocyte count and serum MDA levels, in patients with acute ITP before treatment (r: -0.356, P<0.001) and acute ITP after treatment (r: -0.356, P<0.001) and chronic ITP (r: -0.356, P<0.001). We also found a negative correlation between thrombocyte count and serum OSI, in patients with acute ITP before treatment (r: -0.494, P<0.001) and acute ITP after treatment (r: -0.494, P<0.001) and chronic ITP (r: -0.494, P<0.001). A negative correlation was found between thrombocyte count and TOS, in patients with acute ITP before treatment (r: -0.470, P<0.001) and acute ITP after treatment (r: -0.470, P<0.001) and chronic ITP (r: -0.470, P<0.001). In conclusion, increased MDA, TOS and OSI, and decreased TAC levels were found in patients with acute and chronic ITP. On the basis of these findings, we suggest that free oxygen radicals may have an effect on the structural and functional damage of platelets, and on the mechanism of thrombocytopenia in both, acute and chronic ITP.