Decrease In Total Antioxidant Capacity Research Articles

Altered Hematological and Biochemical Parameters in Schoolchildren Living in an Agricultural Community of Merida State, Venezuela

Epidemiological studies have found that children living in a pesticide treated farmland have higher risk of developing cancer or other serious health problems. Their exposure to pesticides could be limited by periodic health assessments; however, there are few biomarkers for pesticide exposure. The aim of this work was to examine the effects of chronic exposure to pesticides on hematological and biochemical parameters in farm-resident children compared to urban-resident control children. A cross-sectional study was conducted in 72 farm schoolchildren and 41 controls; a follow-up study was done two years later on 20 participants. The children underwent a clinical examination, nutritional assessment, and blood sampling for complete hemogram and biochemical analysis of liver and renal functions, lipid and glucose metabolism, plasma cholinesterase, thyroid hormones and total antioxidant capacity. A prevalence of malnutrition and undernutrition were found in both exposed and control children. The most important hematological results were thrombocytosis in 48% of farm children, increased mean lymphocyte and monocyte counts, and decreased mean neutrophil counts compared to control. Butyrylcholinesterase activity was diminished in 35% of farm children. Alterations in biochemical parameters were observed between exposed and control groups, however, most of the results were within normal limits, except for the significant decrease in total antioxidant capacity. Follow-up study 2 years later showed normalized platelet and lymphocyte counts, however, decreased neutrophil counts was still observed. This study demonstrates that children living in an agricultural community are exposed to the health hazards of pesticides. Undernutrition and improper dental hygiene affect children’s overall health status and are likely to increase their vulnerability to toxic effects of pesticides.

Antiretroviral Therapy Initiation Alters the Redox System of Asymptomatic HIV-Infected Individuals: A Longitudinal Study.

Background. The combination antiretroviral therapy (cART) increases the oxidative stress in HIV-infected people, which in turn favors the onset and aggravation of non-AIDS comorbidities, a common situation affecting these individuals. We aimed to evaluate the influence of cART initiation on oxidative stress parameters. This is a longitudinal study including 30 asymptomatic patients divided according to their CD4+ T cell count (G1: <500 cell/mL; G2: >500 cell/mL) before (M0) and after (M1) cART initiation. We analyzed total antioxidant capacity (TAC), fat-soluble vitamins, malondialdehyde, 8-isoprostane, and DNA damage. Results. Results showed a decrease in TAC, retinol, α-tocopherol, and some carotenoids, in addition to a significant increase in DNA damage at M1. These changes were more evident in G2 subjects. Moreover, there was a significant 8-isoprostane increase at M1 in individuals belonging to G1. Conclusion. The results indicate that cART interfered in the redox system, mainly by reducing the antioxidant defenses. In addition, patients who had CD4+ T counts higher than 500 cells/mm3 showed more susceptibility to genotoxicity, while patients with less CD4+ T counts displayed more damage triggered by lipoperoxidation. Considering the early beginning of cART, its chronic use, and its capacity to alter the redox status, further long-term studies on larger cohorts are needed to define the best time to initiate therapy and to investigate new strategies to delay the development of non-AIDS diseases.

Effects of Propofol on Oxidative Stress Parameters in Selected Parts of the Brain in a Rat Model of Parkinson Disease.

Propofol is an intravenous sedative-hypnotic agent that is commonly used to induce and maintain general anaesthesia. This drug has antioxidant properties, which are partly caused by a phenolic structure similar to α-tocopherol. The present study aimed to evaluate the effect of propofol on the level of oxidative stress biomarkers in the frontal cortex, striatum, thalamus, hippocampus and cerebellum in rats with experimental Parkinson's disease (PD). The experiment was performed on 24 male Wistar rats assigned to the following groups: 1 - control; 2 - PD; 3 - PD with propofol. The dopaminergic systems were damaged with 6-hydroxydopamine (6-OHDA) administered to each lateral ventricle (2x15 μg/5 μl). 60 mg/kg of propofol was later given to the 8-week-old rats intraperitoneally. The activities of superoxide dismutase (SOD) and its enzymes Cu/ZnSOD and MnSOD, together with the malondialdehyde (MDA) concentration, total oxidative status (TOS) and total antioxidant capacity (TAC), were measured. In the 2nd group, a significant increase in MDA concentration in the striatum, hippocampus and thalamus, and an increase of TOS in the striatum, thalamus and cerebellum were noted, along with a TAC decrease in the cortex, striatum and thalamus. Propofol caused a significant decrease in MDA levels in the cortex, striatum, hippocampus and thalamus, and a decrease in TOS levels in the cortex, striatum and cerebellum, with increased TAC in all evaluated structures. A shortage of natural antioxidants is observed in PD, along with an increase in pro-oxidants in many brain areas. Propofol inhibits oxidative stress in the brain, which shows its neuroprotective properties against oxidative damage.

Response of osmotic adjustment and ascorbate-glutathione cycle to heat stress in a heat-sensitive and a heat-tolerant genotype of wucai (Brassica campestris L.)

High temperature stress (>30°C) from late summer to early fall is one of the main limiting factors in wucai (Brassica campestris L.) growth in southern China. To assess the osmotic and antioxidative reponses of two wucai genotypes (WS-6 and WS-1) differing in heat tolerance, three-week-old seedlings were subjected to three heat-stress treatments for 5 days. Heat treatments above at 30°C resulted in significant decreases in leaf area and leaf relative water content (RWC) in both genotypes, but being more in heat-sensitive WS-6. This was due to greater accumulations of osmolytes including soluble sugar, soluble protein and proline (Pro), as well as higher levels of reduced ascorbic acid (AsA) and glutathione (GSH) in heat-tolerant WS-1 under heat stress as compared to those in heat-sensitive WS-6. It is worthy noting that mild hyperthermia (30°C) caused significant increases of AsA and GSH in both genotypes, which might be resulted from their enhanced activities of monodehydroascorbate reductase (MDAR), dehydroascorbate reductase (DHAR) and glutathione reductase (GR), helping recycle AsA and GSH. In contrast, the AsA and GSH levels of both genotypes were decreased markedly at 40°C, especially in heat-sensitive WS-6, despite that the enzymes (DHAR and GR) activities involved in their regeneration remained high levels as compared to their respective controls. In addition, larger decrease in total antioxidant capacity (T-AOC) by heat stress was observed in WS-6 than in WS-1. Our results indicated that the heat-sensitive and the heat-tolerant genotype of wucai might possess the same pathway but different capacities of antioxidant defences to cope with heat stress.

Nephroprotection of punicalagin in rat model of endotoxemic acute kidney injury

The potential nephroprotection of punicalagin (PNG) against lipopolysaccharide (LPS)-induced acute kidney injury in rats was investigated. Rats received a single i.v. dose of LPS (5 mg/kg), and treated with PNG (50 mg/kg, i.p.), 1 h before, and 1 h following LPS administration. LPS caused significant increases of serum creatinine and neutrophil gelatinase-associated lipocalin. LPS also resulted in significant increases in interleukin-18, tumor necrosis factor-α, interleukin-6, malondialdehyde, nitric oxide, Bax/Bcl-2 ratio and myeloperoxidase, inducible nitric oxide synthase, caspases 3, 8 and 9 activities, and a significant decrease in total antioxidant capacity in kidney tissues. PNG significantly ameliorated the alterations in the measured parameters. Additionally, PNG attenuated the histopathological injury and reduced kidney injury molecule-1 expression in kidneys of rats that received LPS. It was concluded that PNG ameliorated endotoxemic acute kidney injury in rats by counteracting inflammation, oxidative/nitrative stress and apoptosis.

Abstract 3593: Electronic cigarettes induce significant DNA damage and reduce cellular antioxidant levels

Abstract Background: Cigarette smoking is the leading preventable cause of mortality in the world and the main risk factor for lung and head and neck cancer. E-cigarettes (ECs) are battery-operated devices that deliver nicotine via inhaled aerosols. Although ECs are marketed as a less harmful alternative to tobacco cigarettes and a smoking cessation aid, the health risks posed by exposure to EC aerosols are unknown. Nonetheless, the use of ECs has increased exponentially since 2003, with EC users reporting inhaling on average 200 puffs a day. EC aerosols have been reported to contain variable levels of genotoxins, including carcinogenic substances and reactive oxygen species (ROS). Some toxins in EC aerosols have been reported to reach the levels of similar to those in tobacco smoke. However, the genotoxicity of EC aerosols has not been characterized. Aims: (1) To determine the cytotoxicity and genotoxicity of short and long-term exposure to EC aerosols on human epithelial normal and cancer cell lines. (2) To evaluate whether exposure of EC aerosols modifies the cellular total antioxidant capacity (TAC). Methods: EC extracts were prepared from NJOY (12 or 18 mg/ml of nicotine) and Oakley eGo-T (0, 12 or 18 mg/ml of nicotine). Standard tobacco extracts were used for comparison. To assess the effects of short-term exposure, human epithelial normal (NuLi-1) and cancer (UD-SCC1) cell lines were exposed for 1 hour to various EC extract concentrations. To assess the effects of long-term exposure, cells lines were exposed every other day for 2 weeks to EC extracts. Cytotoxicity, DNA damage and TAC were evaluated at 1 h and 2 weeks. Cell viability was determined by MTT assay. DNA damage was quantified using the primer anchored DNA damage detection assay (PADDA). TAC was determined by the Antioxidant Assay Kit (Cayman). Data were analyzed by Student's t-test. Results: At the range of EC extract concentrations used in this study and expected to occur in EC users (1 to 100 puffs/5 L of blood), no cytotoxicity was observed for either normal or cancer cells. However, significant levels of DNA damage were observed in cancer cells exposed to 10 or more puffs/5 L of EC extracts and in normal cells exposed to100 puffs/5 L. Long-term exposure to EC extracts resulted in a significant decrease in TAC, a measure of free radical scavengers. Conclusion: Even short-term exposure to low levels of EC aerosols can cause significant DNA damage. Our study emphasizes the need to further investigate the carcinogenic potential of EC aerosols and highlights the importance of regulating EC use. Grant support: This work was supported by the Oklahoma Tobacco Research Center (LQ). Dr. Queimado holds a Presbyterian Health Foundation Endowed Chair in Otorhinolaryngology. Citation Format: Vengatesh Ganapathy, Jimmy Manyanga, Lacy Brame, David Rubenstein, Theodore L. Wagener, Ilangovan Ramachandran, Lurdes Queimado. Electronic cigarettes induce significant DNA damage and reduce cellular antioxidant levels. [abstract]. In: Proceedings of the 107th Annual Meeting of the American Association for Cancer Research; 2016 Apr 16-20; New Orleans, LA. Philadelphia (PA): AACR; Cancer Res 2016;76(14 Suppl):Abstract nr 3593.

Decreased activity of butyrylcholinesterase in blood plasma of patients with chronic obstructive pulmonary disease.

IntroductionButyrylcholinesterase (BChE) is involved in the metabolism of endogenous lipids and xenobiotics, such as esters of carboxylic or phosphoric acids. Butyrylcholinesterase activity is associated with both inflammation and oxidative stress. Changes in the activity of this enzyme have been observed in various diseases such as liver cirrhosis, diabetes, neurodegenerative disease and others.Material and methodsThe study involved 30 patients with chronic obstructive pulmonary disease (COPD) and 18 healthy subjects. The COPD patients were divided according to the severity of the disease by applying the classification of COPD based on GOLD standards for forced expiratory volume in 1 s (FEV1) and the FEV1/forced expiratory volume (FVC) ratio. The control group comprised blood samples collected from healthy subjects without concomitant diseases related to the respiratory system. Butyrylcholinesterase activity, lipid peroxidation and total antioxidant capacity (TAC) were determined in the blood plasma.ResultsA significant (p < 0.05) decrease in the activity of BChE, associated with an increase in lipid peroxidation and a decrease in the total antioxidant capacity, was observed in blood plasma of patients with chronic obstructive pulmonary disease.ConclusionsThe study shows for the first time that activity of BChE in the blood plasma of patients diagnosed with chronic obstructive pulmonary disease is considerably reduced compared with healthy subjects. These changes were accompanied by a decrease of TAC and an increase of lipid peroxidation, which suggests that they may be related to the oxidative stress induced by COPD disease.

Biochemical responses induced by co-exposition to arsenic and titanium dioxide nanoparticles in the estuarine polychaete Laeonereis acuta.

The production and use of nanoparticles, as titanium dioxide (nanoTiO2) is growing exponentially in the last years and their release into aquatic environment seem be inevitable. Once into environment, this nanomaterial can interact with other contaminant, as arsenic, and to exert toxic effect in living organisms. So, the objective of present study was to evaluate if the co-exposure to nanoTiO2 (1mg/L) can alter the As effect (nominal concentration of 50μg/L) in the estuarine polychaeta Laeonereis acuta after 48h of exposure. Were performed biochemical analyses such ROS production, enzymatic activities (GST, GR and GSTΩ), total antioxidant capacity against peroxyl radicals and damage to macromolecules (lipid and DNA), besides also were determined the accumulation of total arsenic and arsenic speciation in the worms. The results showed that co-exposure induced an increase in the ROS levels, decrease in total antioxidant capacity, increase in GR activity, and damage in lipid and DNA. Also, the co-exposure showed to affect the metabolization capacity of arsenic characterized by increase in dimethylated arsenic forms, a compound moderately toxic. So, these results suggest that the co-exposure to both contaminants is harmful to this species and the use of nanoTiO2 to treatment of contaminated water by arsenic should be considered of a toxicological point of view.

Evaluation of oxidant/antioxidant status, trace mineral levels, and erythrocyte osmotic fragility in goats naturally infected with Anaplasma ovis

Anaplasma ovis, an arthropod-borne pathogen that infects erythrocytes, is the major cause of ovine and caprine anaplasmosis. This study was performed to assess in goats infected with A. ovis the osmotic fragility of erythrocytes, antioxidant status, and serum levels of microminerals. Blood samples were collected from 104 mixed breed goats in Ahvaz area, southwest Iran and subjected to parasitologic, hematologic, oxidant/antioxidant, and micromineral assessment. Anaplasma infection was detected in 30 samples (28.8%) by microscopic examination of blood smears while PCR-RFLP analysis revealed infection with A. ovis in 68 samples (65.4%). Studied animals were divided into three groups based on A. ovis infection: Uninfected goats as control group (group 1), PCR positive without parasitemia (group 2) and PCR positive with parasitemia (group 3). Hematological evaluation showed significantly increased lymphocyte and monocyte counts in Anaplasma-infected groups (group 2 and 3). A significantly lower MCHC and higher MCV were also observed in infected groups. In group 3 significant rises in erythrocyte's osmotic fragility in different salt concentrations and also in median corpuscular fragility (MCF) was seen. Evaluation of the antioxidant defense system of the erythrocytes revealed a decrease in total antioxidant capacity (TAC) and superoxide dismutase (SOD) activity in group 3. There was no significant difference in serum micromineral levels between infected and uninfected animals. Overall, the observed substantial decrease in the antioxidant enzyme activities with remarkable elevated levels of erythrocyte osmotic fragility indicate high exposure of erythrocytes to oxidative damage in Anaplasma-infected goats. These results also suggest that the disturbed antioxidant defense mechanisms in caprine anaplasmosis can promote the development of anemia.

Modulation of the neurological and vascular complications by grape seed extract in a rat model of spinal cord ischemia-reperfusion injury by downregulation of both osteopontin and cyclooxygenase-2.

In this study, we investigated the effects of grape seed extract (GSE) on the expression of osteopontin (OPN) and cyclooxygenase-2 (COX-2) in a rat model of spinal cord ischemia-reperfusion injury (SC-IRI). Fifty male rats were divided into 5 groups: control (CON); control + GSE (CON + GSE) (received GSE for 28 days); sham operated (Sham); IRI; and IRI + GSE. SC-IRI was induced by clamping the aorta just above the bifurcation for 45 min, and then the clamp was released for 48 h for reperfusion. IRI + GSE group received GSE for 28 days before SC-IRI. Sensory, motor, and placing/stepping reflex assessment was performed. Prostaglandin E2 (PGE2), thiobarbituric acid reactive substances (TBARs), and total antioxidant capacity (TAC) were measured in spinal cord homogenate. Immunohistochemical examination of the spinal cord for OPN and COX-2 were carried out. SC-IRI resulted in significant increase in plasma nitrite/nitrate level and spinal cord homogenate levels of TBARs and PGE2, and OPN and COX-2 expression with significant decrease in TAC. GSE improves the sensory and motor functions through decreasing OPN and COX-2 expression with reduction of oxidative stress parameters. We conclude a neuroprotective effect of GSE in SC-IRI through downregulating COX-2 and OPN expression plus its antioxidants effects.

Blood Levels of Oxidant/Antioxidant Parameters in Rats Infected with Toxoplasma gondii.

Toxoplasmosis is a common parasitic infection in the world. Since increased free radicals and oxidative stress are reported in many parasitic diseases the purpose of the present study was to evaluate the oxidative stress in acute and chronic toxoplasmosis. RH strains of Toxoplasma tachyzoites were used in the present study. Twenty-five female rats were infected with the parasite while 25 other rats were as the control group that received normal saline. Zero-, 5-, 7-, 10-, and 45-day postinfection (DPI) blood samples were taken. Some parameters related to oxidant and antioxidants such as antioxidant enzymes, malondialdehyde, and total antioxidant capacity were measured. On day 7 after infection, GPX activity and GSH level were significantly increased and in the mentioned day the amount of total antioxidant capacity was significantly reduced. In other cases, there were no significant differences between the groups in different days. Overall, based on the results it seems that, on day 7 after infection, in infected rats responses to oxidative stress were triggered and led to decrease of total antioxidant capacity. Furthermore, glutathione was increased to cope with stress. It seems that probably antioxidant defense system entered the infection to the chronic phase and changed the parasites stage.

Protective Effects of Royal Jelly on Oxymetholone-Induced Liver Injury in Mice.

Background:The present study was carried out to investigate the possible protective effects of royal jelly (RJ) on oxymetholone (OXM)-induced oxidative liver injuries in mice.Methods:In total, 32 adult male NMRI mice were divided into four groups of eight mice each. Mice in groups 1 and 2 were orally administered 5 mg/kg/day OXM for 30 days. At the same time, mice in group 3 received RJ at a dose of 100 mg/kg/day. Saline control and RJ control groups were also included in this study.Results:Administration of 5 mg/kg OXM resulted in a significant decrease in total antioxidant capacity and catalase activity, as well as a significant increase in malondialdehyde (P<0.05). In addition, OXM-administrated mice showed a slight increase in liver enzymes, including alanine amino transferase, aspartate amino transferase, and alkaline phosphatase. Although OXM caused histopathological changes in the liver, RJ could significantly improve all of the above-mentioned parameters at a dose of 100 mg/kg.Conclusion:The results of the present study indicated that RJ has a partially protective effect on OXM-induced liver toxicity in mice.

Protective Effects of Caffeic Acid Phenethyl Ester on Fluoxetine-Induced Hepatotoxicity: An Experimental Study.

Background. The aim of the study was to analyse the effect of caffeic acid phenethyl ester (CAPE) on fluoxetine-induced hepatotoxicity in rats. Materials and Methods. Group I served as control. Group II received CAPE intraperitoneally. Group III received fluoxetine per orally. Group IV received fluoxetine and CAPE. The total antioxidant capacity (TAC), total oxidant status (TOS), oxidative stress index (OSI), and liver enzymes including paraoxonase-1 (PON-1), aspartate transaminase, and alanine transaminase levels were measured. Liver tissues were processed histopathologically for evaluation of liver injury and to validate the serum enzyme levels. Results. An increase in TOS and OSI and a decrease in TAC and PON-1 levels in serum and liver tissues of Group III were observed compared to Groups I and II. After treatment with CAPE, the level of TOS and OSI decreased while TAC and PON-1 increased in serum and liver in Group IV. Histopathological examination of the liver revealed hepatic injury after fluoxetine treatment and reduction of injury with CAPE treatment. Conclusion. Our results suggested that CAPE treatment provided protection against fluoxetine toxicity. Following CAPE treatment with fluoxetine-induced hepatotoxicity, TOS and OSI levels decreased, whereas PON-1 and TAC increased in the serum and liver.

Chronic Periodontitis in Type 2 Diabetes Mellitus: Oxidative Stress as a Common Factor in Periodontal Tissue Injury.

The prevalence of periodontitis is significantly higher among people with poorly controlled diabetes mellitus. Majority of tissue destruction in periodontitis is considered to be the result of an aberrant inflammatory/immune response to microbial plaque and involve prolonged release of reactive oxygen species (ROS). There is increased evidence for compromised antioxidant capacity in periodontal tissues and fluids which may be an added factor for tissue damage in periodontitis. To study the possible role of Reactive oxygen species (ROS) and antioxidant status in blood among chronic periodontitis patients with and without Type 2 Diabetes mellitus. The study comprised of total 100 subjects among which 25 were normal healthy controls, 25 were gingivitis patients, 25 were chronic periodontitis patients (CP) and 25 were having chronic periodontitis with type 2 diabetes (CP with DM). ROS levels were determined as MDA (Malondialdehyde) and antioxidant status as plasma total antioxidant capacity (TAC), vitamin C and erythrocyte Superoxide dismutase (SOD) and catalase activity. There was significant increase in MDA levels in all the patient groups compared with healthy controls (p<0.05). The decrease in TAC, Vitamin C and SOD levels among CP with DM patients as compared to controls was highly significant (p<0.01). There was a positive correlation between the probing pocket depth and MDA levels among periodontitis patients with diabetes (r=0.566, p=0.003). There is increased oxidative stress in chronic periodontitis with and without type 2 diabetes indicating a common factor involvement in tissue damage. More severe tissue destruction in periodontitis is associated with excessive ROS generation which is positively correlated in type 2 diabetic subjects.

Exercise Increases Cystathionine-γ-lyase Expression and Decreases the Status of Oxidative Stress in Myocardium of Ovariectomized Rats.

Exercise could be a therapeutic approach for cardiovascular dysfunction induced by estrogen deficiency. Our previous study has shown that estrogen maintains cystathionine-γ-lyase (CSE) expression and inhibits oxidative stress in the myocardium of female rats. In the present study, we investigated whether exercise improves CSE expression and oxidative stress status and ameliorates isoproterenol (ISO)-induced cardiac damage in ovariectomized (OVX) rats. The results showed that treadmill training restored the ovariectomy-induced reduction of CSE and estrogen receptor (ER)α and decrease of total antioxidant capacity (T-AOC) and increase of malondialdehyde (MDA). The level of CSE was positively correlated to T-AOC and ERα while inversely correlated to MDA. OVX rats showed increases in the serum levels of creatine kinase (CK) and lactate dehydrogenase (LDH) and the percentage of TUNEL staining in myocardium upon ISO insult compared to sham rats. Exercise training significantly reduced the serum levels of LDH and CK and the percentage of TUNEL staining in myocardium upon ISO insult in OVX rats. In cultured cardiomyocytes, ISO treatment decreased cell viability and increased LDH release, while overexpression of CSE increased cell viability and decreased LDH release in the cells upon ISO insult. The results suggest that exercise training improves the oxidative stress status and ameliorates the cardiac damage induced by oxidative stress in OVX rats. The improvement of oxidative stress status by exercise might be at least partially due to upregulation of CSE/H2S signaling.

Developmental effects of two different copper oxide nanomaterials in sea urchin (Lytechinus pictus) embryos

Copper oxide nanomaterials (nano-CuOs) are widely used and can be inadvertently introduced into estuarine and marine environments. We analyzed the effects of different nano-CuOs (a synthesized and a less-pure commercial form), as well as ionic copper (CuSO4) on embryo development in the white sea urchin, a well-known marine model. After 96 h of development with both nano-CuO exposures, we did not detect significant oxidative damage to proteins but did detect decreases in total antioxidant capacity. We show that the physicochemical characteristics of the two nano-CuOs play an essential role in their toxicities. Both nano-CuOs were internalized by embryos and their differential dissolution was the most important toxicological parameter. The synthesized nano-CuO showed greater toxicity (EC50 = 450 ppb of copper) and had increased dissolution (2.5% by weight over 96 h) as compared with the less-pure commercial nano-CuO (EC50 = 5395 ppb of copper, 0.73% dissolution by weight over 96 h). Copper caused specific developmental abnormalities in sea urchin embryos including disruption of the aboral-oral axis as a result in changes to the redox environment caused by dissolution of internalized nano-CuO. Abnormal skeleton formation also occurred.

Apple Peel is a Promising Source of Natural Bioactive Compounds That Promote Human Health

Antioxidant capacities (AC) and total phenolic content (TPC) of sixteen apple varieties obtained from different regions of Turkey and six commercial apple juices were examined. Trolox Equivalent Antioxidant Capacity (TEAC) and 2,2-diphenyl-1-picrylhydrazyl (DPPH) radical scavenging capacity assays were used for AC measurement while Folin-Ciocalteu method was applied for TPC measurements. ‘Ankara Agustos’ cultivar showed the highest antioxidant capacity (7.60 µmol TE/g FW) followed by ‘Bursa Gloster’ (3.10 µmol TE/g FW), and ‘Antalya Red Chief’ (2.90 µmol TE/g FW), whereas ‘Antalya Granny Smith’ exhibited the lowest antioxidant capacity (1.50 µmol TE/g FW). AC’s of commercial apple juices were found to be 2.8-fold less than the average of naturally produced juices with range of 0.38-2.56 µmol TE/g FW. Total antioxidant capacity changes at 4°C over time were also monitored for three varieties. A significant decrease in total antioxidant capacity after five weeks was observed. Moreover, the high correlation between AC and TPC of naturally produced apple juices (R2>0.97) indicated that phenolic compounds are a major contributor to the antioxidant activity of apple fruit.

The Effect of Soy Intake on Metabolic Profiles of Women With Gestational Diabetes Mellitus.

To our knowledge, no study has examined the effects of soy intake on metabolic status of women with gestational diabetes mellitus (GDM). This study was designed to assess the effects of soy intake on metabolic status of GDM women. A randomized clinical trial was performed among 68 women with GDM. Women were randomly assigned to receive either a control diet containing 0.8-g/kg protein (70% animal and 30% plant proteins) (n = 34) or a soy diet containing the same amount of protein with 35% animal protein, 35% soy protein, and 30% other plant proteins (n = 34) for 6 weeks. Compared with soy protein consumption, the control group significantly increased fasting plasma glucose (+1.4 ± 11.6 vs -12.7 ± 13.2 mg/dL, P < .001), serum insulin levels (+5.0 ± 11.6 vs -0.9 ± 10.0 μIU/mL, P = .02), homeostasis model of assessment-insulin resistance (+1.2 ± 2.7 vs -0.8 ± 2.2, P = .002), and decreased quantitative insulin sensitivity check index (-0.007 ± 0.02 vs +0.01 ± 0.03, P = .004). Administration of the control diet resulted in a significant difference in serum triglycerides changes (+31.3 ± 38.0 vs +8.9 ± 46.1 mg/dL, P = .03) compared with soy protein. There were a significant decrease in total antioxidant capacity (-35.0 ± 136.2 vs +81.8 ± 188.8 mmol/L, P = .005) and glutathione (-41.3 ± 145.7 vs +53.3 ± 117.3 μmol/L, P = .004) by the control diet intake compared with soy protein. The control diet group had a higher incidence of newborn hyperbilirubinemia (32.4% vs 8.8%, P = .01) and newborn hospitalization (20.6% vs 2.9%, P = .02) compared with soy protein. Soy protein consumption in women with GDM significantly improved the glucose homeostasis parameters, triglycerides, and biomarkers of oxidative stress, as well as reductions in the incidence of newborn hyperbilirubinemia and hospitalizations.

Mitochondrial Dysfunction and Its Relationship with mTOR Signaling and Oxidative Damage in Autism Spectrum Disorders.

Mitochondria are organelles that play a central role in processes related to cellular viability, such as energy production, cell growth, cell death via apoptosis, and metabolism of reactive oxygen species (ROS). We can observe behavioral abnormalities relevant to autism spectrum disorders (ASDs) and their recovery mediated by the mTOR inhibitor rapamycin in mouse models. In Tsc2(+/-) mice, the transcription of multiple genes involved in mTOR signaling is enhanced, suggesting a crucial role of dysregulated mTOR signaling in the ASD model. This review proposes that the mTOR inhibitor may be useful for the pharmacological treatment of ASD. This review offers novel insights into mitochondrial dysfunction and the related impaired glutathione synthesis and lower detoxification capacity. Firstly, children with ASD and concomitant mitochondrial dysfunction have been reported to manifest clinical symptoms similar to those of mitochondrial disorders, and it therefore shows that the clinical manifestations of ASD with a concomitant diagnosis of mitochondrial dysfunction are likely due to these mitochondrial disorders. Secondly, the adenosine triphosphate (ATP) production/oxygen consumption pathway may be a potential candidate for preventing mitochondrial dysfunction due to oxidative stress, and disruption of ATP synthesis alone may be related to impaired glutathione synthesis. Finally, a decrease in total antioxidant capacity may account for ASD children who show core social and behavioral impairments without neurological and somatic symptoms.

Oxidative stress during cystic ovarian disease in water buffalo

Follicular fluid and serum concentrations of antioxidants such as catalase, ascorbic acid (AA) and total antioxidant capacity (TAC) along with reactive oxygen species (ROS) and degree of oxidative damage to follicular cells, using protein carbonyl (PC) as marker of oxidative stress, were investigated during cystic ovarian disease in buffalo. Follicular fluid was aspirated from cystic follicles (&gt;20 mm) and also from large size (10-17 mm) of cycling buffaloes. Estradiol and progesterone were estimated to determine functional status (E: P ratio) of the follicles. Cystic follicles had greater concentrations of ROS and PC and lesser concentrations of catalase, ascorbic acid and TAC than normal follicles. An interesting finding was a simultaneous decrease of TAC and increase of ROS in serum of cystic buffaloes. Results indicated a pronounced follicular fluid oxidant-antioxidant imbalance and oxidative damage to follicular proteins during cystogenesis. In conclusion, this study provided evidence about role of oxidative stress in pathogenesis of cystic ovarian disease.