Antioxidant Defense Status Research Articles

Single and mixture exposure to atrazine and ciprofloxacin on Clarias gariepinus antioxidant defense status, hepatic condition and immune response

Atrazine (ATRA) and ciprofloxacin (CPRO) are widely detected, persistent and co-existing aquatic pollutants. This study investigated effects of 14-day single and joint ATRA and CPRO exposure on juvenile Clarias gariepinus. Standard bioassay methods were used to determine responses of oxidative stress, hepatic condition, and immunological biomarkers on days 7 and 14. Seven groups were used: Control, CPROEC, CPROSubl, ATRAEC, ATRASubl, CPROEC+ATRAEC, and CPROSubl+ATRASubl. The test substances caused decreased activity of superoxide dismutase, catalase, and glutathione peroxidase. Lipid peroxidation was elevated, especially in CPRO-ATRA mixtures. Serum aminotransferases (ALT, and AST), and alkaline phosphatase activity increased significantly. Total protein, albumin, total immunoglobulin, and respiratory burst decreased significantly. Therefore, single and joint exposure to CPRO and ATRA poses adverse consequences on aquatic life.

Mitochondria-targeted antioxidant, mitoQ protects hepatic tissue from N-nitrosodiethylamine-induced damage by modulating mitochondrial function and redox status

BackgroundTargeting mitochondrial oxidative stress can be a promising strategy for the prevention of hepatocellular carcinoma (HCC). In the current study, we investigated the modulatory effect of mitochondria-targeted antioxidant, mitoQ against N-nitrosodiethylamine (NDEA)-induced hepatic damage in mouse. MethodsBALB/c mice were administered NDEA (10 mg/kg b. w., single dose, intraperitoneally) and the hepatoprotective effect of mitoQ was studied by administering mitoQ (0.125 mg/kg b. w., orally once a week) to the animals. The administration of mitoQ started two weeks prior the NDEA administration. The animals were sacrificed 24 h following NDEA administration after which the blood samples and hepatic tissues were collected. Serum was used for the estimation of liver injury markers and hepatic tissues were analyzed for histopathological changes, antioxidant defense status, mitochondrial functional status, level of mitochondrial reactive oxygen species (mtROS) and mitochondrial lipid peroxidation (mtLPO). ResultsMitoQ treatment to the NDEA-challenged group normalized liver injury markers, level of mtROS and mtLPO. MitoQ treatment also improved the status of mitochondrial antioxidant defense system, mitochondrial complex enzymes. ConclusionOur findings indicate that mito-Q significantly protected against NDEA-induced hepatic damage by modulating mitochondrial function and redox status which may be one of the causes of its purported chemopreventive effect.

Anticancer therapeutic potential of multimodal targeting agent- "phosphorylated galactosylated chitosan coated magnetic nanoparticles" against N-nitrosodiethylamine-induced hepatocellular carcinoma.

Superparamagnetic iron oxide nanoparticles (SPIONs) are extensively used as carriers in targeted drug delivery and has several advantages in the field of magnetic hyperthermia, chemodynamic therapy and magnet assisted radionuclide therapy. The characteristics of SPIONs can be tailored to deliver drugs into tumor via "passive targeting" and they can also be coated with tissue-specific agents to enhance tumor uptake via "active targeting". In our earlier studies, we developed HCC specific targeting agent- "phosphorylated galactosylated chitosan"(PGC) for targeting asialoglycoprotein receptors. Considering their encouraging results, in this study we developed a multifunctional targeting system- "phosphorylated galactosylated chitosan-coated magnetic nanoparticles"(PGCMNPs) for targeting HCC. PGCMNPs were synthesized by co-precipitation method and characterized by DLS, XRD, TEM, VSM, elemental analysis and FT-IR spectroscopy. PGCMNPs were evaluated for in vitro antioxidant properties, uptake in HepG2 cells, biodistribution, in vivo toxicity and were also evaluated for anticancer therapeutic potential against NDEA-induced HCC in mice model in terms of tumor status, electrical properties, antioxidant defense status and apoptosis. The characterization studies confirmed successful formation of PGCMNPs with superparamagnetic properties. The internalization studies demonstrated (99-100)% uptake of PGCMNPs in HepG2 cells. These results were also supported by biodistribution studies in which increased iron content (296%) was noted inside the hepatocytes. Further, PGCMNPs exhibited no in vivo toxicity. The anticancer therapeutic potential was evident from observation that PGCMNPs treatment decreased tumor bearing animals (41.6%) and significantly (p ≤ 0.05) lowered tumor multiplicity. Overall, this study indicated that PGCMNPs with improved properties are efficiently taken-up by hepatoma cells and has therapeutic potential against HCC. Further, this agent can be tagged with 32P and hence can offer multimodal cancer treatment options via radiation ablation as well as magnetic hyperthermia.

The effect of bisphenol A on antioxidant defense and the structure and function of the liver of Siberian sturgeon (Acipenser baerii).

The present study was conducted to investigate the biochemical and histological changes of liver tissue in Siberian sturgeon (Acipenser baerii) exposed to different doses of bisphenol A (BPA). One hundred and eighty pieces of 1-year-old A. baerii with an average weight of 200-250 g bought and randomly distributed in 18 tanks (n = 10). After 2 weeks of adaptation, the fish received intraperitoneal injections of 1, 10, and 100 μg/g/week BPA and μg/g/week of 17β-estradiol intraperitoneally. The solvent control group received only peanut oil, while the control group did not receive any injections. In order to investigate histological changes of the liver, after 2 weeks the liver samples were taken, fixed in 10% formalin solution and slides prepared by routine histological methods. For assaying antioxidant defense status, the liver tissue from three fish of each replicates was captured and after homogenization, activity of catalase, superoxide dismutase, and glutathione peroxidase and malondialdehyde measured. The most important histological changes observed in the liver tissue were: vacuolation of hepatocytes, nuclear hypertrophy, necrosis of liver cells, expansion of sinusoids, and accumulation of fat cells. In the highest dose, the intensity of tissue changes increased. Activity of antioxidant enzymes and malondialdehyde content increased in fish exposed to 100 μg/g/week BPA in compare with other groups (p < .05). According to our findings, it could be concluded that liver histology was affected by BPA and tissue damage had occurred, which had led to changes in blood parameters. Also, the obtained results showed that the high concentrations of BPA used in this study stimulate the antioxidant defense. RESEARCH HIGHLIGHTS: BPA evoke oxidative stress in Siberian sturgeons in high dose of exposure. Severity of liver histologic lesions was dose dependent.

Effect of Liver Enzymes, Oxidative Stress and Vitamin D3 in Psoriatic Patients

Psoriasis is one of the skin’s chronic inflammatory diseases. Psoriasis etiology isn’t exactly known. Recently, it has been suggested that the imbalances in oxidant-antioxidant status happening because of the increase in reactive oxygen species production (ROS) and/or deficient function regarding the antioxidant system might be included in psoriasis pathogenesis. The major goal is to evaluate the antioxidant defense status in patients experiencing psoriasis and oxidative stresses represented by malondialdehyde (MDA) level and evaluate liver enzymes and vitamin D3. There are some tests of biochemical parameters and vitamins (GSH, MDA, VitD3, SOD, GPx, CAT, AST, ALT, and ALP) are conducted on 35 patients experiencing psoriasis. The results indicated that the significant increase in MDA in psoriatic patients in comparison to the control at (P&lt;0.05), while the level of glutathione (GSH), superoxide dismutase (SOD), glutathione peroxidase (GPX), and catalase (CAT) decreased significantly in psoriatic subjects compare to control. No significances differences in levels of liver enzymes in psoriatic patients compared to the control group.

Mito-TEMPO mitigates 5-fluorouracil-induced intestinal injury via attenuating mitochondrial oxidative stress, inflammation, and apoptosis: an in vivo study

BackgroundRecent evidences highlight role of mitochondria in the development of 5-fluorouracil (5-FU)-induced intestinal toxicity. Mitochondria-targeted antioxidants are well-known for their protective effects in mitochondrial oxidative stress- mediated diseases. In the present study, we investigated protective effect of Mito-TEMPO in 5-FU-induced intestinal toxicity.MethodsMito-TEMPO (0.1 mg/kg b.w.) was administered intraperitoneally to male BALB/c mice for 7 days, followed by co-administration of 5-FU for next 4 days (intraperitoneal 12 mg/kg b.w.). Protective effect of Mito-TEMPO on intestinal toxicity was assessed in terms of histopathological alterations, modulation in inflammatory markers, apoptotic cell death, expression of 8-OhDG, mitochondrial functional status and oxidative stress.Results5-FU administered animals showed altered intestinal histoarchitecture wherein a shortening and atrophy of the villi was observed. The crypts were disorganized and inflammatory cell infiltration was noted. Mito-TEMPO pre-protected animals demonstrated improved histoarchitecture with normalization of villus height, better organized crypts and reduced inflammatory cell infiltration. The inflammatory markers and myeloperoxidase activity were normalized in mito-TEMPO protected group. A significant reduction in intestinal apoptotic cell death and expression of 8-OhDG was also observed in mito-TEMPO group as compared to 5-FU group. Further, mtROS, mtLPO and mitochondrial antioxidant defense status were improved by mito-TEMPO.ConclusionMito-TEMPO exerted significant protective effect against 5-FU-induced intestinal toxicity. Therefore, it may be used as an adjuvant in 5-FU chemotherapy.

The Role of Selected Trace Elements in Oxidoreductive Homeostasis in Patients with Thyroid Diseases.

Impaired levels of selenium (Se), zinc (Zn), copper (Cu), iron (Fe), manganese (Mn) and iodine (I) in the organism may adversely affect the thyroid endocrine system. These trace elements play a role in the fight against oxidative stress as components of enzymes. Oxidative-antioxidant imbalance is considered a possible factor in many pathological conditions, including various thyroid diseases. In the available literature, there are few scientific studies showing a direct correlation of the effect of supplementation of trace elements on slowing down or preventing the occurrence of thyroid diseases in combination with the improvement of the antioxidant profile, or through the action of these elements as antioxidants. Among the available studies, it has been shown that an increase in lipid peroxidation levels and a decrease in the overall antioxidant defense status occur during such thyroid diseases as thyroid cancer, Hashimoto's thyroiditis and dysthyroidism. In studies in which trace elements were supplemented, the following were observed: a decrease in the level of malondialdehyde after supplementation with Zn during hypothyroidism and reduction in the malondialdehyde level after Se supplementation with a simultaneous increase in the total activity status and activity of antioxidant defense enzymes in the course of autoimmune thyroiditis. This systematic review aimed to present the current state of knowledge about the relationship between trace elements and thyroid diseases in terms of oxidoreductive homeostasis.

Astaxanthin mitigates oxidative stress caused by microplastics at the expense of reduced skin pigmentation in discus fish

Microplastics (MPs) exposure generally triggers oxidative stress in fish species and vertebrate pigmentation is commonly influenced by oxidative stress, but MPs-induced oxidative stress on fish pigmentation and body color phenotype has not been reported. The aim of this study is to determine whether astaxanthin could mitigate the oxidative stress caused by MPs but at the expense of reduced skin pigmentation in fish. Here, we induced oxidative stress in discus fish (red skin color) by 40 or 400 items/L MPs under both astaxanthin (ASX) deprivation and supplementation. We found that lightness (L*) and redness (a*) values of fish skin were significantly inhibited by MPs under ASX deprivation. Moreover, MPs exposure significantly reduced ASX deposition in fish skin. The total antioxidant capacity (T-AOC) and superoxide dismutase (SOD) activity in fish liver and skin were both significantly increased with the increase of MPs concentration, but content of glutathione (GSH) in fish skin showed a significant decrease. For ASX supplementation, the L*, a* values and ASX deposition were significantly improved by ASX, including the skin of MPs-exposed fish. The T-AOC and SOD levels changed non-significantly in fish liver and skin under the interaction of MPs and ASX, but ASX significantly reduced GSH content in fish liver. Biomarker response index indicated that ASX could improve the moderately altered antioxidant defense status of MPs-exposed fish. This study suggests that the oxidative stress caused by MPs was mitigated by ASX but at expense of reduced fish skin pigmentation.

Leaf extract of Anacardium occidentale ameliorates biomarkers of neuroinflammation, memory loss, and neurobehavioral deficit in N(ω)-nitro-L-arginine methyl ester (L-NAME) treated rats

Purpose Anacardium occidentale commonly known as Cashew is a plant that is widely used in African traditional medicine. It is endowed with phytochemical constituents that are responsible for its medicinal properties. Methods Twenty-five male Wistar rats were grouped as follows: Control (Group A), Group B (L-NAME 40 mg/kg), Group C (100 mg/kg Anacardium occidentale extract plus 40 mg/kg L-NAME), Group D (200 mg/kg extract plus 40 mg/kg L-NAME) and Group E (10 mg/kg of Lisinopril plus 40 mg/kg L-NAME). The animals were treated with oral administration of either the extracts or Lisnopril daily for 4 weeks. Neuro-behavioural tests such as the Morris Water Maze and Hanging Wire Grip tests were carried out to evaluate memory/spatial learning and muscular strength, respectively. Makers of oxidative stress, antioxidant enzymes and immunohistochemical staining of Glial Fibrillary Acidic Protein and Ionised Calcium Binding Adaptor molecule 1 were assessed. Results L-NAME administration caused significant increases in biomarkers of oxidative stress, decreased antioxidant status, acetylcholinesterase activity, altered neuro-behavioural changes, astrocytosis, and microgliosis. However, Anacardium occidentale reversed exaggerated oxidative stress biomarkers and improved neuro-behavioural changes. Conclusions Combining all, Anacardium occidentale enhanced brain antioxidant defence status, improved memory and muscular strength, thus, suggesting the neuroprotective properties of Anacardium occidentale.

Antioxidant Defense and Pseudoexfoliation Syndrome: An Updated Review.

Oxidative stress (OS) affects the anterior ocular tissues, rendering them susceptible to several eye diseases. On the other hand, protection of the eye from harmful factors is achieved by unique defense mechanisms, including enzymatic and non-enzymatic antioxidants. The imbalance between oxidants and antioxidants could be the cause of pseudoexfoliation syndrome (PEXS), a condition of defective extracellular matrix (ECM) remodeling. A systematic English-language literature review was conducted from May 2022 to June 2022. The main antioxidant enzymes protecting the eye from reactive oxygen species (ROS) are superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPx), which catalyze the reduction of specific types of ROS. Similarly, non-enzymatic antioxidants such as vitamins A, E and C, carotenoids and glutathione (GSH) are involved in removing ROS from the cells. PEXS is a genetic disease, however, environmental and dietary factors also influence its development. Additionally, many OS products disrupting the ECM remodeling process and modifying the antioxidative defense status could lead to PEXS. This review discusses the antioxidative defense of the eye in association with PEXS, and the intricate link between OS and PEXS. Understanding the pathways of PEXS evolution, and developing new methods to reduce OS, are crucial to control and treat this disease. However, further studies are required to elucidate the molecular pathogenesis of PEXS.

Physiological responses of channel catfish (Ictalurus punctatus) reared at different stocking densities in a recirculating aquaculture system

This study investigated the physiological responses of channel catfish (Ictalurus punctatus) reared under different stocking densities (SDs). Juvenile channel catfish with an average initial body weight of 40.6 ± 2.23 g were reared at three densities of 2.03 (low SD; LSD), 6.09 (medium SD; MSD), and 12.18 (high SD; HSD) kg m−3 for 60 days. Serum biochemistry, antioxidant defense status, immune parameters, and hepatic heat shock proteins (hsps) mRNA expression were analyzed. Serum cortisol levels are significantly elevated in MSD and HSD. A significant increase in lysozyme (LZM) activity and the contents of immunoglobulin M (IgM) and complement component 3 (C3) were observed with the increased SD. Total antioxidant capacity (T-AOC) and the activities of superoxide dismutase (SOD) and glutathione peroxidase (GPx) did not significantly affect SD. I. punctatus reared in HSD showed significantly increased catalase (CAT) activity, malonaldehyde (MDA) content, and nitric oxide (NO) levels. Hepatic hsp70 and hsp90 mRNA expression were significantly downregulated in HSD compared to LSD. Overall, HSD caused chronic stress in I. punctatus, leading to biochemical and immune function variations

Recent Approaches to Determine Static and Dynamic Redox State-Related Parameters

Oxidative stress refers to an imbalance between oxidant and antioxidant molecules, which is usually associated with oxidative damage to biomolecules and mitochondrial malfunction. Redox state-related parameters include (1) the direct measurement of ROS, (2) the assessment of the antioxidant defense status, and (3) the analysis of the resulting oxidative damage to molecules. Directly measuring ROS appears to be the preferred method among scientists, but most ROS are extremely unstable and difficult to measure. The processes of determining both the oxidative damage to biomolecules and the antioxidant system status, although both are indirect approaches, provide a reliable method to measure oxidative stress on a given sample. Recently, the Seahorse XF and the Oroboros O2k systems have provided new insights into the redox state from a more dynamic point of view. These techniques assess mitochondrial oxidative phosphorylation function and bioenergetics on isolated mitochondria, cultured cells, or specific tissues such as permeabilized fibers. This review describes a range of methodologies to measure redox state-related parameters, their strengths, and their limitations. In conclusion, all these techniques are valid and none of them can be replaced by another. Indeed, they have the potential to complement each other for a complete evaluation of the redox state of a given sample.

Correlations between Elemental Status and Indicators of Oxidative Metabolism in Residents of the Khanty-Mansi Autonomous Okrug with Its Poor-Quality Water Treatment

Introduction: Trace elements found in natural drinking water can play a key role in making up the chemical composition of the human body in the area of residence. Objective: To study the relationship between indicators characterizing the elemental status and oxidative metabolism of residents of the Khanty-Mansi Autonomous Okrug and poor-quality tap water treatment. Materials and methods: Hair concentrations of iron, manganese, calcium, magnesium, zinc, and selenium were established in 155 regional residents using atomic emission and inductively coupled plasma mass spectrometry. Contents of the products of lipid peroxidation (lipid hydroperoxide and thiobarbituric acid reactive substances) and antioxidant defense of the body (total antioxidant capacity and thiol status) were determined in blood serum using test kits. The oxidative stress index was calculated as lipid hydroperoxide × thiobarbituric acid reactive substances / total antioxidant capacity × thiol status. Results: The residents of the northern Russian cities notorious for poor-quality water treatment have elevated hair levels of Fe and Mn (p &lt; 0.001) and a decreased Se concentration (p = 0.012) combined with a statistically higher level of lipid hydroperoxides, thiobarbituric acid reactive substances, oxidative stress index (p &lt; 0.001), and a low level of antioxidant defense of the body (p &lt; 0.001–0.002). We established a direct correlation between selenium levels in hair and indicators of antioxidant defense status (r = +0,784 ... r = +0,531) and an inverse correlation with lipid peroxidation parameters (r = –0,679 ... r = –0,465). Accumulation of iron and manganese in the human body is closely related to activation of lipid peroxidation (r = +0,472 ... r = +0,413) and suppression of the antioxidant defense status (r = –0,521 ... r = –0,379). Conclusion: The observed relationships between the parameters of oxidative metabolism give evidence of a weakening of antioxidant protection and activation of lipid peroxidation in the population of the cities of the Khanty-Mansi Autonomous Okrug supplied with poor-quality tap water.

Comparative study of micropropagated plants of Grand Naine banana during in vitro regeneration and ex vitro acclimatization

An improved micropropagation protocol was established from field grown sword suckers of Banana Grand Naine (Musa acuminata AAA) by evaluating the mircopropagules combating reactive oxygen species (ROS) during acclimatization. Optimization of surface sterilization of sprouted apical meristematic buds and pre-culture on Shoot Bud Induction Medium [MS + 4.0 mg l −1 BA under dark conditions for 3 weeks] resulted ideal number of multiple shoot clusters (12.20 ± 0.30). Subculture of these shoot clusters on Shoot Bud Multiplication Medium (SBMM) fortified with 2 mg l −1 BA and 20 mg l −1 AdS induced highest shoot buds (15.00 ± 0.75) in 3 weeks and showed consistent till seven passages. The individual in vitro shoots upon transferring onto MS + 2 mg l −1 KN +1.0 mg l −1 IBA + activated charcoal (3 g l −1) resulted in elongated shoots and in vitro rooting after 3 weeks at a photoperiod of 16 h light and 8 h dark conditions. Evaluation of antioxidant defense status in micropropagated plantlets during acclimatization revealed altered levels of MDA, chlorophyll, catalase, ascorbate peroxidase and glutathione reductase. Our study throws an insight into decisive/differential role of cytokinins (Kinetin) in combating oxidative stress during acclimatization of in vitro regenerated plantlets. The present investigation facilitates the massive propagation (90% survival rate) of healthy and quality in vitro plantlets of banana.

Protective effect of Zataria multiflora Boiss against sodium nitrite-induced hepatotoxicity in rats.

Objective:Sodium nitrite (NaNO2) is used as a color stabilizer and antimicrobial agent in preservation of cured meat and fish. However, extensive use of this agent in the meat industries increased worries about its detrimental effects on human health. Zataria multiflora (Z. multiflora) is a well-known plant with therapeutic properties in the traditional medicine. Therefore, the present study was conducted to investigate the protective effect of this plant against sodium nitrite-induced hepatotoxicity.Materials and methods:Thirty-two male Wistar rats were divided into 4 groups: Control (without any treatment), nitrite (350 mg/kg by gavage for 60 days), NaNO2 plus Z. multiflora (rats treated with NaNO2 350 mg/kg gavage for 60 days and simultaneously received Z. multiflora extract at 200 mg/kg, ip) and Z. multiflora group (rats treated with Z. multiflora extract at 200 mg/kg, ip). At the end of the study, rats were euthanized and liver tissue samples were taken and studied under microscopy. Also, serum levels of liver function enzymes and antioxidant defense systems were measured. The results were analyzed using SPSS software and a p<0.0.5 was considered significant. Results:Results showed that NaNO2 induces liver injuries and altered hepatic histo-architecture. Also, NaNO2 significantly altered the biochemical profiles and antioxidant defense parameters of the liver. However, treatment with Z. multiflora improved tissue integrity as well as antioxidant defense status and biochemical conditions of the liver. Conclusion:Administration of Z. multiflora extract has beneficial effects on the NaNO2-induced histological and functional toxicity in the liver.

Антиоксидантный профиль ретроплацентарной крови при физиологической беременности и преэклампсии

The pathogenesis of pre-eclampsia (PE) is based on the disorders of placental circulation, which develop due to the impaired migration of extravillous trophoblast. Local processes at the maternal-fetal interface can be assessed through the retroplacental blood (RB) which flows during placental separation. Objective. To study the parameters of antioxidant status of RB in uncomplicated pregnancy and PE. Patients and methods. The study included 50 pregnant women: 36 women with uncomplicated pregnancy and 14 women with PE. Total antioxidant capacity (TAC) of plasma was measured by the luminol chemiluminescence method. Results. In uncomplicated pregnancy, total antioxidant capacity of RB was increased compared to peripheral blood (PB) (1236 ± 344 sec vs. 852 ± 246 sec; p &lt; 0.0001), which indicates that RB provides a balance of pro-oxidants and antioxidants at the maternal-placental-fetal interface. The increase in total antioxidant capacity of RB plasma in PE compared to uncomplicated pregnancy (1716 ± 922 sec vs. 1236 ± 344 sec; p = 0.007) may be both compensatory and pathogenetic mechanisms of the disease. Thus, the prevention and treatment of PE with antioxidants should be discussed. The increase in total antioxidant capacity of RB plasma was observed in severe PE (2304 ± 948 sec vs. 1236 ± 344 sec, p &lt; 0.0001), which is associated with an unfavorable prognosis. Conclusion. Our pilot study of the antioxidant defense status of retroplacental blood shows that pre-eclampsia leads to a significant imbalance between pro-oxidants and antioxidants at the maternal-placental-fetal interface. Key words: antioxidants, antioxidant capacity, pre-eclampsia, retroplacental blood, chemiluminescence

Impaired Antioxidant Defence Status Is Associated With Metabolic-Inflammatory Risk Factors in Preterm Children With Extrauterine Growth Restriction: The BIORICA Cohort Study.

Introduction: An impaired antioxidant status has been described during foetal growth restriction (FGR). Similarly, the antioxidant defence system can be compromised in preterm children with extrauterine growth restriction (EUGR). The aim of this prospective study was to evaluate the antioxidant status in prepubertal children with a history of prematurity without FGR, with and without EUGR, compared to a healthy group.Methods: In total, 211 children were recruited and classified into three groups: 38 with a history of prematurity and EUGR; 50 with a history of prematurity and adequate extrauterine growth (AEUG); and 123 control children born at term. Catalase (CAT), superoxide dismutase (SOD), glutathione peroxidase (GPx) and glutathione reductase (GR) activities were assessed in lysed erythrocytes with spectrophotometric methods. Plasma levels of the antioxidants α-tocopherol, retinol and β-carotene were determined through solvent extraction and ultra-high-pressure liquid chromatography coupled to mass spectrometry.Results: Children with the antecedent of EUGR and prematurity had lower CAT activity than the other two groups and lower GPx activity than the control children. Lower SOD, GPx and GR activities were observed in the AEUG group compared to the controls. However, higher concentrations of α-tocopherol and β-carotene were found in the EUGR group compared to the other groups; retinol levels were also higher in EUGR than in AEUG children. In EUGR and AEUG children, enzymatic antioxidant activities and plasma antioxidants were associated with metabolic syndrome components and pro-inflammatory biomarkers.Conclusions: This study reveals, for the first time, that the EUGR condition and prematurity appear to be linked to an impairment of the antioxidant defence status, which might condition an increased risk of adverse metabolic outcomes later in life.

Fructose Induces Visceral Adipose Tissue Inflammation and Insulin Resistance Even Without Development of Obesity in Adult Female but Not in Male Rats.

Introduction: Obesity and related metabolic disturbances are frequently related to modern lifestyle and are characterized by excessive fructose intake. Visceral adipose tissue (VAT) inflammation has a central role in the development of insulin resistance, type 2 diabetes (T2D), and metabolic syndrome. Since sex-related differences in susceptibility and progression of metabolic disorders are not yet fully understood, our aim was to examine inflammation and insulin signaling in VAT of fructose-fed female and male adult rats.Methods: We analyzed effects of 9-week 10% fructose-enriched diet on energy intake, VAT mass and histology, and systemic insulin sensitivity. VAT insulin signaling and markers of VAT inflammation, and antioxidative defense status were also evaluated.Results: The fructose diet had no effect on VAT mass and systemic insulin signaling in the female and male rats, while it raised plasma uric acid, increased PPARγ level in the VAT, and initiated the development of a distinctive population of small adipocytes in the females. Also, adipose tissue insulin resistance, evidenced by increased PTP1B and insulin receptor substrate 1 (IRS1) inhibitory phosphorylation and decreased Akt activity, was detected. In addition, fructose stimulated the nuclear accumulation of NFκB, increased expression of proinflammatory cytokines (IL-1β, IL-6, and TNFα), and protein level of macrophage marker F4/80, superoxide dismutase 1, and glutathione reductase. In contrast to the females, the fructose diet had no effect on plasma uric acid and VAT inflammation in the male rats, but less prominent alterations in VAT insulin signaling were observed.Conclusion: Even though dietary fructose did not elicit changes in energy intake and led to obesity in the females, it initiated the proliferation of small-sized adipocytes capable of storing fats further. In contrast to the males, this state of VAT was accompanied with enhanced inflammation, which most likely contributed to the development of insulin resistance. The observed distinction could possibly originate from sex-related differences in uric acid metabolism. Our results suggest that VAT inflammation could precede obesity and start even before the measurable increase in VAT mass, making it a silent risk factor for the development of T2D. Our results emphasize that adipose tissue dysfunction, rather than its simple enlargement, could significantly contribute to the onset and development of obesity and related metabolic disorders.

Mitoquinol mesylate (MITOQ) attenuates diethyl nitrosamine-induced hepatocellular carcinoma through modulation of mitochondrial antioxidant defense systems.

Diethyl nitrosamine (DEN) induced cirrhosis-hepatocellular carcinoma (HCC) model associates cancer progression with oxidative stress and mitochondrial dysfunction. This study investigated the effects of mitoquinol mesylate (MitoQ), a mitochondrial-targeted antioxidant on DEN-induced oxidative damage in HCC Wistar rats. Fifty male Wistar rats were randomly divided into five groups. Healthy control, DEN, and MitoQ groups were orally administered exactly 10mg/kgof distilled water, DEN, and MitoQ, respectively for 16weeks. Animals in the MitoQ + DEN group were pre-treated with MitoQ for a week followed by co-administration of 10mg/kg each of MitoQ and DEN. DEN + MitoQ group received DEN for 8weeks, then co-administration of 10mg/kg each of DEN and MitoQ till the end of 16th week. Survival index, tumour incidence, hematological profile, liver function indices, lipid profile, mitochondrial membrane composition, mitochondrial respiratory enzymes, and antioxidant defense status in both mitochondrial and post-mitochondrial fractions plus expression of antioxidant genes were assessed. In MitoQ + DEN and DEN + MitoQ groups, 80% survival occurred while tumour incidence decreased by 60% and 40% respectively, compared to the DEN-only treated group. Similarly, MitoQ-administered groups showed a significant (p<0.05) decrease in the activities of liver function enzymes while hemoglobin concentration, red blood cell count, and packed cell volume were significantly elevated compared to the DEN-only treated group. Administration of MitoQ to the DEN-intoxicated groups successfully enhanced the activities of mitochondrial F1F0-ATPase and succinate dehydrogenase; and up-regulated the expression and activities of SOD2, CAT, and GPx1. Macroscopic and microscopic features indicated a reversal of DEN-induced hepatocellular degeneration in the MitoQ + DEN and DEN + MitoQ groups. These data revealed that MitoQ intervention attenuated DEN-induced oxidative stress through modulation of mitochondrial antioxidant defense systems and alleviated the burden of HCC as a chemotherapeutic agent.

Impact of CuO nanoparticles on maize: Comparison with CuO bulk particles with special reference to oxidative stress damages and antioxidant defense status

The present study aimed to systematically investigate the particle size effects of copper (II) oxide [CuO nanoparticles (<50 nm) and CuO bulk particles (<10 μm)] on maize (Zea mays L.). Bioaccumulation of Cu, in vivo ROS generation, membrane damage, transcriptional modulation of antioxidant genes, cellular redox status of glutathione and ascorbate pool, expression patterns of COPPER TRANSPORTER 4 and stress responsive miRNAs (miR398a, miR171b, miR159f-3p) with their targets were investigated for better understanding of the underlying mechanisms and the extent of CuO nanoparticles and CuO bulk particles induced oxidative stress damages. More restricted seedling growth, comparatively higher membrane injury, marked decline in the levels of chlorophylls and carotenoids and severe oxidative burst were evident in CuO bulk particles challenged leaves. Dihydroethidium and CM-H2DCFDA staining further supported elevated reactive oxygen species generation in CuO bulk particles stressed roots. CuO bulk particles exposed seedlings accumulated much higher amount of Cu in roots as compared to CuO nanoparticles stressed plants with low root-to-shoot Cu translocation. Moderately high GR expression with maintenance of a steady GSH-GSSG ratio in CuO nanoparticles challenged leaves might be accountable for their rather improved performance under stressed condition. miR171b-mediated enhanced expression of SCARECROW 6 might participate in the marked decline of chlorophyll content in CuO bulk particles exposed leaves. Ineffective recycling of AsA pool is another decisive feature of inadequate performance of CuO bulk particles stressed seedlings in combating oxidative stress damages. Taken together, our findings revealed that toxicity of CuO bulk particles was higher than CuO nanoparticles and the adverse effects of CuO bulk particles on maize seedlings might be due to higher Cu ions dissolution.