Oxidative Medicine and Cellular Longevity http://www.hindawi.com The latest articles from Hindawi Publishing Corporation © 2015 , Hindawi Publishing Corporation . All rights reserved. Xanthine Oxidoreductase Reference Values in Platelet-Poor Plasma and Platelets in Healthy Volunteers Tue, 20 Jan 2015 08:48:19 +0000 http://www.hindawi.com/journals/omcl/2015/341926/ Introduction. Xanthine oxidoreductase (XOR) is an enzyme belonging to the class of hydroxylases. XOR is stated, inter alia, in the kidneys, liver, and small intestine as well as in leukocytes and platelets and endothelial cells of capillaries. Its main role is to participate in the conversion of hypoxanthine to xanthine and the uric acid. It occurs in two isoforms: dehydrogenase (XD) and oxidase (XO), which is considered one of the sources of reactive oxygen species. Aim of the Study. Determination of reference values of xanthine oxidoreductase activity in PPP and platelets. Materials and Methods. Study group consisted of 70 healthy volunteers. The isoform activities of xanthine oxidoreductase were determined by kinetic spectrophotometry. Results. A statistically significant difference between the activity of the XOR in PPP and platelets (). The highest activity of XO was found in both PPP and blood platelets. Significant differences between the activity of the various isoforms in PPP () and platelets () were also found. Conclusions. The healthy volunteers showed the highest activity XO (prooxidant) and the lowest XD (antioxidant), which indicates a slight oxidative stress and confirmed physiological effects of XOR. Elżbieta Cecerska-Heryć, Anna Jesionowska, Szupiluk Klaudyna, Siewierska Katarzyna, Mączka Dominika, Pawlak Dominika, Urbańska Marta, and Barbara Dołęgowska Copyright © 2015 Elżbieta Cecerska-Heryć et al. All rights reserved. Naphthoquinone Derivative PPE8 Induces Endoplasmic Reticulum Stress in p53 Null H1299 Cells Sun, 18 Jan 2015 14:22:57 +0000 http://www.hindawi.com/journals/omcl/2015/453679/ Endoplasmic reticulum (ER) plays a key role in synthesizing secretory proteins and sensing signal function in eukaryotic cells. Responding to calcium disturbance, oxidation state change, or pharmacological agents, ER transmembrane protein, inositol-regulating enzyme 1 (IRE1), senses the stress and triggers downstream signals. Glucose-regulated protein 78 (GRP78) dissociates from IRE1 to assist protein folding and guard against cell death. In prolonged ER stress, IRE1 recruits and activates apoptosis signal-regulating kinase 1 (ASK1) as well as downstream JNK for cell death. Naphthoquinones are widespread natural phenolic compounds. Vitamin K3, a derivative of naphthoquinone, inhibits variant tumor cell growth via oxygen uptake and oxygen stress. We synthesized a novel naphthoquinone derivative PPE8 and evaluated capacity to induce ER stress in p53 null H1299 and p53 wild-type A549 cells. In H1299 cells, PPE8 induced ER enlargement, GRP78 expression, and transient IER1 activation. Activated IRE1 recruited ASK1 for downstream JNK phosphorylation. IRE1 knockdown by siRNA attenuated PPE8-induced JNK phosphorylation and cytotoxicity. Prolonged JNK phosphorylation may be involved in PPE8-induced cytotoxicity. Such results did not arise in A549 cells, but p53 knockdown by siRNA restored PPE8-induced GRP78 expression and JNK phosphorylation. We offer a novel compound to induce ER stress and cytotoxicity in p53-deficient cancer cells, presenting an opportunity for treatment. Jin-Cherng Lien, Chien-Chun Huang, Te-Jung Lu, Chih-Hsiang Tseng, Ping-Jyun Sung, Hong-Zin Lee, Bo-Ying Bao, Yueh-Hsiung Kuo, and Te-Ling Lu Copyright © 2015 Jin-Cherng Lien et al. All rights reserved. The Synergistic Effects of Heat Shock Protein 70 and Ginsenoside Rg1 against Tert-Butyl Hydroperoxide Damage Model In Vitro Thu, 15 Jan 2015 11:13:39 +0000 http://www.hindawi.com/journals/omcl/2015/437127/ Neural stem cells (NSCs) transplanted is one of the hottest research to treat Alzheimer’s disease (AD), but cholinergic neurons from stem cells were also susceptible to cell death which Heat shock protein 70 (HSP70) was affirmed to reverse. Related to cognitive impairment, cholinergic nervous cells should be investigated and ginsenoside Rg1 (G-Rg1) was considered to increase them. We chose tert-butyl hydroperoxide (t-BHP) damage model to study in vitro. Functional properties of our recombination plasmid pEGFP-C2-HSP70 were affirmed by SH-SY5Y cells. To opposite the transitory appearance of HSP70, NSCs used as the vectors of HSP70 gene overexpressed HSP70 for at least 7 days in vitro. After transfection for 3 days, G-Rg1 pretreatment for 4 hours, and coculture for 3 days, the expression of acetylcholinesterase (ChAT), synaptophysin, and the ratio of NeuN and GFAP were assessed by western blot; Morphological properties were detected by 3D reconstruction and immunofluorescence. ChAT was markedly improved in the groups contained G-Rg1. In coculture system, the ratio of neurons/astrocytes and the filaments of neurons were increased; apoptosis cells were decreased, compared to monotherapy (). In conclusion, we demonstrated that, as a safe cotreatment affirmed in vitro, overexpression of HSP70 in NSCs plus G-Rg1 promoted nervous cells regeneration from chronic oxidative damage. Dan Lu, Anding Xu, Hongcheng Mai, Jiayi Zhao, Chanjuan Zhang, Renbin Qi, Huadong Wang, Daxiang Lu, and Lihong Zhu Copyright © 2015 Dan Lu et al. All rights reserved. Neuroprotective Effect of Dexmedetomidine on Hyperoxia-Induced Toxicity in the Neonatal Rat Brain Tue, 13 Jan 2015 09:56:19 +0000 http://www.hindawi.com/journals/omcl/2015/530371/ Dexmedetomidine is a highly selective agonist of α2-receptors with sedative, anxiolytic, analgesic, and anesthetic properties. Neuroprotective effects of dexmedetomidine have been reported in various brain injury models. In the present study, we investigated the effects of dexmedetomidine on neurodegeneration, oxidative stress markers, and inflammation following the induction of hyperoxia in neonatal rats. Six-day-old Wistar rats received different concentrations of dexmedetomidine (1, 5, or 10 µg/kg bodyweight) and were exposed to 80% oxygen for 24 h. Sex-matched littermates kept in room air and injected with normal saline or dexmedetomidine served as controls. Dexmedetomidine pretreatment significantly reduced hyperoxia-induced neurodegeneration in different brain regions of the neonatal rat. In addition, dexmedetomidine restored the reduced/oxidized glutathione ratio and attenuated the levels of malondialdehyde, a marker of lipid peroxidation, after exposure to high oxygen concentration. Moreover, administration of dexmedetomidine induced downregulation of IL-1β on mRNA and protein level in the developing rat brain. Dexmedetomidine provides protections against toxic oxygen induced neonatal brain injury which is likely associated with oxidative stress signaling and inflammatory cytokines. Our results suggest that dexmedetomidine may have a therapeutic potential since oxygen administration to neonates is sometimes inevitable. Marco Sifringer, Clarissa von Haefen, Maria Krain, Nadine Paeschke, Ivo Bendix, Christoph Bührer, Claudia D. Spies, and Stefanie Endesfelder Copyright © 2015 Marco Sifringer et al. All rights reserved. Sesquiterpene Lactones Inhibit Advanced Oxidation Protein Product-Induced MCP-1 Expression in Podocytes via an IKK/NF-κB-Dependent Mechanism Mon, 12 Jan 2015 14:00:58 +0000 http://www.hindawi.com/journals/omcl/2015/934058/ Inflammation is a relevant factor in the pathogenesis of diabetes nephropathy (DN). Sesquiterpene lactones (SLs), originally isolated from Tanacetum parthenium, have been reported to exhibit anti-inflammatory effects but few studies have examined their effects on DN. To determine whether advanced oxidation protein products (AOPPs) can induce the expression of chemokine monocyte chemoattractant protein- (MCP-) 1 in cultured mouse podocytes and to explore the mechanisms of the potential renoprotection of SLs, we treated podocytes with AOPPs and SLs (parthenolide and its derivatives micheliolide, compound 1, and compound 2). MCP-1 mRNA and protein expression were tested using quantitative real-time PCR and ELISA, respectively, and the protein levels of IKKβ, phospho-IKKβ, IκBα, NF-κB p65, phospho-NF-κB p65, and tubulin were analyzed by Western blotting. AOPPs activated the expression of MCP-1 mRNA and protein in a dose- and time-dependent manner, activated IKKβ and NF-κB p65, and promoted IκBα degradation. The IKK/NF-κB inhibitor parthenolide decreased AOPP-induced MCP-1 expression. Pretreatment with SLs inhibited MCP-1 mRNA and protein expression and suppressed IKKβ and NF-κB p65 phosphorylation and IκBα degradation. Taken together, these findings provide a novel explanation for the anti-inflammatory effects of SLs that will ultimately benefit DN and potentially other inflammatory and immune renal diseases. Yan Zhao, Si-jia Chen, Jian-cheng Wang, Hong-xin Niu, Qian-qian Jia, Xiao-wen Chen, Xiao-yan Du, Lu Lu, Bo Huang, Quan Zhang, Yue Chen, and Hai-bo Long Copyright © 2015 Yan Zhao et al. All rights reserved. The Role of Flavonoids on Oxidative Stress in Epilepsy Sun, 11 Jan 2015 11:50:00 +0000 http://www.hindawi.com/journals/omcl/2015/171756/ Backgrounds. Oxidative stress can result from excessive free-radical production and it is likely implicated as a possible mechanism involved in the initiation and progression of epileptogenesis. Flavonoids can protect the brain from oxidative stress. In the central nervous system (CNS) several flavonoids bind to the benzodiazepine site on the GAB-receptor resulting in anticonvulsive effects. Objective. This review provides an overview about the role of flavonoids in oxidative stress in epilepsy. The mechanism of action of flavonoids and its relation to the chemical structure is also discussed. Results/Conclusions. There is evidence that suggests that flavonoids have potential for neuroprotection in epilepsy. Tâmara Coimbra Diniz, Juliane Cabral Silva, Sarah Raquel Gomes de Lima-Saraiva, Fernanda Pires Rodrigues de Almeida Ribeiro, Alessandra Gomes Marques Pacheco, Rivelilson Mendes de Freitas, Lucindo José Quintans-Júnior, Jullyana de Souza Siqueira Quintans, Rosemairy Luciane Mendes, and Jackson Roberto Guedes da Silva Almeida Copyright © 2015 Tâmara Coimbra Diniz et al. All rights reserved. New Antioxidant Drugs for Neonatal Brain Injury Mon, 05 Jan 2015 09:31:39 +0000 http://www.hindawi.com/journals/omcl/2015/108251/ The brain injury concept covers a lot of heterogeneity in terms of aetiology involving multiple factors, genetic, hemodynamic, metabolic, nutritional, endocrinological, toxic, and infectious mechanisms, acting in antenatal or postnatal period. Increased vulnerability of the immature brain to oxidative stress is documented because of the limited capacity of antioxidant enzymes and the high free radicals (FRs) generation in rapidly growing tissue. FRs impair transmembrane enzyme Na+/K+-ATPase activity resulting in persistent membrane depolarization and excessive release of FR and excitatory aminoacid glutamate. Besides being neurotoxic, glutamate is also toxic to oligodendroglia, via FR effects. Neuronal cells die of oxidative stress. Excess of free iron and deficient iron/binding metabolising capacity are additional features favouring oxidative stress in newborn. Each step in the oxidative injury cascade has become a potential target for neuroprotective intervention. The administration of antioxidants for suspected or proven brain injury is still not accepted for clinical use due to uncertain beneficial effects when treatments are started after resuscitation of an asphyxiated newborn. The challenge for the future is the early identification of high-risk babies to target a safe and not toxic antioxidant therapy in combination with standard therapies to prevent brain injury and long-term neurodevelopmental impairment. Maria Luisa Tataranno, Serafina Perrone, Mariangela Longini, and Giuseppe Buonocore Copyright © 2015 Maria Luisa Tataranno et al. All rights reserved. Antioxidant Activity, Antitumor Effect, and Antiaging Property of Proanthocyanidins Extracted from Kunlun Chrysanthemum Flowers Thu, 01 Jan 2015 11:07:23 +0000 http://www.hindawi.com/journals/omcl/2015/983484/ The objective of the present study was to evaluate the antioxidant activity, antitumor effect, and antiaging property of proanthocyanidins from Kunlun Chrysanthemum flowers (PKCF) grown in Xinjiang. In vitro antioxidant experiments results showed that the total antioxidant activity and the scavenging capacity of hydroxyl radicals (•OH) and 1,1-diphenyl-2-picrylhydrazyl (DPPH•) radicals increased in a concentration-dependent manner and were stronger than those of vitamin C. To investigate the antioxidant activity of PKCF in vivo, we used serum, liver, and kidney from mouse for the measurement of superoxide dismutase (SOD), malondialdehyde (MDA), and total antioxidant capacity (T-AOC). Results indicated that PKCF had antioxidative effect in vivo which significantly improved the activity of SOD and T-AOC and decreased MDA content. To investigate the antitumor activity of PKCF, we used H22 cells, HeLa cells, and Eca-109 cells with Vero cells as control. Inhibition ratio and IC50 values were measured by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay; PKCF showed great inhibitory activity on H22 cells and HeLa cells. We also used fruit flies as a model for analyzing the anti-aging property of PKCF. Results showed that PKCF has antiaging effect on Drosophila. Results of the present study demonstrated that PKCF could be a promising agent that may find applications in health care, medicine, and cosmetics. Siqun Jing, Xiaoming Zhang, and Liang-Jun Yan Copyright © 2015 Siqun Jing et al. All rights reserved. The Combined Extract of Purple Waxy Corn and Ginger Prevents Cataractogenesis and Retinopathy in Streptozotocin-Diabetic Rats Wed, 31 Dec 2014 11:29:04 +0000 http://www.hindawi.com/journals/omcl/2014/789406/ Based on the crucial roles of oxidative stress and aldose reductase on diabetic complications and the protective effect against diabetic eye complication of purple waxy corn and ginger (PWCG) together with the synergistic effect concept, we aimed to determine anticataract and antiretinopathy effects of the combined extract of purple waxy corn and ginger (PWCG). The streptozotocin diabetics with the blood glucose levels >250 mg·dL−1 were orally given the extract at doses of 50, 100, and 200 mg/kg·BW−1 for 10 weeks. Then, lens opacity and histopathology of retina were determined. The changes of MDA together with the activities of SOD, CAT, GPx, and AR in lens were also determined using biochemical assays. All doses of PWCG decreased lens opacity, MDA, and AR in the lens of diabetic rats. The elevation of CAT and GPx activities was also observed. The antiretinopathy property of the combined extract was also confirmed by the increased number of neurons in ganglion cell layer and thickness of total retina and retinal nuclear layer in diabetic rats. PWCG is the potential functional food to protect against diabetic cataract and retinopathy. However, further studies concerning toxicity and clinical trial are still essential. Paphaphat Thiraphatthanavong, Jintanaporn Wattanathorn, Supaporn Muchimapura, Wipawee Thukham-mee, Kamol Lertrat, and Bhalang Suriharn Copyright © 2014 Paphaphat Thiraphatthanavong et al. All rights reserved. Stresses, Aging, and Age-Related Disorders Tue, 30 Dec 2014 10:01:02 +0000 http://www.hindawi.com/journals/omcl/2014/320564/ Xiaotao Li, Robb E. Moses, Jianping Jin, Weiguo Cao, and Carlos Caulin Copyright © 2014 Xiaotao Li et al. All rights reserved. SIRT1 Functions as an Important Regulator of Estrogen-Mediated Cardiomyocyte Protection in Angiotensin II-Induced Heart Hypertrophy Mon, 29 Dec 2014 12:27:01 +0000 http://www.hindawi.com/journals/omcl/2014/713894/ Background. Sirtuin 1 (SIRT1) is a member of the sirtuin family, which could activate cell survival machinery and has been shown to be protective in regulation of heart function. Here, we determined the mechanism by which SIRT1 regulates Angiotensin II- (AngII-) induced cardiac hypertrophy and injury in vivo and in vitro. Methods. We analyzed SIRT1 expression in the hearts of control and AngII-induced mouse hypertrophy. Female C57BL/6 mice were ovariectomized and pretreated with 17β-estradiol to measure SIRT1 expression. Protein synthesis, cardiomyocyte surface area analysis, qRT-PCR, TUNEL staining, and Western blot were performed on AngII-induced mouse heart hypertrophy samples and cultured neonatal rat ventricular myocytes (NRVMs) to investigate the function of SIRT1. Results. SIRT1 expression was slightly upregulated in AngII-induced mouse heart hypertrophy in vivo and in vitro, accompanied by elevated cardiomyocyte apoptosis. SIRT1 overexpression relieves AngII-induced cardiomyocyte hypertrophy and apoptosis. 17β-Estradiol was able to protect cardiomyocytes from AngII-induced injury with a profound upregulation of SIRT1 and activation of AMPK. Moreover, estrogen receptor inhibitor ICI 182,780 and SIRT1 inhibitor niacinamide could block SIRT1’s protective effect. Conclusions. These results indicate that SIRT1 functions as an important regulator of estrogen-mediated cardiomyocyte protection during AngII-induced heart hypertrophy and injury. Tao Shen, Ling Ding, Yang Ruan, Weiwei Qin, Yajun Lin, Chao Xi, Yonggang Lu, Lin Dou, Yuping Zhu, Yuan Cao, Yong Man, Yunfei Bian, Shu Wang, Chuanshi Xiao, and Jian Li Copyright © 2014 Tao Shen et al. All rights reserved. Oxidative Stress Associated with Neuronal Apoptosis in Experimental Models of Epilepsy Mon, 29 Dec 2014 09:19:52 +0000 http://www.hindawi.com/journals/omcl/2014/293689/ Epilepsy is considered one of the most common neurological disorders worldwide. Oxidative stress produced by free radicals may play a role in the initiation and progression of epilepsy; the changes in the mitochondrial and the oxidative stress state can lead mechanism associated with neuronal death pathway. Bioenergetics state failure and impaired mitochondrial function include excessive free radical production with impaired synthesis of antioxidants. This review summarizes evidence that suggest what is the role of oxidative stress on induction of apoptosis in experimental models of epilepsy. Marisela Méndez-Armenta, Concepción Nava-Ruíz, Daniel Juárez-Rebollar, Erika Rodríguez-Martínez, and Petra Yescas Gómez Copyright © 2014 Marisela Méndez-Armenta et al. All rights reserved. Correlation between Serum RANTES Levels and the Severity of Parkinson’s Disease Mon, 22 Dec 2014 08:16:17 +0000 http://www.hindawi.com/journals/omcl/2014/208408/ Inflammatory mediators may reflect a role of systemic inflammation in the neurodegenerative process of Parkinson’s disease (PD). Interleukin-6 (IL-6) and chemokine ligand 5 (CCL5), also known as RANTES (regulated on activation, normal T cell expressed and secreted), have been implicated in neurodegenerative diseases including PD. Serum levels of RANTES and IL-6 of 78 consecutive PD patients and age-matched 80 controls were measured. Patients with PD had higher RANTES and IL-6 levels compared with the controls. We found that serum RANTES levels strongly correlated with Hoehn-Yahr score and disease duration in PD patients. This study indicated that patients with PD have an on-going systemic inflammatory profile where the elevated peripheral production of RANTES may play a role in the neurodegenerative process. Peng Tang, Li Chong, Xiaoqing Li, Yue Liu, Peng Liu, Chen Hou, and Rui Li Copyright © 2014 Peng Tang et al. All rights reserved. Free Radicals in Adolescent Varicocele Testis Sun, 14 Dec 2014 11:19:29 +0000 http://www.hindawi.com/journals/omcl/2014/912878/ We examine the relationship between the structure and function of the testis and the oxidative and nitrosative stress, determined by an excessive production of free radicals and/or decreased availability of antioxidant defenses, which occur in the testis of adolescents affected by varicocele. Moreover, the effects of surgical treatment on oxidative stress were provided. We conducted a PubMed and Medline search between 1980 and 2014 using “adolescent,” “varicocele,” “free radicals,” “oxidative and nitrosative stress,” “testis,” and “seminiferous tubules” as keywords. Cross-references were checked in each of the studies, and relevant articles were retrieved. We conclude that increased concentration of free radicals, generated by conditions of hypoxia, hyperthermia, and hormonal dysfunction observed in adolescent affected by varicocele, can harm germ cells directly or indirectly by influencing nonspermatogenic cells and basal lamina. With regard to few available data in current literature, further clinical trials on the pre- and postoperative ROS and RNS levels together with morphological studies of the cellular component of the testis are fundamental for complete comprehension of the role played by free radicals in the pathogenesis of adolescent varicocele and could justify its pharmacological treatment with antioxidants. Carmelo Romeo and Giuseppe Santoro Copyright © 2014 Carmelo Romeo and Giuseppe Santoro. All rights reserved. Cucurbitacin E Has Neuroprotective Properties and Autophagic Modulating Activities on Dopaminergic Neurons Tue, 09 Dec 2014 12:11:17 +0000 http://www.hindawi.com/journals/omcl/2014/425496/ Natural molecules are under intensive study for their potential as preventive and/or adjuvant therapies for neurodegenerative disorders such as Parkinson’s disease (PD). We evaluated the neuroprotective potential of cucurbitacin E (CuE), a tetracyclic triterpenoid phytosterol extracted from the Ecballium elaterium (Cucurbitaceae), using a known cellular model of PD, NGF-differentiated PC12. In our postmitotic experimental paradigm, neuronal cells were treated with the parkinsonian toxin 1-methyl-4-phenylpyridinium (MPP+) to provoke significant cellular damage and apoptosis or with the potent N,N-diethyldithiocarbamate (DDC) to induce superoxide () production, and CuE was administered prior to and during the neurotoxic treatment. We measured cellular death and reactive oxygen species to evaluate the antioxidant and antiapoptotic properties of CuE. In addition, we analyzed cellular macroautophagy, a bulk degradation process involving the lysosomal pathway. CuE showed neuroprotective effects on MPP+-induced cell death. However, CuE failed to rescue neuronal cells from oxidative stress induced by MPP+ or DDC. Microscopy and western blot data show an intriguing involvement of CuE in maintaining lysosomal distribution and decreasing autophagy flux. Altogether, these data indicate that CuE decreases neuronal death and autophagic flux in a postmitotic cellular model of PD. Anne-Marie Arel-Dubeau, Fanny Longpré, Julie Bournival, Cindy Tremblay, Julie Demers-Lamarche, Pavlina Haskova, Everaldo Attard, Marc Germain, and Maria-Grazia Martinoli Copyright © 2014 Anne-Marie Arel-Dubeau et al. All rights reserved. Relevance of the Glutathione System in Temporal Lobe Epilepsy: Evidence in Human and Experimental Models Sun, 30 Nov 2014 00:10:26 +0000 http://www.hindawi.com/journals/omcl/2014/759293/ Oxidative stress, which is a state of imbalance in the production of reactive oxygen species and nitrogen, is induced by a wide variety of factors. This biochemical state is associated with diseases that are systemic as well as diseases that affect the central nervous system. Epilepsy is a chronic neurological disorder, and temporal lobe epilepsy represents an estimated 40% of all epilepsy cases. Currently, evidence from human and experimental models supports the involvement of oxidative stress during seizures and in the epileptogenesis process. Hence, the aim of this review was to provide information that facilitates the processing of this evidence and investigate the therapeutic impact of the biochemical status for this specific pathology. Noemí Cárdenas-Rodríguez, Elvia Coballase-Urrutia, Claudia Pérez-Cruz, Hortencia Montesinos-Correa, Liliana Rivera-Espinosa, Aristides Sampieri III, and Liliana Carmona-Aparicio Copyright © 2014 Noemí Cárdenas-Rodríguez et al. All rights reserved. Dietary Blueberry and Bifidobacteria Attenuate Nonalcoholic Fatty Liver Disease in Rats by Affecting SIRT1-Mediated Signaling Pathway Thu, 27 Nov 2014 06:26:56 +0000 http://www.hindawi.com/journals/omcl/2014/469059/ NAFLD model rats were established and divided into NAFLD model (MG group), SIRT1 RNAi (SI group), blueberry juice (BJ group), blueberry juice + bifidobacteria (BJB group), blueberry juice + SIRT1 RNAi (BJSI group), and blueberry juice + bifidobacteria + SIRT1 RNAi groups (BJBSI group). A group with normal rats was a control group (CG). BJB group ameliorated NAFLD, which was better than BJ group (). The lipid accumulation was lower in CG, BJ, and BJB groups than that in MG, SI, BJSI, and BJBSI groups (). The levels of SIRT1 and PPAR-α were higher in CG, BJ, and BJB groups than those in MG, SI, BJSI, and BJBSI groups (). The levels of SREBP-1c were lower in CG, BJ, and BJB groups than those in MG, SI, BJSI, and BJBSI groups (). The biochemical indexes SOD, GSH, and HDL-c were improved from CG to BJB group (). Inversely, the levels of AST and ALT, TG, TC, LDL-c, and MDA were decreased from CG to BJB group (). These changes enhance antioxidative capability and biochemical index of rats. Blueberry juice and bifidobacteria improve NAFLD by activating SIRTI-mediating signaling pathway. Tingting Ren, Chao Huang, and Mingliang Cheng Copyright © 2014 Tingting Ren et al. All rights reserved. Antioxidant Function of Steen Solution Sun, 23 Nov 2014 00:00:00 +0000 http://www.hindawi.com/journals/omcl/2014/578353/ Mohamed S. A. Mohamed Copyright © 2014 Mohamed S. A. Mohamed. All rights reserved. Protective Effects of Gelam Honey against Oxidative Damage in Young and Aged Rats Wed, 19 Nov 2014 14:04:31 +0000 http://www.hindawi.com/journals/omcl/2014/673628/ Aging is characterized by progressive decline in physiological and body function due to increase in oxidative damage. Gelam honey has been accounted to have high phenolic and nonphenolic content to attenuate oxidative damage. This study was to determine the effect of local gelam honey on oxidative damage of aged rats. Twenty-four male Spraque-Dawley rats were divided into young (2 months) and aged (19 months) groups. Each group was further divided into control (fed with plain water) and supplemented with 2.5 mg/kg body weight of gelam honey for 8 months. DNA damage level was determined by comet assay and plasma malondialdehyde (MDA) by high performance liquid chromatography (HPLC). The activity of blood and cardiac antioxidant enzymes was determined by spectrophotometer. The DNA damage and MDA level were reduced in both gelam honey supplemented groups. Gelam honey increases erythrocytes CAT and cardiac SOD activities in young and cardiac CAT activity in young and aged groups. The DNA damage was increased in the aged group compared to young group, but reduced at the end of the study. The decline of oxidative damage in rats supplemented with gelam honey might be through the modulation of antioxidant enzyme activities. Zulaikha Sahhugi, Siti Maisarah Hasenan, and Zakiah Jubri Copyright © 2014 Zulaikha Sahhugi et al. All rights reserved. Evaluation of Neonatal Streptozotocin Induced Diabetic Rat Model for the Development of Cataract Wed, 19 Nov 2014 08:19:07 +0000 http://www.hindawi.com/journals/omcl/2014/463264/ Type 2 diabetes (T2D) generally follows prediabetes (PD) conditions such as impaired fasting glucose (IFG) and/or impaired glucose tolerance (IGT). Although studies reported an association of IGT or IFG with cataract, the experimental basis for PD associated cataract is not known. Hence, we evaluated neonatal streptozotocin (nSTZ) induced rat model to study PD associated cataractogenesis by injecting STZ to two-day old rats. While majority (70%) of nSTZ injected pups developed IGT (nSTZ-PD) by two months but not cataract even after seven months, remaining (30%) nSTZ rats developed hyperglycemia (nSTZ-D) by two months and mature cataract by seven months. Lens biochemical analysis indicated increased oxidative stress as indicated by increased SOD activity, lipid peroxidation, and protein carbonyl levels in nSTZ-D cataractous lens. There was also increased polyol pathway as assessed by aldose reductase activity and sorbitol levels. Though nSTZ-PD animals have not shown any signs of lenticular opacity, insolubilization of proteins along with enhanced polyol pathway was observed in the lens. Further there was increased oxidative stress in lens of IGT animals. These results suggest that oxidative stress along with increased polyol pathway might play a role in IGT-associated lens abnormalities. In conclusion, nSTZ-PD rat model could aid to investigate IGT-associated lens abnormalities. Madhoosudan A. Patil, Palla Suryanarayana, Uday Kumar Putcha, Myadara Srinivas, and G. Bhanuprakash Reddy Copyright © 2014 Madhoosudan A. Patil et al. All rights reserved. Association between Paraoxonases Gene Expression and Oxidative Stress in Hepatotoxicity Induced by CCl4 Mon, 17 Nov 2014 00:00:00 +0000 http://www.hindawi.com/journals/omcl/2014/893212/ Objectives. The purpose of the study is to evaluate the hepatoprotective effect of rutin in carbon tetrachloride- (CCl4-) induced liver injuries in rat model. Methods. Forty male Wistar albino rats were divided into four groups. Group I was the control group and received dimethyl sulphoxide (DMSO) and olive oil. Group II received rutin. Groups III was treated with CCl4. Group IV was administered rutin after 48 h of CCl4 treatment. Liver enzymes level, lipid profile, lipid peroxidation, and hydrogen peroxide were measured. The genes expression levels were monitored by real time RT-PCR and western blot techniques. Results. CCl4 group showed significant increase in alanine aminotransferase (ALT), aspartate aminotransferase (AST), thiobarbituric acid reactive substances (TBAR), hydrogen peroxide (H2O2), and lipid profile and a significant decrease in glutathione peroxidase (GPx), glutathione S transferase (GST), catalase (CAT), paraoxonase-1 (PON-1), paraoxonase-3 (PON-3), peroxisome proliferator activated receptor delta (PPAR-δ), and ATP-binding cassette transporter 1 (ABAC1) genes expression levels. Interestingly, rutin supplementation completely reversed the biochemical and gene expression levels induced by CCl4 to control values. Conclusion. CCl4 administration causes aberration of genes expression levels in oxidative stress pathway resulting in DNA damage and hepatotoxicity. Rutin causes hepatoprotective effect through enhancing the antioxidant genes. Mohamed M. Hafez, Othman A. Al-Shabanah, Naif O. Al-Harbi, Mohamed M. Al-Harbi, Salim S. Al-Rejaie, Saad M. Alsurayea, and Mohamed M. Sayed-Ahmed Copyright © 2014 Mohamed M. Hafez et al. All rights reserved. The Effects of Quinacrine, Proglumide, and Pentoxifylline on Seizure Activity, Cognitive Deficit, and Oxidative Stress in Rat Lithium-Pilocarpine Model of Status Epilepticus Sun, 16 Nov 2014 12:29:37 +0000 http://www.hindawi.com/journals/omcl/2014/630509/ The present data indicate that status epilepticus (SE) induced in adult rats is associated with cognitive dysfunctions and cerebral oxidative stress (OS). This has been demonstrated using lithium-pilocarpine (Li-Pc) model of SE. OS occurring in hippocampus and striatum of mature brain following SE is apparently due to both the increased free radicals production and the limited antioxidant defense. Pronounced alterations were noticed in the enzymatic, glutathione-S transferase (GST), catalase (CAT), and superoxide dismutase (SOD), as well as in the nonenzymatic; thiobarbituric acid (TBARS) and reduced glutathione (GST), indices of OS in the hippocampus and striatum of SE induced animals. Quinacrine (Qcn), proglumide (Pgm), and pentoxifylline (Ptx) administered to animals before inducing SE, were significantly effective in ameliorating the seizure activities, cognitive dysfunctions, and cerebral OS. The findings suggest that all the drugs were effective in the order of Ptx < Pgm < Qcn indicating that these drugs are potentially antiepileptic as well as antioxidant; however, further studies are needed to establish this fact. It can be assumed that these antiepileptic substances with antioxidant properties combined with conventional therapies might provide a beneficial effect in treatment of epilepsy through ameliorating the cerebral OS. Mohammad Ahmad, Gasem M. Abu-Taweel, Ahmad E. Aboshaiqah, and Jamaan S. Ajarem Copyright © 2014 Mohammad Ahmad et al. All rights reserved. Antiosteoporotic Effect of Combined Extract of Morus alba and Polygonum odoratum Wed, 12 Nov 2014 12:25:16 +0000 http://www.hindawi.com/journals/omcl/2014/579305/ Due to the limitation of osteoporosis therapy, the alternative therapies from natural sources have been considered. In this study, we aimed to determine the antiosteoporotic effect of the combined extract of Morus alba and Polygonum odoratum leaves. Ovariectomized rats, weighing 200–220 g, were orally given the combined extract at doses of 5, 150, and 300 mg·kg−1 BW for 3 months. At the end of study, blood was collected to determine serum osteocalcin, calcium, and alkaline phosphatase level. In addition, tibia bone was isolated to determine bone oxidative stress markers, cortical bone thickness, and density of osteoblast. The combined extract decreased oxidative stress and osteoclast density but increased osteoblast density and cortical thickness. The elevation of serum calcium, alkaline phosphatase, and osteocalcin was also observed. These results suggested the antiosteoporotic effect of the combined extract via the increased growth formation together with the suppression of bone resorption. However, further studies concerning chronic toxicity and the underlying mechanism are required. Sudarat Sungkamanee, Jintanaporn Wattanathorn, Supaporn Muchimapura, and Wipawee Thukham-mee Copyright © 2014 Sudarat Sungkamanee et al. All rights reserved. Fumigant Activity of the Psidium guajava Var. Pomifera (Myrtaceae) Essential Oil in Drosophila melanogaster by Means of Oxidative Stress Wed, 12 Nov 2014 11:21:51 +0000 http://www.hindawi.com/journals/omcl/2014/696785/ The guava fruit, Psidium guajava var. pomifera (Myrtaceae family), is a native plant from South America. Its leaves and fruits are widely used in popular medicine in tropical and subtropical countries. Drosophila melanogaster has been used as one of the main model organisms in genetic studies since the 1900s. The extensive knowledge about this species makes it one of the most suitable organisms to study many aspects of toxic compound effects. Due to the lack of studies on the effects of the bioactive compounds present in the P. guajava var. pomifera essential oil, we performed a phytochemical characterization by CG-MS and evaluated the toxicity induced by the essential oil in the D. melanogaster insect model. In order to understand the biochemical mechanisms of toxicity, changes on the Nrf2 signaling as well as hallmarks of oxidative stress response were followed in the exposed flies. Our results showed that exposure of insects to the P. guajava oil increased mortality and locomotor deficits in parallel with an oxidative stress response signaling. Therefore, it suggested a bioinsecticidal activity for P. guajava volatile compounds by means of oxidative stress. Further studies are ongoing to identify which oil compounds are responsible for such effect. Antonio Ivanildo Pinho, Gabriel Luz Wallau, Mauro Eugenio Medina Nunes, Nadghia Figueiredo Leite, Saulo Relison Tintino, Litiele Cezar da Cruz, Francisco Assis Bezerra da Cunha, José Galberto Martins da Costa, Henrique Douglas Melo Coutinho, Thais Posser, and Jeferson Luis Franco Copyright © 2014 Antonio Ivanildo Pinho et al. All rights reserved. A Novel Contrast-Induced Acute Kidney Injury Model Based on the 5/6-Nephrectomy Rat and Nephrotoxicological Evaluation of Iohexol and Iodixanol In Vivo Tue, 11 Nov 2014 13:06:49 +0000 http://www.hindawi.com/journals/omcl/2014/427560/ Contrast-induced acute kidney injury (CI-AKI) is a serious complication in patients after administration of iodinated contrast media. Proper animal models of CI-AKI can help understand the mechanisms involved and prevent the disorder. We used the 5/6-nephrectomized (NE) rat to develop a CI-AKI model and to evaluate differences in the toxic effects on the kidney between iohexol and iodixanol. We found that six weeks after ablative surgery was the preferred time to induce CI-AKI. We compared multiple pretreatment plans and found that dehydration for 48 hours before iodixanol (320, 10 mL/kg) administration was optimal to induce CI-AKI in the 5/6 NE rats. Compared with iodixanol, iohexol induced a significantly greater reduction in renal function, severe renal tissue damage, intrarenal hypoxia, and apoptotic tubular cells. Iohexol and iodixanol resulted in similarly marked increases in levels of inflammation and oxidative stress. In summary, the 5/6 NE rat combined with dehydration for 48 hours is a useful pretreatment to establish a novel and reliable CI-AKI model. Iohexol induced more severe CI-AKI than iodixanol in this model. Tong-qiang Liu, Wei-li Luo, Xiao Tan, Yi Fang, Jing Chen, Hui Zhang, Xiao-fang Yu, Jie-ru Cai, and Xiao-qiang Ding Copyright © 2014 Tong-qiang Liu et al. All rights reserved. CAT, GPX1, MnSOD, GSTM1, GSTT1, and GSTP1 Genetic Polymorphisms in Chronic Myeloid Leukemia: A Case-Control Study Tue, 11 Nov 2014 00:00:00 +0000 http://www.hindawi.com/journals/omcl/2014/875861/ Oxidative damage at the DNA level may be promoted by high levels of reactive oxygen species (ROS), leading to genomic instability and increased neoplastic risk. Superoxide dismutase (SOD), glutathione peroxidase (GPX), and catalase (CAT) enzymes are implicated in the prevention of DNA damage by ROS. The aim of the study was to investigate the relationships between CAT C262T, GPX1 Pro198Leu, MnSOD Ala16Val, GSTM1, GSTT1, and GSTP1 Ile105Val polymorphisms and the risk of CML. No association was observed between CML and variant genotypes of GPX1, MnSOD, GSTM1, and GSTT1 polymorphisms in any of the investigated cases. Our study suggests that the homozygous variant genotype of the GSTP1 Ile105Val gene polymorphisms may be associated with the risk of developing CML (; 95% –5.7; P value = 0.02), while the heterozygous genotype of the CAT C262T polymorphism seems to have a protective effect against CML (, 95% –0.89, P value = 0.01). In most cases, no association was found between laboratory parameters and prognostic factors and the variant genotype of investigated gene polymorphisms. We concluded that CAT, GPX, MnSOD, GSTM1, and GSTT1 gene polymorphisms are not associated with the risk of CML. Variant genotype of the GSTP1 Ile105Val gene polymorphisms may contribute to the risk of developing CML. Claudia Bănescu, Adrian P. Trifa, Septimiu Voidăzan, Valeriu G. Moldovan, Ioan Macarie, Erzsebeth Benedek Lazar, Delia Dima, Carmen Duicu, and Minodora Dobreanu Copyright © 2014 Claudia Bănescu et al. All rights reserved. Exercise-Induced Neuroprotection of Hippocampus in APP/PS1 Transgenic Mice via Upregulation of Mitochondrial 8-Oxoguanine DNA Glycosylase Wed, 05 Nov 2014 00:00:00 +0000 http://www.hindawi.com/journals/omcl/2014/834502/ Improving mitochondrial function has been proposed as a reasonable therapeutic strategy to reduce amyloid-β (Aβ) load and to modify the progression of Alzheimer’s disease (AD). However, the relationship between mitochondrial adaptation and brain neuroprotection caused by physical exercise in AD is poorly understood. This study was undertaken to investigate the effects of long-term treadmill exercise on mitochondrial 8-oxoguanine DNA glycosylase-1 (OGG1) level, mtDNA oxidative damage, and mitochondrial function in the hippocampus of APP/PS1 transgenic mouse model of AD. In the present study, twenty weeks of treadmill training significantly improved the cognitive function and reduced the expression of Aβ-42 in APP/PS1 transgenic (Tg) mice. Training also ameliorated mitochondrial respiratory function by increasing the complexes I, and IV and ATP synthase activities, whereas it attenuated ROS generation and mtDNA oxidative damage in Tg mice. Furthermore, the impaired mitochondrial antioxidant enzymes and mitochondrial OGG1 activities seen in Tg mice were restored with training. Acetylation level of mitochondrial OGG1 and MnSOD was markedly suppressed in Tg mice after exercise training, in parallel with increased level of SIRT3. These findings suggest that exercise training could increase mtDNA repair capacity in the mouse hippocampus, which in turn would result in protection against AD-related mitochondrial dysfunction and phenotypic deterioration. Hai Bo, Weimin Kang, Ning Jiang, Xun Wang, Yong Zhang, and Li Li Ji Copyright © 2014 Hai Bo et al. All rights reserved. Exercise Training Preserves Ischemic Preconditioning in Aged Rat Hearts by Restoring the Myocardial Polyamine Pool Thu, 23 Oct 2014 00:00:00 +0000 http://www.hindawi.com/journals/omcl/2014/457429/ Background. Ischemic preconditioning (IPC) strongly protects against myocardial ischemia reperfusion (IR) injury. However, IPC protection is ineffective in aged hearts. Exercise training reduces the incidence of age-related cardiovascular disease and upregulates the ornithine decarboxylase (ODC)/polyamine pathway. The aim of this study was to investigate whether exercise can reestablish IPC protection in aged hearts and whether IPC protection is linked to restoration of the cardiac polyamine pool. Methods. Rats aging 3 or 18 months perform treadmill exercises with or without gradient respectively for 6 weeks. Isolated hearts and isolated cardiomyocytes were exposed to an IR and IPC protocol. Results. IPC induced an increase in myocardial polyamines by regulating ODC and spermidine/spermine acetyltransferase (SSAT) in young rat hearts, but IPC did not affect polyamine metabolism in aged hearts. Exercise training inhibited the loss of preconditioning protection and restored the polyamine pool by activating ODC and inhibiting SSAT in aged hearts. An ODC inhibitor, α-difluoromethylornithine, abolished the recovery of preconditioning protection mediated by exercise. Moreover, polyamines improved age-associated mitochondrial dysfunction in vitro. Conclusion. Exercise appears to restore preconditioning protection in aged rat hearts, possibly due to an increase in intracellular polyamines and an improvement in mitochondrial function in response to a preconditioning stimulus. Weiwei Wang, Hao Zhang, Guo Xue, Li Zhang, Weihua Zhang, Lina Wang, Fanghao Lu, Hongzhu Li, Shuzhi Bai, Yan Lin, Yu Lou, Changqing Xu, and Yajun Zhao Copyright © 2014 Weiwei Wang et al. All rights reserved. Reduced Oxidative Stress Contributes to the Lipid Lowering Effects of Isoquercitrin in Free Fatty Acids Induced Hepatocytes Wed, 22 Oct 2014 09:10:58 +0000 http://www.hindawi.com/journals/omcl/2014/313602/ Oxidative stress interferes with hepatic lipid metabolism at various levels ranging from benign lipid storage to so-called second hit of inflammation activation. Isoquercitrin (IQ) is widely present flavonoid but its effects on hepatic lipid metabolism remain unknown. We used free fatty acids (FFA) induced lipid overload and oxidative stress model in two types of liver cells and measured cell viability, intracellular lipids, and reactive oxygen species (ROS) within hepatocytes. In addition, Intracellular triglycerides (TG), superoxide dismutase (SOD), and malondialdehyde (MDA) were examined. A novel in vitro model was used to evaluate correlation between lipid lowering and antioxidative activities. Furthermore, 34 major cytokines and corresponding ROS levels were analyzed in FFA/LPS induced coculture model between hepatocytes and Kupffer cells. At molecular level AMPK pathway was elucidated. We showed that IQ attenuated FFA induced lipid overload and ROS within hepatocytes. Further, IQ reversed FFA induced increase in intracellular TG SOD and MDA. It was shown that antioxidative activity of IQ correlates with its lipid lowering potentials. IQ reversed major proinflammatory cytokines and oxidative stress in FFA/LPS induced coculture model. Finally, AMPK pathway was found responsible for metabolic benefits at molecular level. IQ strikingly manifests antioxidative and related lipid lowering activities in hepatocytes. Waseem Hassan, Gao Rongyin, Abdelkader Daoud, Lin Ding, Lulu Wang, Jun Liu, and Jing Shang Copyright © 2014 Waseem Hassan et al. All rights reserved. Magnolin Protects against Contrast-Induced Nephropathy in Rats via Antioxidation and Antiapoptosis Tue, 21 Oct 2014 10:00:25 +0000 http://www.hindawi.com/journals/omcl/2014/203458/ Background. Magnolin is the major active ingredient of the herb Magnolia fargesii which has anti-inflammatory and antioxidative effects. Oxidative stress and apoptosis are involved in the pathogenesis of contrast-induced nephropathy (CIN). We hypothesize that Magnolin could protect against CIN through antioxidative and antiapoptotic properties. Methods. To test whether Magnolin could attenuate CIN, oxidative stress and apoptosis, in vivo and in vitro, we utilized a rat model of ioversol-induced CIN and a cell model of oxidative stress in which HK2 cells were treated with H2O2. Rats were assigned to 4 groups ( per group): control group, ioversol group (ioversol-induced CIN), vehicle group (CIN rats pretreated with vehicle), and Magnolin group (CIN rats pretreated with 1 mg/kg Magnolin). Results. The results showed that magnolin ameliorated the renal tubular necrosis, apoptosis, and the deterioration of renal function (). Furthermore, Magnolin reduced the renal oxidative stress, suppressed caspase-3 activity, and increased Bcl-2 expression in vivo and in vitro. Conclusion. Magnolin might protect CIN in rats through antioxidation and antiapoptosis. Feng Wang, Guangyuan Zhang, Yang Zhou, Dingkun Gui, Junhui Li, Tao Xing, and Niansong Wang Copyright © 2014 Feng Wang et al. All rights reserved.