Trimetazidine potentiates the antiepileptic activity and ameliorates the metabolic changes associated with pentylenetetrazole kindling in rats treated with valproic acid

2017 ◽  
Vol 95 (6) ◽  
pp. 686-696
Author(s):  
Amina Ahmed Sedky ◽  
Osama Mahmoud Hassan El Serafy ◽  
Olfat Ahmed Hassan ◽  
Hala Salah Abdel-kawy ◽  
Amany Helmy Hasanin ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Valproic Acid ◽  
Metabolic Changes ◽  
Anticonvulsant Effect ◽  
Histopathological Changes ◽  
Atherosclerotic Vascular Disease ◽  
Antiepileptic Activity ◽  
Increased Risk ◽  
The Impact ◽  
Oxidative Effect

Oxidative stress is implicated in epileptogenesis as well as in the metabolic changes associated with increased risk of atherosclerotic vascular disease in epilepsy. The present work investigated the impact of the antioxidant trimetazidine (TMZ) on the antiepileptic activity of valproic acid (VPA) and on the metabolic and histological changes in hippocampal, aortic, and hepatic tissues associated with epilepsy and (or) VPA. Rats were divided into non-pentylenetetrazole (non-PTZ) group subdivided into control and VPA-treated groups, and PTZ-treated group subdivided into PTZ, PTZ/VPA, PTZ/TMZ, and PTZ/VPA + TMZ groups. VPA treatment in PTZ rats resulted in an antioxidant effect with improvement in oxidative stress, metabolic and histopathological changes induced by PTZ in hippocampus, aortic, and hepatic tissues. TMZ exhibited anticonvulsant activity and potentiated the anticonvulsant effect of VPA. Combination of TMZ with VPA induced a greater reduction in oxidative stress, improvement in the metabolic and histopathological changes compared to VPA treatment. In contrast, VPA administration in non-PTZ-treated rats induced a pro-oxidative effect, associated with metabolic and histopathological changes in aortic and hepatic tissues. These findings suggest that co-administration of TMZ with VPA in epilepsy might antagonize not only the oxidative stress associated with epilepsy but might also counteract a potential pro-oxidative effect of VPA.

scholarly journals The Effect of Coenzyme Q10 on Liver Injury Induced by Valproic Acid and Its Antiepileptic Activity in Rats

Biomedicines ◽  
2022 ◽  
Vol 10 (1) ◽  
pp. 168
Author(s):  
Fahad Alqarni ◽  
Hala S. Eweis ◽  
Ahmed Ali ◽  
Aziza Alrafiah ◽  
Mohammed Alsieni ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Valproic Acid ◽  
Coenzyme Q10 ◽  
Intraperitoneal Injection ◽  
Therapeutic Potential ◽  
Acid Group ◽  
Control Group ◽  
Anticonvulsant Effect ◽  
Antiepileptic Activity ◽  
Stress Markers

Valproic acid (VPA) has toxic metabolites that can elevate oxidative stress markers, and the hepatotoxicity of VPA has been reported. Coenzyme Q10 (CoQ10) is one of the most widely used antioxidants. The effect of CoQ10 on epileptogenesis and VPA hepatotoxicity were examined. Rats were randomly divided into five groups: the control group received 0.5% methylcellulose by oral gavages daily and saline by intraperitoneal injection three times weekly. The PTZ group received 1% methylcellulose by gavages daily and 30 mg/kg PTZ by intraperitoneal injection three times weekly. The valproic acid group received 500 mg/kg valproic acid by gavage and 30 mg/kg PTZ, as above. The CoQ10 group received 200 mg/kg CoQ10 by gavages daily and 30 mg/kg PTZ, as above. The Valproic acid + CoQ10 group received valproic acid and CoQ10, as above. Results: CoQ10 exhibited anticonvulsant activity and potentiated the anticonvulsant effect of VPA. CoQ10 combined with VPA induced a more significant reduction in oxidative stress and improved the histopathological changes in the brain and liver compared to VPA treatment. In addition, CoQ10 reduced the level of toxic VPA metabolites. These findings suggest that the co-administration of CoQ10 with VPA in epilepsy might have therapeutic potential by increasing antiepileptic activity and reducing the hepatotoxicity of VPA.

scholarly journals Oxidative Stress Biomarker Decreased in Preterm Neonates Treated With Kangaroo Mother Care

2020 ◽  
Vol 22 (2) ◽  
pp. 188-196 ◽  
Author(s):  
Dorothy Forde ◽  
Douglas D. Deming ◽  
John C. Tan ◽  
Raylene M. Phillips ◽  
Eileen K. Fry-Bowers ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Maternal Separation ◽  
Intervention Group ◽  
Kangaroo Mother Care ◽  
Energy Utilization ◽  
Infrared Spectrometry ◽  
Control Group ◽  
Increased Risk ◽  
The Impact ◽  
Incubator Care

Objective: Due to physiological and metabolic immaturity, prematurely born infants are at increased risk because of maternal separation in many neonatal intensive care units (NICUs). The stress induced from maternal–infant separation can lead to well-documented short-term physiologic instability and potentially lifelong neurological, sociological, or psychological sequelae. Based on previous studies of kangaroo mother care (KMC) that demonstrated improvement in physiologic parameters, we examined the impact of KMC on physiologic measures of stress (abdominal temperature, heart rate, oxygen saturation, perfusion index, near-infrared spectrometry), oxidative stress, and energy utilization/conservation in preterm infants. Methods: In this randomized, stratified study of premature neonates, we compared the effects on urinary concentrations of biomarkers of energy utilization and oxidative stress of 1 hr of KMC versus incubator care on Day 3 of life in intervention-group babies ( n = 26) and control-group babies ( n = 25), respectively. On Day 4, both groups received 1 hr of KMC. Urinary samples were collected 3 hr before and 3 hr after intervention/incubator care on both days. Energy utilization was assessed by measures of adenosine triphosphate (ATP) degradation (i.e., hypoxanthine, xanthine, and uric acid). Oxidative stress was assessed using urinary allantoin. Mixed-models analysis was used to assess differences in purine/allantoin. Results: Mean allantoin levels over Days 3 and 4 were significantly lower in the KMC group than in the control group ( p = .026). Conclusions: Results provide preliminary evidence that KMC reduces neonatal oxidative stress processes and that urinary allantoin could serve as an effective noninvasive marker for future studies.

scholarly journals The impact of melatonin on antioxidant defense mechanisms in Alzheimer’s disease

2018 ◽  
Vol 72 ◽  
pp. 1114-1122
Author(s):  
Daria Malicka ◽  
Dominika Markowska ◽  
Jarosław Nuszkiewicz ◽  
Karolina Szewczyk-Golec
Keyword(s):  
Oxidative Stress ◽  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Defense Mechanisms ◽  
Senile Plaques ◽  
Biological Clock ◽  
Cell Functions ◽  
Increased Risk ◽  
The Impact ◽  
Phosphorylated Tau Protein

During aging, the increased risk of neurodegenerative disease development is observed. One of the most common and most serious disorders is Alzheimer’s disease manifested by the loss of nerve cell functions. In the course of the disease, extracellular senile plaques consisting of beta-amyloid and intracellular neurofibrillary tangles of hyper-phosphorylated tau protein are formed. As a result of aging, the repair potential of damaged nerve cells is reduced. Free radicals formed in excess generate augmented oxidative stress, which contributes to the damaging of biomolecules and the development of pathological changes. This mechanism is favored by a decrease in the efficiency of antioxidant enzymes and the deficiency of antioxidants, observed in aging organism. With age, the secretion of the pineal hormone melatonin, functioning as a biochemical biological clock, is significantly reduced. This compound has been proved to be a very effective antioxidant that plays a key role in protecting cells against excessive damage, especially in nervous tissue. Studies have shown that supplementation with exogenous melatonin can prevent oxidative stress-induced degeneration of neurons. Considering the action of melatonin and the pathogenesis of Alzheimer’s disease, the idea of using the hormone supplementation in the prevention and alleviation of the effects of the disease seems to be extremely interesting.

scholarly journals Advanced maternal age compromises fetal growth and induces sex-specific changes in placental phenotype in rats

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Tina Napso ◽  
Yin-Po Hung ◽  
Sandra T. Davidge ◽  
Alison S. Care ◽  
Amanda N. Sferruzzi-Perri
Keyword(s):  
Oxidative Stress ◽  
Health Outcomes ◽  
Maternal Age ◽  
Advanced Maternal Age ◽  
Placental Lactogen ◽  
Rat Offspring ◽  
Placental Transport ◽  
Increased Risk ◽  
Glucocorticoid Metabolism ◽  
The Impact

AbstractAdvanced maternal age is associated with an increased risk of pregnancy complications. It programmes sex-specific cardiovascular dysfunction in rat offspring, however the intrauterine mechanisms involved remain unknown. This study in the rat assessed the impact of advanced maternal age on placental phenotype in relation to the growth of female and male fetuses. We show that relative to young (3–4 months) dams, advanced maternal age (9.5–10 months) compromises growth of both female and male fetuses but affects the placental phenotype sex-specifically. In placentas from aged versus young dams, the size of the placental transport and endocrine zones were increased and expression of Igf2 (+41%) and placental lactogen (Prl3b1: +59%) genes were upregulated in female, but not male fetuses. Placental abundance of IGF2 protein also decreased in the placenta of males only (−95%). Moreover, in placentas from aged versus young dams, glucocorticoid metabolism (11β-hsd2: +63% and 11β-hsd1: −33%) was higher in females, but lower in males (11β-hsd2: −50% and 11β-hsd1: unaltered). There was however, no change in the placental abundance of 11β-HSD2 protein in aged versus young dams regardless of fetal sex. Levels of oxidative stress in the placenta were increased in female and male fetuses (+57% and +90%, respectively) and apoptosis increased specifically in the placenta of males from aged rat dams (+700%). Thus, advanced maternal age alters placental phenotype in a sex-specific fashion. These sexually-divergent changes may play a role in determining health outcomes of female and male offspring of aged mothers.

scholarly journals Profile Of Oxidative Stress Genes In Response To Obesity Treatment

2021 ◽  
Author(s):  
Amira Ahmed ◽  
Huda Farah ◽  
Omnia Ahmed ◽  
Dina Elsayegh ◽  
Abdelrahman Elgamal ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Skeletal Muscle ◽  
Body Weight ◽  
Skeletal Muscles ◽  
Bioactive Compound ◽  
Treated Group ◽  
The Body ◽  
Tissue Samples ◽  
Increased Risk ◽  
The Impact

Background: Oxidative stress (OS) is an imbalance between free radical production and the antioxidants defense in the body. Previous studies demonstrated the correlation of OS to the increased risk of developing metabolic disorders such as obesity. Sulforaphane (SFN), a bioactive compound, can protect against inflammation and OS, thus an effective anti-obesity supplement. Aim: This study explores the impact of SNF on OS in diet induced obese (DIO) mice via profiling of OS genes and pathways in skeletal muscles related to the anti-obesity effect. Methods: Wild-type CD1 male mice and the knockout of nuclear factor (erythroid-derived 2) like 2 (NrF2) mice were fed a high-fat diet (HFD) for 16 weeks; to induce obesity. Subsequently, each group was subdivided into two subgroups and received either Vehicle (25μl) or SFN (5 mg/kg BW) for four weeks. Body weight was measured daily, and a glucose tolerance test (GTT) was performed after 21 days of treatment. Afterward, mice were decapitated, blood and tissue samples were collected and snap-frozen immediately. Total RNA was extracted from Skeletal muscle and epididymal white adipose tissue (eWAT), leptin expression was measured in (eWAT), and 84 OS genes in skeletal muscle were examined using RT-PCR. Results: Significant reduction in body weight in SFN treated WT mice, while no change in KO mice. Plasma glucose, leptin, and leptin gene expression (eWAT) were significantly reduced in the WT-DIO SFN treated group, while no changes were detected in KO mice. SFN decreases OS damage in skeletal muscles, such as lipid peroxidation and production of reactive oxygen species (ROS). Conclusion: This study demonstrated that SFN had lowered body weight in WT-DIO mice by decreasing OS damage in skeletal muscles through the NrF2 pathway and can be a potential anti-obesity drug.

Zinc Depletion Increases Readmission in Older Patients: An Example of Interactions Between Nutrition and Disease

2017 ◽  
Vol 87 (1-2) ◽  
pp. 10-16 ◽  
Author(s):  
Salah Gariballa ◽  
Awad Alessa
Keyword(s):  
Nutritional Status ◽  
Inductively Coupled Plasma ◽  
Older Patients ◽  
Controlled Trial ◽  
Prognostic Indicators ◽  
Hospitalised Patients ◽  
Increased Risk ◽  
Co Morbidity ◽  
The Impact ◽  
Poor Nutrition

Abstract. Background: ill health may lead to poor nutrition and poor nutrition to ill health, so identifying priorities for management still remains a challenge. The aim of this report is to present data on the impact of plasma zinc (Zn) depletion on important health outcomes after adjusting for other poor prognostic indicators in hospitalised patients. Methods: Hospitalised acutely ill older patients who were part of a large randomised controlled trial had their nutritional status assessed using anthropometric, hematological and biochemical data. Plasma Zn concentrations were measured at baseline, 6 weeks and at 6 months using inductively- coupled plasma spectroscopy method. Other clinical outcome measures of health were also measured. Results: A total of 345 patients assessed at baseline, 133 at 6 weeks and 163 at 6 months. At baseline 254 (74%) patients had a plasma Zn concentration below 10.71 μmol/L indicating biochemical depletion. The figures at 6 weeks and 6 months were 86 (65%) and 114 (70%) patients respectively. After adjusting for age, co-morbidity, nutritional status and tissue inflammation measured using CRP, only muscle mass and serum albumin showed significant and independent effects on plasma Zn concentrations. The risk of non-elective readmission in the 6-months follow up period was significantly lower in patients with normal Zn concentrations compared with those diagnosed with Zn depletion (adjusted hazard ratio 0.62 (95% CI: 0.38 to 0.99), p = 0.047. Conclusions: Zn depletion is common and associated with increased risk of readmission in acutely-ill older patients, however, the influence of underlying comorbidity on these results can not excluded.

Thrombophilia and risk of VTE recurrence according to the age at the time of first VTE manifestation

VASA ◽  
2015 ◽  
Vol 44 (4) ◽  
pp. 313-323 ◽  
Author(s):  
Lea Weingarz ◽  
Marc Schindewolf ◽  
Jan Schwonberg ◽  
Carola Hecking ◽  
Zsuzsanna Wolf ◽  
...  
Keyword(s):  
Factor V Leiden ◽  
Cox Proportional Hazards ◽  
First Episode ◽  
Factor V ◽  
Factor V Leiden Mutation ◽  
Younger Patients ◽  
Risk Of Recurrence ◽  
G20210a Mutation ◽  
Increased Risk ◽  
The Impact

Abstract. Background: Whether screening for thrombophilia is useful for patients after a first episode of venous thromboembolism (VTE) is a controversial issue. However, the impact of thrombophilia on the risk of recurrence may vary depending on the patient’s age at the time of the first VTE. Patients and methods: Of 1221 VTE patients (42 % males) registered in the MAISTHRO (MAin-ISar-THROmbosis) registry, 261 experienced VTE recurrence during a 5-year follow-up after the discontinuation of anticoagulant therapy. Results: Thrombophilia was more common among patients with VTE recurrence than those without (58.6 % vs. 50.3 %; p = 0.017). Stratifying patients by the age at the time of their initial VTE, Cox proportional hazards analyses adjusted for age, sex and the presence or absence of established risk factors revealed a heterozygous prothrombin (PT) G20210A mutation (hazard ratio (HR) 2.65; 95 %-confidence interval (CI) 1.71 - 4.12; p < 0.001), homozygosity/double heterozygosity for the factor V Leiden and/or PT mutation (HR 2.35; 95 %-CI 1.09 - 5.07, p = 0.030), and an antithrombin deficiency (HR 2.12; 95 %-CI 1.12 - 4.10; p = 0.021) to predict recurrent VTE in patients aged 40 years or older, whereas lupus anticoagulants (HR 3.05; 95%-CI 1.40 - 6.66; p = 0.005) increased the risk of recurrence in younger patients. Subgroup analyses revealed an increased risk of recurrence for a heterozygous factor V Leiden mutation only in young females without hormonal treatment whereas the predictive value of a heterozygous PT mutation was restricted to males over the age of 40 years. Conclusions: Our data do not support a preference of younger patients for thrombophilia testing after a first venous thromboembolic event.

Percutaneous Coronary Intervention in Patients with Diabetes and Multivessel or Left Main Disease – a Review

2012 ◽  
Vol 7 (1) ◽  
pp. 37
Author(s):  
Donald E Cutlip ◽  
Keyword(s):  
Percutaneous Coronary Intervention ◽  
Coronary Artery ◽  
Statistical Significance ◽  
Bare Metal Stents ◽  
Coronary Intervention ◽  
Metal Stents ◽  
Increased Risk ◽  
Percutaneous Coronary ◽  
Patients With Diabetes ◽  
The Impact

Coronary artery disease in patients with diabetes is frequently a diffuse process with multivessel involvement and is associated with increased risk for myocardial infarction and death. The role of percutaneous coronary intervention (PCI) versus coronary artery bypass grafting (CABG) in patients with diabetes and multivessel disease who require revascularisation has been debated and remains uncertain. The debate has been continued mainly because of the question to what degree an increased risk for in-stent restenosis among patients with diabetes contributes to other late adverse outcomes. This article reviews outcomes from early trials of balloon angioplasty versus CABG through later trials of bare-metal stents versus CABG and more recent data with drug-eluting stents as the comparator. Although not all studies have been powered to show statistical significance, the results have been generally consistent with a mortality benefit for CABG versus PCI, despite differential risks for restenosis with the various PCI approaches. The review also considers the impact of mammary artery grafting of the left anterior descending artery and individual case selection on these results, and proposes an algorithm for selection of patients in whom PCI remains a reasonable strategy.

Working conditions and occupational pathology of coal miners in the Arctic

2019 ◽  
pp. 452-457 ◽  
Author(s):  
S. A. Gorbanev ◽  
S. A. Syurin ◽  
N. M. Frolova
Keyword(s):  
Coal Mining ◽  
Working Conditions ◽  
Occupational Diseases ◽  
Climatic Factors ◽  
Coal Mines ◽  
The Arctic ◽  
Morbidity Rate ◽  
Coal Miners ◽  
Increased Risk ◽  
The Impact

Introduction. Due to the impact of adverse working conditions and climate, workers in coal-mining enterprises in the Arctic are at increased risk of occupational diseases (OD).The aim of the study was to study the working conditions, causes, structure and prevalence of occupational diseases in miners of coal mines in the Arctic.Materials and methods. Th e data of social and hygienic monitoring “Working conditions and occupational morbidity” of the population of Vorkuta and Chukotka Autonomous District in 2007–2017 are studied.Results. It was established that in 2007–2017 years, 2,296 ODs were diagnosed for the first time in 1851 coal mines, mainly in the drifters, clearing face miners, repairmen and machinists of mining excavating machines. Most often, the ODs occurred when exposed to the severity of labor, fibrogenic aerosols and hand-arm vibration. The development of professional pathology in 98% of cases was due to design flaws of machines and mechanisms, as well as imperfections of workplaces and technological processes. Diseases of the musculoskeletal system (36.2%), respiratory organs (28.9%) and nervous system (22.5%) prevailed in the structure of professional pathology of miners of coal mines. Among the three most common nosological forms of OD were radiculopathy (32.1%), chronic bronchitis (27.7%) and mono-polyneuropathy (15.4%). In 2017, coal miners in the Arctic had a professional morbidity rate of 2.82 times higher than the national rates for coal mining.Conclusions. To preserve the health of miners of coal mining enterprises, technical measures to improve working conditions and medical interventions aimed at increasing the body’s resistance to the effects of harmful production and climatic factors are necessary.

Assessment of Superoxide Dismutase and Catalase Evolution in Different Stages of an Experimental Endometriosis

2017 ◽  
Vol 68 (6) ◽  
pp. 1381-1383
Author(s):  
Allia Sindilar ◽  
Carmen Lacramioara Zamfir ◽  
Eusebiu Viorel Sindilar ◽  
Alin Constantin Pinzariu ◽  
Eduard Crauciuc ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Superoxide Dismutase ◽  
Antioxidant Enzymes ◽  
Reproductive Function ◽  
Female Rats ◽  
Oxygen Species ◽  
Efficient Treatment ◽  
Endometrial Cells ◽  
Gynecological Disorder ◽  
The Impact

Endometriosis is described as a gynecological disorder characterized by the presence of endometrial tissue outside the uterus; extensively explored because of its increasing incidency, with an indubitable diagnostic only after invasive surgery, with no efficient treatment, it has still many aspects to be elucidated. A growing body of facts sustain oxidative stress as a crucial factor between the numerous incriminated factors implicated in endometriosis ethiopathogeny. Reactive oxygen species(ROS) act to decline reproductive function. Our study intends to determine if an experimental model of endometriosis may be useful to assess the impact of oxidative stress on endometrial cells; we have used a murine model of 18 adult Wistar female rats. A fragment from their left uterine horn was implanted in the abdominal wall. After 4 weeks, a laparatomy was performed, 5 endometrial implants were removed, followed by biochemical tissue assay of superoxide dismutase(SOD) and catalase(CAT). At the end of the experiment, the rats were sacrificed, the implants were removed for histopathological exam and biochemical assay of antioxidant enzymes. The results revealed decreased levels of antioxidant enzymes, pointing on significant oxidative stress involvement.

Sign in / Sign up

Export Citation Format

Share Document