Free Radical Oxidative Stress Research Articles

MYRICETIN ISOLATED FROM TURBINARIA ORNATA AMELIORATES ROTENONE INDUCED PARKINSONISM IN DROSOPHILA MELANOGASTER

Objective: Parkinson’s disease (PD) is a neurodegenerative disorder which affects the elderly population. Free radicals overproduction, oxidative stress, apoptosis, inflammation and abnormalities in mitochondria are critical mediators of the neuronal degeneration. In the present study neuroprotective activity of myricetin, a flavonoid isolated from brown seaweed Turbinaria ornata have been investigated in rotenone induced experimental PD models of Drosophila melanogaster.Methods: Male fruit flies (Drosophila melanogaster) were fed with an effective dose of 0.1% myricetin three hours before to the treatment with 500 µM of Rotenone (LD 50) for seven days and on 8th day through behavioral analysis the neuroprotective effect of myricetin was investigated for motor coordination in fruit flies. Lipid peroxidation was analyzed by estimating the levels of TBARS. Oxidative stress was determined by estimating the activities of enzymatic antioxidants superoxide dismutase, catalase, and glutathione peroxidase along with the level of reduced glutathione. Dopamine level was estimated in HPLC column detected at 280 nm with UV detectors and degree of apoptosis was studied apoptotic marker Bcl-2, Bax, caspases-3 and 9, cytochrome c and β-actin expressions in the whole body homogenate of fruit flies of experimental groups homogenized in 500μL of 0.1 M phosphate buffers (ice cold, pH, 7.4) containing 1 mmol EDTA.Results: Myricetin maintains the positive behavioral patterns against motor impairments due to the rotenone toxicity, it creates a balance in oxidant and antioxidant status, reduces the oxidative stress and inhibits apoptosis to retard neurodegeneration and maintains the dopamine level with a significant (p<0.05) difference compared to the rotenone treated group.Conclusion: The flavonoid myricetin by reducing the oxidative stress, maintaining the enzymatic antioxidants status and by inhibiting apoptosis prevents the degeneration of dopaminergic neurons. The dopaminergic neurons prevention reduces the depletion of dopamine and thereby promotes the muscular coordination and psychological well being of fruit flies of experimental group. Further in depth molecular level studies are in need to explore the preventive mechanisms of myricetin in Parkinson’s disease.

Inhibitory effects of Tabernaemontana divaricata root extract on oxidative stress and neuronal loss induced by amyloid β25–35 peptide in mice

In Alzheimer's disease, there are numerous amyloid plaques, neurofibrillary tangles, and neuronal loss in several brain areas. Oxidative stress is involved in the mechanisms of Aβ-peptide induced neurotoxicity by the generation of free radical oxidative stress that may lead to neurodegeneration. Tabernaemontana divaricata has various medical properties in Thai folklore medicine including prevent forgetfulness or improve memory. The present study aimed to investigate the effects of T. divaricata root extract (TDE) on Aβ25–35 peptides induced neuronal loss and oxidative stress in mice. Male ICR mice were administered with vehicle or TDE (250, 500, and 1000 mg/kg b.w., p.o.) for 28 consecutive days. Then, these mice were given a single intracerebroventricular (i.c.v.) injection of Aβ25–35 or phosphate buffer saline (PBS) (10 μg/mouse). The novel object recognition (NOR) test was used to determine memory disturbance. In addition, the neuronal cells in the cerebral cortex and hippocampus were measured by using crystal violet staining and lipid peroxidation was determined by measuring the formation of thiobarbituric acid reactive substances. An i.c.v. injection of Aβ25–35 peptides could significantly induce memory impairment, increase level of lipid peroxidation including the neuronal loss in CA3 of hippocampus. However, the mice pretreated with TDE could prevent the memory loss, neuronal loss and decrease lipid peroxidation. These results suggest the potential therapeutic value in dementia of TDE through its antioxidant property.

Polyphenol Supplementation Attenuates Apoptotic Signaling Following Acute Resistance Exercise in Untrained Males

Research has demonstrated an increase in free radical production, oxidative stress, and apoptotic signaling following resistance exercise. Thus, identifying dietary strategies to prevent or attenuate exercise-induced cellular stress and apoptotic activity are of interest. PURPOSE: To examine the effects of 28-days of supplementation with an aqueous proprietary polyphenol blend (PPB) sourced from Camellia sinensis on intramuscular apoptotic signaling following an acute lower-body resistance exercise protocol and subsequent recovery. METHODS: Untrained males (n=38, 21.8 ± 2.7 y, 1.7 ± 0.1 m, 77.6 ± 14.6 kg) were randomized to PPB (n = 14), placebo (PL; n = 14) or control (CON; n = 10). Participants completed a lower-body muscle-damaging resistance exercise protocol comprised of 10 repetitions at 70% of 1-RM for the squat (6 sets), leg press (4 sets) and leg extension (4 sets), with 90 seconds of rest between sets. Skeletal muscle microbiopsies were obtained from the vastus lateralis pre-exercise (PRE), 1-hour (1HR), 5-hour (5HR), and 48-hours (48HR) post-resistance exercise. Apoptotic signaling pathways were quantified using multiplex signaling assay kits to quantify total proteins (Caspase 3, 8, 9) and markers of phosphorylation status (JNK, FADD, p53, BAD, Bcl-2). Change scores from PRE were calculated for each group (PBB, PL, CON) and analyzed by magnitude based inferences to compare the effects of each condition on intramuscular signaling following resistance exercise. The precision of the magnitude inference was set at 90% confidence limits using the p value corresponding to the t-statistic. RESULTS: Magnitude based inferences indicated a “likely” decrease in total Caspase 3 and “possibly” decreased total Caspase 9 in PPB compared to PL from PRE-5H. JNK phosphorylation was “likely” decreased from PRE-5H in PPB compared to PL. BAD was “very likely” decreased from PRE-5H in PPB when compared to PL and Bcl-2 was “likely” decreased from PRE-1H and PRE-5H in PPB compared to PL. Phosphorylation of p53 was “likely increased” in PPB compared to PL from PRE-1H and PRE-48H. CONCLUSION: These data indicate that chronic supplementation with PPB may attenuate or delay indices of apoptosis in skeletal muscle following an acute muscle-damaging resistance exercise. Supported by Kemin Foods L.C.

Cyto-genotoxicity and oxidative stress in common carp (Cyprinus carpio) exposed to a mixture of ibuprofen and diclofenac.

Thirty million people worldwide consume each day nonsteroidal anti-inflammatory drugs (NSAIDs), a heterogeneous group of pharmaceuticals used for its analgesic, antipyretic, and anti-inflammatory properties. Recent studies report high NSAID concentrations in wastewater treatment plant effluents, in surface, ground, and drinking water, and in sediments. NSAIDs are also known to induce toxicity on aquatic organisms. However, toxicity in natural ecosystems is not usually the result of exposure to a single substance but to a mixture of toxic agents, yet only a few studies have evaluated the toxicity of mixtures. The aim of this study was to evaluate the toxicity induced by diclofenac (DCF), ibuprofen (IBP), and their mixture on a species of commercial interest, the common carp Cyprinus carpio. The median lethal concentration of IBP and DCF was determined, and oxidative stress was evaluated using the following biomarkers: lipid peroxidation and activity of the antioxidant enzymes superoxide dismutase, catalase and glutathione peroxidase. Cyto-genotoxicity was evaluated by micronucleus test, comet assay, and the specific activity of caspase-3. Results show that DCF, IBP, and a mixture of these pharmaceuticals induced free radical production, oxidative stress and cyto-genotoxicity in tissues of C. carpio. However, a greater effect was elicited by the mixture than by either pharmaceutical alone in some biomarkers evaluated, particularly in gill. © 2016 Wiley Periodicals, Inc. Environ Toxicol 32: 1637-1650, 2017.

中医阴阳循行的量子元素

量子生物学以微观的波粒二重性突破古典力学对于粒子受制于热力学定律的局限，赋予人类遗传物质得以稳定实现演化的规则性和可预测性。在此之前，去相干的古典物理特性明显遮蔽了我们对量子行为的观察，乃至于面对病理表症的解决之道因为缺少分子尺度的微观考虑，从而限制许许多多医学上重大的发现。巨大个体的生长发育过程会遭遇热力学干扰，最终呈现的是我们所熟悉的古典力学样貌，这现象在物理学上称为去相干，在人类则称为老化。换句话说，当生命体呈现古典定律的粒子性僵硬轨迹，而原本具有波顺应性的量子特性被过滤掉了，这是生命先在性的老化宿命。显现出肌肉皮肤萎缩、弹性下降、皱纹产生、粒线体功能失衡、自由基氧化压力、慢性发炎反应等表症。中医《内经》：「营卫阴阳，如环无端。」依照这个规律而有顺序的循行振动，实现生趣盎然的生命现象。此一生生不息的波、粒二重性，在于法阴阳，和术数，饮食有节，起居有常，不妄作劳，故形与神俱，而终其天年，度百岁乃去。这个源自黄帝内经的组件当可以为人类逆转老化的议题提供值得思考的可能性。 Quantum microscopic biological systems with duality are concerned with the influence of non-trivial quantum phenomena, as opposed to the so-called trivial quantum mechanics present in all biology by reduction to fundamental physics and the law of thermodynamics. These characteristics give the human genetic DNA stable evolution and are able to predictive property. Because the lack of molecular microscopic scale and classical physics of gravity theory interfere with objects wave-like behavior, it limits many of the medical intervention and achievement about human diseases. Quantum phenomena present in the processes of individual biological development system will interfere with an entanglement of physics of gravity theory and thermodynamics. This phenomenon is called de- coherent in physics, and it is also illustrated as ageing in human beings. In other words, when the living environment full with the rigid track of the particles characterization could be considered as a class of quantum phenomena in biological systems are excluded, which may illustrate as the fate of life on aging. Manifestations include muscle and skin atrophy, loose skin elasticity, wrinkling production, mitochondria dysfunction, free radical oxidative stress, chronic inflammation and body function imbalance. This can lead to accelerating ageing. And, of course, it is eventually as scene of death. The yellow Emperor’s classic of Chinese medicine said that yin and yang are interdependent and transform as a circle that is always round endless. Following the yin and yang rhythm, integrated technol-ogy and culture, we will have a regular diet, and not be tired and exhausted in a routine living style. In addition, people should remain calm and avoid excessive desires and fantasies, maintaining the natural purity and clarity of the mind, thus illness and disease can be avoided. The concept supporting the yin-yang-pair model is potentially based on fundamental quantum effects. In ancient times, yin- yang theory advised people to guard themselves against disease-causing factors, and the role of yin-yang recurrence can be subtle as quantum microscale mechanisms. We may consider a biological system that exploits coherent superposition of states of yin-yang recurrence for some practical purposes and provide the possibility for mankind reversing ageing issues, making people happy and have healthy life.

Antioxidant and Total Phenolic Content of Catharanthus roseus Using Deep Eutectic Solvent

Deep eutectic solvents as a new type of eco-friendly solvents have attracted attention in chemistry, medicine, and other fields for the extraction and separation of target compounds from medicinal plants. Deep eutectic solvents are easy to prepare and have many advantages as solvents, such as chemical inertness with water, low cost, easy biodegradability, and pharmaceutically acceptable toxicity. In this study, a deep eutectic solvent made up of choline chloride-glycerol (1:2) was used for the extraction of flavonoids from Catharanthus roseus plant parts (flower petal, leaves, stem, and root). The highest amount of phenolic content was detected in flower petal, that is, 194.50 mg GAE/g. In DPPH test, the maximum amount of antioxidant activity determined in the flower petal was 73.13%; IC50 was calculated by using a linear regression equation; IC50 value of the standard, stem, root, leaf, and flower petal was 13.22, 90.44, 83.93, 120.14, 79.49 μg/ml, respectively. The result of this research is that Catharanthus roseus has a compatible antioxidant activity. This can be helpful for the treatment of diseases caused by free-radical oxidative stress.

Effect of Lawsonia inermis Linn. Ethanol Extract on the Superoxyde Dismutase Activity in Hyperglycemic Rattus norvegicus

Background: Alloxan causes experimental diabetic conditions (hyperglycemia) in experi­mental animals through oxidation and the formation of free radicals (oxidative stress) that damage pancreatic β cells. The ethanol extract of the henna leaves can decrease oxidative stress. The purpose of this study is to know the effect of ethanol extract of henna leaves to decrease blood sugar level and increase superoksida enzyme activity. Subjects and Methods: This study is an experimental study. The study design of posttest only control group design , using mice (Rattus norvegicus) strains of wistar, was randomized in five groups: negative control, positive control, group obtaining ethanol extract of henna leaves 200 mg/kg BW, 400 mg/kg BW and 600 mg/kg BW. Results: This study showed a significant reduction in blood glucose levels when compared to the control group. Superoxide dismutase enzyme activity increased but was not statistically significant. Conclusion: Ethanol extract of henna leaves 400 mg/kg BW significantly decreased mice blood glucose level, there was no significant difference in the increase of superoxide dis­mutase enzyme activity. Keywords: Alloxan, antioxidant, flavonoids, hyperglycemia, oxidative stress. Correspondence: Maya Anjelir Antika. Masters Program of Biomedic, Faculty of Medicine, University of North Sumatera. Indonesian Journal of Medicine (2017), 2(2): 79-85 https://doi.org/10.26911/theijmed.2017.02.02.01

Hepatoprotective activity of quercetin against paracetamol-induced liver toxicity in rats

Background Paracetamol (PCM) overdose induces hepatotoxicity in both humans and experimental animals. The pathogenesis and progression of PCM hepatic toxicity are associated with free radical injury and oxidative stress, which could be partially attenuated by antioxidants and free radical scavengers. Aim The present study was undertaken to examine the effects of quercetin on PCM-induced hepatic toxicity in rats. Material and methods In this experimental study, forty adult male rats were divided into four groups: control, quercetin, PCM groups, and the protective group that was pretreated with quercetin orally [50 mg/kg body weight (b.w.)] daily for 16 days and thereafter received both quercetin (same dose) and PCM (500 mg/kg b.w.) for another 5 days. Twenty-four hours after the administration of PCM, the rats were killed to measure serum hepatotoxic markers, levels of tumor necrosis factor-α, and oxidative stress biomarkers. Results Oral administration of PCM (500 mg/kg b.w.) for 5 days resulted in a significant elevation of liver enzymes in serum such as aspartate transaminase, alanine transaminase, alkaline phosphatase, and total bilirubin, and in levels of tumor necrosis factor-α as well as reducing hepatic total protein and albumin concentrations when compared with the results in the control group. As regards oxidative stress biomarkers, there were increased tissue levels of malondialdehyde and decreases in the activity of liver enzymes [superoxide dismutase, catalase, glutathione, glutathione peroxidase, and glutathione-s-transferase] in the group treated with PCM. All of these results were ameliorated by coadministration of quercetin. Conclusion These results suggest that the protective role of quercetin in the prevention of PCM-induced hepatic toxicity in rats was associated with a decrease of oxidative stress in hepatic tissues. However, clinical studies are warranted to investigate such an effect in humans.

(Z)-ligustilide increases ferroportin1 expression and ferritin content in ischemic SH-SY5Y cells

The mechanisms involved in the antioxidant and anti-apoptotic properties of (Z)-ligustilide (LIG) are not fully elucidated. Based on the accumulated data, we hypothesized that LIG might be able to reduce ischemia/reperfusion-induced increase in brain iron by regulating expression of iron transport proteins. We therefore investigated the effects of LIG on iron uptake protein transferrin receptor 1, iron exporter protein ferroportin 1, iron storage protein ferritin light chain and also hypoxia inducible factor-1 alpha (HIF-1 alpha) in oxygen-glucose deprivation/reoxygenation (OGD/R)-treated SH-SY5Y cells, using Western blot analysis. We demonstrated that LIG completely reversed the OGD/R-induced reduction of ferroportin 1, increased ferritin light chain content, and also suppressed the OGD-induced increase in HIF-1 alpha in SH-SY5Y cells. These findings imply that LIG might reduce the OGD/R-induced increase in brain iron by promoting cell iron release and iron corporation into ferritin, and also by inhibiting the HIF-1 alpha-induced increase in transferrin-bound iron uptake and iron accumulation in the brain, consequently attenuating iron-mediated free radical formation, oxidative stress and apoptosis.

Annihilation of Leishmania by daylight responsive ZnO nanoparticles: a temporal relationship of reactive oxygen species-induced lipid and protein oxidation.

Lipid and protein oxidation are well-known manifestations of free radical activity and oxidative stress. The current study investigated extermination of Leishmania tropica promastigotes induced by lipid and protein oxidation with reactive oxygen species produced by PEGylated metal-based nanoparticles. The synthesized photodynamic therapy-based doped and nondoped zinc oxide nanoparticles were activated in daylight that produced reactive oxygen species in the immediate environment. Lipid and protein oxidation did not occur in dark. The major lipid peroxidation derivatives comprised of conjugated dienes, lipid hydroperoxides, and malondialdehyde whereas water, ethane, methanol, and ethanol were found as the end products. Proteins were oxidized to carbonyls, hydroperoxides, and thiol degrading products. Interestingly, lipid hydroperoxides were produced by more than twofold of the protein hydroperoxides, indicating higher degradation of lipids compared to proteins. The in vitro evidence represented a significant contribution of the involvement of both lipid and protein oxidation in the annihilated antipromastigote effect of nanoparticles.

Clozapine and olanzapine are better antioxidants than haloperidol, quetiapine, risperidone and ziprasidone in in vitro models.

Although the etiopathogenic mechanisms of schizophrenia (SCZ) are unknown, evidences suggest that excessive free radical production or oxidative stress may be involved in the pathophysiology of SCZ. Antipsychotics are the drugs used in the treatment of SCZ but it remains controversial the impact that typical vs. atypical antipsychotics has on the oxidative stress status in SCZ patients. In vitro, the antioxidant capacity of six antipsychotics was assessed by their ability to: decrease or scavenge reactive oxygen species in the neutrophil respiratory burst; donate hydrogen and stabilize the free radical 2,2-diphenyl-1-picryl-hydrazyl (DPPH); and scavenge 2,2'-azino-di-(3-ethylbenzthiazoline-6-sulphonic acid) (ABTS(+)). This study demonstrated that both clozapine and olanzapine have antioxidant effects, in vitro, by scavenging superoxide anion on the respiratory burst, donating electron in the ABTS(+) assay and stabilizing the radical DPPH. Ziprasidone significantly scavenged ABTS(+) and stabilized the radical DPPH whereas risperidone significantly reduced the respiratory burst. Haloperidol and quetiapine lacked antioxidant effects. The chemical structure-related antioxidant capacity suggests a possible neuroprotective mechanism of these drugs on the top of their antipsychotic mechanism of action.

Iron function and dysfunction in the brain: A pediatric neurologist's perspective

Iron plays a critical role in brain development and physiology, cytoplasmic protein function, and mitochondrial reactions. Brain iron levels are regulated tightly, and pathologies can result from both iron deficiency (learning and memory deficits, neuronal and dendritic developmental alterations, impaired myelin function, and abnormal neurotransmitter regulation) and iron overload (free radical production and oxidative stress, as proposed for Parkinson and Alzheimer diseases as well as rare genetic disorders of iron accumulation). This review briefly summarizes the roles of iron in normal and abnormal brain function, with emphasis on the developing brain, and describes some disorders deriving from deficient or excessive iron levels.

ANTIOXIDANT AND CHEMOPREVENTIVE EFFECT OF AZADIRACHTA INDICA ON LEAD ACETATE INDUCED HEPATOTOXICITY IN RATS

Lead (Pb), a ubiquitous heavy metal is known to be injurious to all systems. Oxidative damage has been shown to be one of the principal mechanisms by which Pb causes toxicity. In this study, hepatic antioxidant status and markers of oxidative stress were assessed in experimental animals orally exposed to lead acetate (PbA) and was compared with groups treated with the methanolic extract of Azadirachta indica at 2 different doses.Seventy rats were used in this study. They were divided into 7 groups each containing 10 animals. Control group (group A) received water only. Group B, C and D were dosed 0.1% lead and was withdrawn after 6 weeks. On withdrawal, Group B received water only while groups C and D were treated with 100mg/kg and 200mg/kg of the methanolic extract of Azadirachta indica respectively for 6 weeks. Similarly, groups E, F, G were given 0.2% lead orally and was withdrawn after 6 weeks. On withdrawal, group E received water only while groups F and G were treated with 100mg/kg and 200mg/kg A. indica respectively for 6 weeks.Exposure of rats to lead acetate led to a significant (p<0.05) reduction in hepatic reduced Glutathione (GSH), Glutathione peroxidase (GPX) and Glutathione S‐ transferase. Similarly, Malondialdehyde (MDA) content increased (p<0.05) significantly in animals dosed PbA alone while there was a significant (p<0.05) reduction in rats treated with A. indica. There was significant (p<0.05) increase in nitric oxide (NO) and H2O2 concentrations in rats treated with PbA alone whereas treatment with A. indica led to significant (p<0.05) reduction in these markers of oxidative stress. Histology showed the presence of high periportal infiltration with inflammatory cells and focal necrosis in PbA treated groups but periportal infiltration was mild in Rats dosed with A. indica. In conclusion, animals exposed to PbA showed hepatotoxicity and disruption of antioxidant defence system through free radical generation and oxidative stress. Treatment of PbA exposed rats with A. indica led to significant amelioration of the hepatotoxicity induced by PbA. In conclusion, this study demonstrated the hepatoprotective effect of A. indica via antioxidant and free radical scavenging activities.Support or Funding InformationNone

Oxidative stress and antioxidant defence markers in muscle tissue of rainbow trout (Oncorhynchus mykiss) after vaccination against Yersinia ruckeri

Abstract Introduction: The goal of this study was to assess the influence of vaccination against enteric redmouth disease on oxidative stress biomarkers and antioxidant defence in the muscle tissue of rainbow trout (Oncorhynchus mykiss Walbaum) vaccinated against Yersinia ruckeri in the first and second month after immunisation. Material and Methods: Healthy fish were vaccinated orally with inactivated whole cells of a virulent strain of Y. ruckeri. One and two months after immunisation the muscle samples were collected. Results: No significant difference was noted in lipid peroxidation level in either the first or second month after vaccination, while aldehydic and ketonic derivatives of oxidatively modified proteins (OMB) in the vaccinated group were significantly lower in the second month compared to those in the first month after vaccination (P < 0.05). The content of ketonic derivatives of OMB in muscles in the first month after immunisation was higher compared to untreated control. All these culminated in a depletion of glutathione peroxidase (GPx) activity and low level of total antioxidant capacity (TAC). Conclusion: Correlations between catalase activity and lipid peroxidation and TAC confirmed the pivotal role of catalase in antioxidant defence during immunisation. From a broader perspective, it is suggested that immunisation of fish with Yersinia vaccine is associated with induced free radical formation and oxidative stress. Free radicals would therefore be at least partially responsible for the induction of both humoral and cellular elements of the immunity and increased protective immunity against Y. ruckeri infection.

Comparison of In vitro Antioxidant Activity of Olmesartan and Amlodipine

International Journal of Pharmacology and Clinical Sciences,2015,4,4,90-93.DOI:10.5530/ijpcs.4.4.4Published:Dec 2015Type:Research ArticleAuthors:Rajathilagam Thiruvengadam, and Seethalakshmi Sankar Author(s) affiliations:Rajathilagam Thiruvengadam* Seethalakshmi Sankar Department of Pharmacology, ESIC Medical College, Chennai, TamilNadu, INDIA. Abstract:Introduction: Free radical oxidative stress has been implicated in the pathology of a wide variety of clinical disorders. Antioxidants are agents which scavenge the free radicals and prevent the damage caused by them. Angiotensin II receptor blockers used in the treatment of hypertension, have also been reported to protect organs such as kidney and heart. Althoug, the mechanisms of these protective effects are not fully understood, it is generally thought that their antioxidant effects likely play a role. Amlodipine, a calcium channel blocker, seems to exert atheroprotective effects through its antioxidant properties related to its chemical structure and independent of its calcium channel-blocking effect. Though research has proved that olmesartan and amlodipine exhibit antioxidant activity independent of their antihypertensive effects, there are not many in vitro studies to analyse which drug is a better antioxidant. Objective: This in vitro study was done to compare the antioxidant activity of olmesartan and amlodipine. Materials and Methods: In this study, we demonstrated the antioxidant activities of 10 mg/ml stock solutions of olmesartan and amlodipine in vitro. DPPH (1,1 Diphenyl 2-picryl hydrazide) and Nitric oxide free radical scavenging assays were done. Results: Olmesartan showed significant (49.48%) and consistent free radical scavenging activity by DPPH and Nitric oxide radical scavenging assays. Free radical scavenging activity of amlodipine was more significant (56.89%) than olmesartan but was inconsistent and non-concentration dependent. Conclusion: Hence this in vitro study has proved that olmesartan has better antioxidant activity than amlodipine. Keywords:Amlodipine, DPPH, Free radicals, Nitric Oxide, Olmesartan, Oxidative StressView:PDF (431.09 KB) PDFClick here to download the PDF file. Images Free radical scavenging activity by DPPH assay

Oxidative stress and life histories: unresolved issues and current needs.

Life-history theory concerns the trade-offs that mold the patterns of investment by animals between reproduction, growth, and survival. It is widely recognized that physiology plays a role in the mediation of life-history trade-offs, but the details remain obscure. As life-history theory concerns aspects of investment in the soma that influence survival, understanding the physiological basis of life histories is related, but not identical, to understanding the process of aging. One idea from the field of aging that has gained considerable traction in the area of life histories is that life-history trade-offs may be mediated by free radical production and oxidative stress. We outline here developments in this field and summarize a number of important unresolved issues that may guide future research efforts. The issues are as follows. First, different tissues and macromolecular targets of oxidative stress respond differently during reproduction. The functional significance of these changes, however, remains uncertain. Consequently there is a need for studies that link oxidative stress measurements to functional outcomes, such as survival. Second, measurements of oxidative stress are often highly invasive or terminal. Terminal studies of oxidative stress in wild animals, where detailed life-history information is available, cannot generally be performed without compromising the aims of the studies that generated the life-history data. There is a need therefore for novel non-invasive measurements of multi-tissue oxidative stress. Third, laboratory studies provide unrivaled opportunities for experimental manipulation but may fail to expose the physiology underpinning life-history effects, because of the benign laboratory environment. Fourth, the idea that oxidative stress might underlie life-history trade-offs does not make specific enough predictions that are amenable to testing. Moreover, there is a paucity of good alternative theoretical models on which contrasting predictions might be based. Fifth, there is an enormous diversity of life-history variation to test the idea that oxidative stress may be a key mediator. So far we have only scratched the surface. Broadening the scope may reveal new strategies linked to the processes of oxidative damage and repair. Finally, understanding the trade-offs in life histories and understanding the process of aging are related but not identical questions. Scientists inhabiting these two spheres of activity seldom collide, yet they have much to learn from each other.

CHANGES IN GLUTATHIONE SYSTEM AND LIPID PEROXIDATION IN RAT BLOOD DURING THE FIRST HOUR AFTER CHLORPYRIFOS EXPOSURE.

Chlorpyrifos (CPF) is a highly toxic organophosphate compound, widely used as an active substance of many insecticides. Along with the anticholinesterase action, CPF may affect other biochemical mechanisms, particularly through disrupting pro- and antioxidant balance and inducing free-radical oxidative stress. Origins and occurrence of these phenomena are still not fully understood. The aim of our work was to investigate the effects of chlorpyrifos on key parameters of glutathione system and on lipid peroxidation in rat blood in the time dynamics during one hour after exposure. We found that a single exposure to 50 mg/kg chlorpyrifos caused a linear decrease in butyryl cholinesterase activity, increased activity of glutathione peroxidase and glutathione reductase, alterations in the levels of glutathione, TBA-active products and lipid hydroperoxides during 1 hour after poisoning. The most significant changes in studied parameters were detected at the 15-30th minutes after chlorpyrifos exposure.

Anti-Inflammatory and Gastroprotective Activities of C udrania Tricuspidata Leaf Extract Against Acute HCl/Ethanol-Induced Gastric Mucosal Injury in Sprague-Dawley Rats

We investigated the inhibitory effect of Cudrania tricuspidata ethanol 10% extract (CTL10) on gastric inflammation induced by acute ethanol treatment in Sprague-Dawley rats. After oral administration of CTL10 (100 or 300 mg/kg) for 7 days, acute gastric inflammation was induced by 70% ethanol and 0.15 M HCl. After 1 h of ethanol administration, the animals were sacrificed. Pretreatment with CTL10 showed attenuation of gastric mucosal injury, hemorrhages and gastric juice secretion induced by ethanol administration. Oral administration of CTL10 significantly decreased the levels of lipid peroxidation and increased superoxide dismutase activity. Additionally, pretreatment with 300 mg/kg CTL10 significantly decreased the expression of nuclear factor-κB, cyclooxygenase-2, interferon-γ, interleukin-6 and tumor necrosis factor-α compared with the gastric inflammation group. Based on this study, CTL10 may be considered a potential agent to control acute gastric inflammation induced by alcohol through the antioxidative effect of CTL10. Practical Applications Ethanol directly and dose-dependently impairs the gastric mucosal barrier, and the molecular mechanisms underlying ethanol-induced gastric inflammation remain incompletely understood. However, there is evidence that free radical production and oxidative stress play a major role in the pathogenesis of acute gastric inflammation by ethanol. We investigated the inhibitory effect of Cudrania tricuspidata ethanol 10% extract (CTL10) on gastric inflammation induced by acute ethanol treatment in Sprague-Dawley (SD) rats. We found that CTL10 has inhibitory effects on gastric inflammation induced by acute ethanol treatment in SD rats. Although the exact mechanism underlying these effects is unclear, the effects on acute gastric inflammation suggest a mechanism involving the antioxidant properties of C. tricuspidata. C. tricuspidata may be a new alternative for the clinical management of gastric inflammation while serving as an antioxidant against oxidative stress.

Role of oxidant stress in rheumatoid arthritis

Oxygen derived free radicals have been implicated in the causation of Rheumatoid arthritis (RA) [1].In this study, evidence of free radical injury and oxidative stress in patients with RA is compared with healthy subjects by estimating superoxide dismutase (SOD) and catalase, which are anti-oxidant enzymes in RBCs, Glucose 6 Phosphate Dehydrogenase (G 6 PD) in RBCs and serum Malon-di-aldehyde (MDA) levels. Serum MDA levels in RA could be used as a biochemical marker of disease activity and for monitoring the response to treatment. There was no definite correlation between enzyme levels of SOD, catalase and G 6 PD and disease activity.

Fish oil provides protection against the oxidative stress in pilocarpine model of epilepsy.

Temporal lobe epilepsy (TLE), the most common form of epilepsy is often resistant to pharmacological treatment. Neuronal loss observed in epileptic brain may be result of an overproduction of free radicals (oxidative stress). Oxidative stress is characterized by an imbalance between antioxidant defenses and oxidizing agents (free radicals), which can lead to tissue injury. The n-3 PUFAs are important for the development and maintenance of central nervous system functions. Research by our group has shown that chronic treatment with fish oil, immediately after status epilepticus (SE), exhibits both neuroprotective effects and effects on neuroplasticity. The main purpose of this research was to evaluate if fish oil exhibits a protective effect against oxidative stress. Animals were subjected to TLE model by pilocarpine administration. After 3h of SE they were randomly divided into the following groups: control animals treated daily with vehicle or with 85mg/kg of fish oil and animals with epilepsy treated daily with vehicle or with 85mg/kg of fish oil. After 90days, superoxide anion production, enzymatic activity of superoxide dismutase (SOD) and catalase (CAT) and protein expression of NAD(P)H oxidase subunits (p47(PHOX) and gp91(PHOX)) were analyzed. Our results showed evidences that reactive oxygen species are increased in animals with epilepsy and that fish oil supplementation could counteract it. Fish oil supplementation promoted protection against oxidative stress by multiple ways, which involved the reduction of activity and expression of NAD(P)H oxidase subunits and increased the activity and expression of antioxidants enzymes, contributing to well-known neuroprotective effect in epilepsy.