Source Of Free Radicals Research Articles

Effect of marigold leaf on hemoglobin levels on Wistar rat expossed cigarette smoking

Background: cigarette smoke is one of the source of free radicals. The influence of free radicals can be suppressed through antioxidant administration. The marigold leaves contain phenolic as antioxidants. This study aims to determine the effect of marigold leaves on hemoglobin levels of the blood of rats exposed to cigarette smoke. Method: the samples were divided into 3 groups (the control group and the treatment group 1 and 2). While the treatment group 1 and 2 were given the exposure to cigarette smoke by giving marigold leaves at a dose of 4.5 grams and 6.3 grams. Blood sampling was carried out on days 0, 7 and 14, measuring the blood sample parameters using the Hematology Analyzer Sysmex KX-21®. Data were analyzed with One Way Anova test, and posthoc the Duncan test. Results: there was a significant effect between the control group against the treatment group 1 and 2 ( p <0.05). There were no significant differences between marigold leaves groups with a dose of 4.5 grams and 6.3 in increasing hemoglobin levels ( p <1.00). Conclusion: there was significant effect of marigold leaf on hemoglobin levels expossed cigarette smoking at a dose of 4.5 gram and 6.3 gram.

Optimization Of Natural Body Scrub Formulation Based On Oilseed Press Cake Of Nyamplung (Calophyllum Inophyllum L) Using D-Optimal Mixture Experimental Design

UV light and air pollution are sources of free radicals that can trigger skin problems. Skin problems can be overcome by using skin treatments that contain antioxidant compounds so that oxidation reactions derived from free radicals can be inhibited (Halliwell and Gutteridge, 2000). Skin care that can overcome skin problems is body scrub preparation. Body scrub cream-based preparations consists of oil and water phase, emulgator, and abrasives. Oilseed press cake or residual product of nyamplung (tamanu) oil (Calophyllum inophyllum L.) has characteristics as an abrasiver and reported degree of hydrolysis that can counteract free radicals using the DPPH method through a % RSA value of 39.82%. Oilseed press cake of nyamplung will be developed as a raw material for the formulation of body scrub that have added value. Body scrub formulation was done by optimizing the emulgator material (stearic acid and triethanolamine) using Expert Design software D-Optimal and the optimal emulgator concentration was obtained (stearic acid 3% and triethanolamine 1%) and physical in stability of the optimum formulation is tested in 28 days in 1,2,3 and 4 week at room temperature by looking at the parameters of organoleptic physical properties, pH, viscosity, spreadability, and adhesion test. Based on physicaly examination, it showed that the formula of oilseed press cake of nyamplung body scrub for 28 days at room temperature is a semi-solid, brown color and smells of apple, pH value is 7,647 ± 0.128; the viscosity value is 3.633.33 ± 152.75 dPas; spreadability is 3,87 ± 0.20 cm, and adhesiveness is 2,3 ± 0,04 second.

Inflammaging: inflammation and oxidative stress as a cause of aging and cognitive decline

According to the theory of inflammaging, aging of the body and the development of age-related diseases are a consequence of a chronic progressive generalized inflammatory process that develops and persists throughout life under the influence of negative factors of an infectious and non-infectious nature. Inflammaging has a number of features that distinguish it from acute inflammation: a chronic nature of inflammation, a low level of inflammation, blurry clinical state (in the early stages of clinical manifestations there may not be any at all). The key pathogenetic role in inflammation plays age-associated changes in the innate immune system, which are referred to in the English literature as “immunosenescence” and oxidative stress. The main source of reactive oxygen species and free radicals in the cells are mitochondria. With age, the concentration of intracellular glutathione, one of the main factors of the antioxidant protection of the cell, decreases and a pathological condition arises in which the rate of production of free radicals and reactive oxygen species significantly exceeds the antioxidant capabilities, which leads to the formation of oxidative stress and disruption of the structure and function of cells. Oxidative stress, inflammation and neuroinflammation are closely related to cognitive impairment, pathological state that is often observed in a group of elderly and senile patients. Further study of the pathogenesis of Inflammaging and the role of oxidative stress in it will potentially lead to development of methods to slow down aging and treat age-related cognitive impairments.

Redox-related biomarkers in physical exercise

Research in redox biology of exercise has made considerable advances in the last 70 years. Since the seminal study of George Pake's group calculating the content of free radicals in skeletal muscle in resting conditions in 1954, many discoveries have been made in the field. The first section of this review is devoted to highlight the main research findings and fundamental changes in the exercise redox biology discipline. It includes: i) the first steps in free radical research, ii) the relation between exercise and oxidative damage, iii) the redox regulation of muscle fatigue, iv) the sources of free radicals during muscle contractions, and v) the role of reactive oxygen species as regulators of gene transcription and adaptations in skeletal muscle.In the second section of the manuscript, we review the available biomarkers for assessing health, performance, recovery during exercise training and overtraining in the sport population. Among the set of biomarkers that could be determined in exercise studies we deepen on the four categories of redox biomarkers: i) oxidants, ii) antioxidants, iii) oxidation products (markers of oxidative damage), and iv) measurements of the redox balance (markers of oxidative stress). The main drawbacks, strengths, weaknesses, and methodological considerations of every biomarker are also discussed.

Czynniki determinujące status oksydacyjno-antyoksydacyjny i jego odpowiedź na wysiłek fizyczny

Nasilenie przemian metabolicznych podczas wysiłku fizycznego sprzyja powstawaniu wolnych rodników i reaktywnych form tlenu, co może zaburzać równowagę oksydacyjno-antyoksydacyjną w kierunku stresu oksydacyjnego. Warunki te sprzyjają uszkodzeniu struktur komórkowych, przyczyniając się do zmęczenia i spadku zdolności wysiłkowych. W pracy omówiono wysiłkowe źródła wolnych rodników tlenowych oraz obronę antyoksydacyjną ustroju, jak też czynniki wpływające na nasilenie powysiłkowego stresu oksydacyjnego. W kolejnej części przedstawiono wyniki badań dotyczących efektywności podawania suplementów antyoksydacyjnych w warunkach wysiłkowych, głównie na przykładzie polifenoli zielonej herbaty. Zwrócono też uwagę na potencjalne zagrożenia związane z przyjmowaniem suplementów antyoksydacyjnych w nadmiernych ilościach. Wynika to z faktu, iż reaktywne formy tlenu odgrywają ważną rolę jako przekaźniki sygnałów komórkowych, umożliwiając uzyskanie adaptacji do wysiłku fizycznego i wzrost zdolności wysiłkowych w odpowiedzi na trening sportowy (siły, wytrzymałości). W dalszej części omówiono czynniki genetyczne warunkujące poziom enzymatycznej obrony antyoksydacyjnej i wrażliwość na stres oksydacyjny, główną uwagę skupiając na polimorfizmach genów kodujących enzymy antyoksydacyjne. Przedstawiono zależność pomiędzy polimorfizmem genu mitochondrialnej dysmutazy ponadtlenkowej (enzymu stanowiącego pierwszą linię obrony przed szkodliwym wpływem wolnych rodników tlenowych na organizm) a zmianami parametrów równowagi oksydacyjno-antyoksydacyjnej w odpowiedzi na trening sportowy. Na koniec podkreślono użyteczność oznaczeń wspomnianego powyżej polimorfizmu w selekcji sportowców podatnych na stres oksydacyjny, w celu indywidualizacji zaleceń żywieniowych dotyczących podaży antyoksydantów w diecie lub w postaci suplementów.

The Protective Antioxidant Effects of Sulforaphane on Germinating Radish Seeds Treated with Hydrogen Peroxide

Free radical chain reactions result when atoms containing unpaired electrons bind with biomolecules and alter their biological functions, contributing to the progression of diseases such as atherosclerosis, cancer, and diabetes. Antioxidants, such as vitamin E and sulforaphane, are effective neutralizers of free radicals and prevent cellular damage. This present study is conducted to determine the relative effectiveness of sulforaphane against free radicals generated by hydrogen peroxide (H2O2) compared with the known antioxidant vitamin E. In this experiment, H2O2 is a source of free radicals and germinating radish seeds are models to test the protective effects of antioxidants against free radicals. Generally, H2O2 diffuses into the cell and dissociates to form hydroxyl radicals through Fenton reactions. Based on current literature, the hypothesis is that sulforaphane is more effective than vitamin E in inhibiting free radicals from 1% H2O2 on germinating radish seeds due to its activation of different antioxidant pathways compared to vitamin E’s direct neutralization of free radicals. The 1% H2O2-treated radish seeds show lower germination rates than seeds treated with sulforaphane and vitamin E with 1% H2O2. Furthermore, the germination rate is higher in sulforaphane with 1% H2O2-treated seeds compared to vitamin E and 1% H2O2 treated seeds. In summary, these experiments show sulforaphane is more effective than vitamin E in neutralizing the free radical effects of H2O2 on radish seed germination. These results point to sulforaphane’s potential use as a dietary supplement to counteract free radical effects on cellular levels, helping to prevent the progression of certain diseases.

Mitochondria as Source of Free Radicals and Reactive Oxygen Species

Mitochondria as Source of Free Radicals and Reactive Oxygen Species

Method to Improve Azo-Compound (AAPH)-Induced Hemolysis of Erythrocytes for Assessing Antioxidant Activity of Lipophilic Compounds

We examined the method of oxidative hemolysis for assessment of antioxidant activity of various compounds, especially lipophilic compounds. 2,2'-Azobis(amidinopropane) dihydrochloride (AAPH) was used as the source of free radicals for the oxidative hemolysis of horse erythrocytes. We found that absorbance at 540 nm is not appropriate for monitoring AAPH-induced hemolysis. Instead, we should use absorbance at 523 nm (an isosbestic point), because AAPH oxidizes the oxygenated hemoglobin to methemoglobin and absorbance at 540 nm does not correctly reflect the amount of released hemoglobin by AAPH-induced hemolysis. The corrected method of AAPH-induced hemolysis was applicable to assess the antioxidant activity of various hydrophilic compounds such as ascorbic acid, (-)-epicatechin, and edaravone. For the assessment of antioxidant activity of lipophilic compounds, we need appropriate dispersing agents for these lipophilic compounds. Among several agents tested, 1,2-dimiristoyl-sn-glycero-3-phosphocholine (DMPC) liposome at a concentration of 0.34 mM was found to be useful. Exogenous α-tocopherol incorporated using DMPC liposome as a dispersing agent was shown to protect erythrocytes from AAPH-induced hemolysis in a concentration-dependent manner.

Hyaluronic Acid Improves Hydrogen Peroxide Modulatory Effects on Calcium Channel and Sodium-Potassium Pump in 4T1 Breast Cancer Cell Line.

Maintaining homeostasis of ion concentrations is critical in cancer cells. Under hypoxia, the levels of channels and pumps in cancer cells are more active than normal cells suggesting ion channels as a suitable therapeutic target. One of the contemporary ways for cancer therapy is oxidative stress. However, the effective concentration of oxidative stress on tumor cells has been reported to be toxic for normal cells as well. In this study, we benefited from the modifying effects of hyaluronic acid (HA) on H2O2, as a free radical source, to make a gradual release of oxidative stress on cancer cells while preventing/decreasing damage to normal cells under normoxia and hypoxic conditions. To do so, we initially investigated the optimal concentration of HA antioxidant capacity by the DPPH test. In the next step, we found optimum H2O2 dose by treating the 4T1 breast cancer cell line with increasing concentrations (0, 10, 20, 50,100, 200, 500, and 1000 μM) of H2O2 alone or H2O2 + HA (83%) for 24 hrs. The calcium channel and the sodium-potassium pumps were then evaluated by measuring the levels of calcium, sodium, and potassium ions using an atomic absorption flame spectrophotometer. The results revealed that treatment with H2O2 or H2O2+ HA led to an intracellular increase of calcium, sodium, and potassium in the normoxic and hypoxic circumstances in a dose-dependent manner. It is noteworthy that H2O2 + HA treatment had more favorable and controllable effects compared with H2O2 alone. Moreover, HA optimizes the antitumor effect of oxidative stress exerted by H2O2 making H2O2 + HA suitable for clinical use in cancer treatment along with chemotherapy.

Effect of Kele Honey (Trigona Sp) in Malondyaldehide and Superoxide Dismutase Serum and Hepatic Tissue of White Rats (Rattus Norvegicus) Exposed to Cigarettes Smoke

Cigarette smoke contains more than 4000 constituents including tar, nicotine, carbonic monoxide, heavy metals, etc.Cigarette smoke is a source of exogenous free radicals. The accumulation of free radicals causes an imbalance of the endogenous antioxidant body system triggering oxidative stress as a risk factor for various degenerative diseases. The purpose of this study was to determine the effect of giving stingless bee honey to of malondialdehyde (MDA) and superoxide dismutase (SOD)levels in serum and hepatic tissue as a marker of oxidative stress in white rats exposed to cigarette smoke. This study was an experimental study with a posttest only control group design. This research was conducted in vivo at the Integrated Biomedical Laboratory, Faculty of Medicine, Udayana University. The research sample was 30 adult male Wistar rats aged 12-14 weeks, weight 200-400 gr. In this study the sample divided into 2 groups, the control group (exposed to cigarette smoke for 4 weeks of research but not given honey) and the treatment group (exposed to cigarette smoke and given stingless bee honey (Kele-honey) for 4 weeks as well). Statistical analysis using SPSS statistics program, the test used was the average comparative analysis by T-independent test(Mann WhitneyTest for nonparametric) to compare MDA and SOD means of rat serum and hepatic tissue exposed to cigarettes smoke. The results showed that the mean of MDA serum among the control group was 0.2247 ± 0.1192, and among the treatment group was 0.2394 ± 01058, ( p>0.05). The mean of MDA hepatic tissue among the control group was 0.5951 ± 0.1029, and among the treatment group was 0.6721 ± 0.6721, (p>0.05). The results showed that the mean of SOD serum among the control group was 1.0724 ± 0.3446, and among the treatment group was 0.6166 ± 0.2841, (p<0.05). The mean of SOD hepatic among the control group was 1.0174 ± 0.3249, and among the treatment group was 0.6721 ± 0.0847, (p<0.05). The result indicated that mean of MDA both in serum and hepatic, of the treatment group higher than the control group, the differences are not significant. Whereas, the mean of SOD both in serum and hepatic, of the intervention group lower than the control group, the differences are significant.

The Role of Oxidative Stress in Early Brain Injury after Subarachnoid Hemorrhage

This review focuses on the problem of oxidative stress in early brain injury (EBI) after spontaneous subarachnoid hemorrhage (SAH). EBI involves complex pathophysiological mechanisms, including oxidative stress. In the first section, we describe the main sources of free radicals in EBI. There are several sources of excessive generation of free radicals from mitochondrial free radicals’ generation and endoplasmic reticulum stress, to hemoglobin and enzymatic free radicals’ generation. The second part focuses on the disruption of antioxidant mechanisms in EBI. The third section describes some newly found molecular mechanisms and pathway involved in oxidative stress after EBI. The last section is dedicated to the pathophysiological mechanisms through which free radicals mediate early brain injury.

Consider Optimizing Glutathione Levels in COVID-19 Symptomatic Patients

Hypothesis: Optimizing glutathione status in symptomatic COVID-19 patients may prevent the development of more severe aspects of the disease During the inflammatory phase in symptomatic COVID-19 patients the oxidant stress has the potential to be massive The observed cytokine storm is a source of free radicals that can cause a major oxidant stress, which in turn leads to a self-fueling vicious cycle of cytokine-mediated oxidant injury SARS-CoV-2 virus uses the angiotensin-converting enzyme 2 (ACE2) receptor to invade the cell ACE2 activation induces an antioxidant response by activating Nrf2 and inhibiting NFκB Nrf2 promotes production of glutathione that could reduce NFκB activation and consequently reduce generation of cytokines Could the glutathione status of individuals account for the unexplained variability in clinical presentations of COVID-19? Elderly subjects are the hardest hit by COVID-19 Beyond their comorbidities, they exhibit a slower protein metabolism explaining the lower level of plasma glutathione reported in this population Obesity is an aggravating factor observed in deaths occurring in elderly and younger COVID-19 patients Beyond the comorbidities such as diabetes, hypertension, cardiovascular diseases associated with obesity, the metabolic syndrome reported in these subjects is associated with lower glutathione levels and oxidant stress Optimizing glutathione levels should be considered in symptomatic subjects with proven COVID-19 Following the action of endogenous gamma-glutamyltranspeptidase, plasma glutathione is an efficient source of substrates for de novo tissue synthesis of glutathione The injection of glutathione might be contemplated in these patients Although injectable glutathione is not yet available on the market, N-acetylcysteine (NAC) could be considered It is an existing and approved form of bioavailable cysteine limiting substrate for glutathione synthesis In a recent review on NAC in COVID-19, the Center for Evidence Based Medicine (University of Oxford, UK) concluded that preclinical data suggest that NAC may have a purpose in viral respiratory infections doi: xxxxx

Detection and identification of ethanal-derived spin-trapped free radicals using headspace thermal desorption gas chromatography-mass spectrometry (TD-GC-MS)

In this study, we demonstrate a novel approach to the detection and identification of the products of spin-trapped free radicals. Hydroxyl free radicals were generated by Fenton-based chemistry in the presence of ethanal and the spin-trapping agent N-tert-butyl-α-phenylnitrone (PBN). The resulting volatile compounds present in the reaction vial headspace were collected using thermal desorption (TD) and analysed by gas chromatography-mass spectrometry (GC-MS). Eleven compounds were detected in the headspace, and their identification was aided by using either a fluorinated or deuterated analogue of PBN as an alternative spin trap and/or deuterated ethanal (CD3CHO) as the secondary source of free radicals. The electron-ionisation (EI) mass spectra clearly demonstrate the “capture” of methyl radicals; two of the compounds detected were identified as containing one methyl group derived from ethanal, and four were shown to contain two methyl groups. This study demonstrates that sampling the reaction headspace using TD-GC-MS is a viable method for analysing products of free radical trapping, and potentially may be applied to a wide range of free radical systems.

Asymptomatic hyperuricemia: are we passing the problem?

Hyperuricemia is a laboratory phenomenon of persistent increase in serum uric acid concentration (above 420 μmol/l). This condition precedes gout, but only in every 5 cases does hyperuricemia develop into gout. The main pathogenic factor in this disease is not uric acid, but the enzyme xanthine oxidase. In treatment, it is important to block it as a source of free radicals, and then we can improve the prognosis in patients. Today, there is no doubt about the association of hyperuricemia with obesity, metabolic syndrome, diabetes, heart failure, hyperlipidemia and hypertension. For example, hypertension in healthy patients occurs with a frequency of 6.39 %, with hyperuricemia, this figure increases to almost 50 %, and in patients with gout – up to 73.9 %. Asymptomatic hyperuricemia is not considered treatable, although ultrasound studies have shown that sodium monourate crystals (MUN) are deposited in soft tissues and joints. Their presence is a marker of asymptomatic hyperuricemia. Therefore, experts have recently begun to talk about a new stage of gout. If earlier we listed asymptomatic hyperuricemia, acute gout attack, intermittent gout and chronic tofus gout, now we are talking about an additional second stage - asymptomatic hyperuricemia with the deposition of MUN crystals. The path from hyperuricemia to chronic gout can take up to 11 years, but after 4 years can develop kidney damage and decreased glomerular filtration rate, after 6 years - hypertension, and after 10 years – heart failure. So is it worth waiting for the development of chronic gout or perhaps you should start treatment for hyperuricemia earlier?

Antioxidant Activity Tests of Extract of Principle Crafts (Phaleria macrocarpa)

Phaleria macrocarpa contains secondary metabolite compounds such as alkaloids, terpenoids, saponins, polyphenols, tannins, sterols, and coumarins. Those metabolites are antioxidants and can be efficacious in the healing of various degenerative diseases such as cervical cancer and diabetes. This plant is widely grown in Tindaki Village, Parigi Mautong, Central Sulawesi. The aim of this study was to determine the antioxidant power of those phaleria macrocarpa fruit extract. This study was conducted by using maceration extraction technique with ethanol as solvent, and compound 2,2-difenil-1-picrilhidrazil (DPPH) as source of free radical, and vitamin C as the positive control. The UV-Vis spectrophotometer was used to measure the absorbance of the extract. Various concentrations of the extract used were 5 ppm, 15 ppm, 25 ppm, and 35 ppm. The results showed that the IC50 value of the fruit extract was 28.242 ppm, while the IC50 value of vitamin C was 19.302 ppm. These IC50 values show that vitamin C was a stronger antioxidant activity than the fruit extract, but the fruit extract was still as a very strong natural antioxidant category.

Selenium and L-carnitine protects from valproic acid-Induced oxidative stress and mitochondrial damages in rat cortical neurons

Oxidative stress and mitochondrial dysfunction have been associated with valproic acid (VPA) induced neurotoxicity. Mitochondria are vulnerable to oxidative damage and are also a major source of superoxide free radicals. Therefore, the need for mitochondrial protective and antioxidant agents for reducing valporic acid toxicity in central nerve system (CNS) is essential. In the present study, we investigated the potential beneficial effects of sodium selenite (SS) and L-carnitine (LC) against valproic acid -induced oxidative stress and mitochondrial dysfunction in isolated rat cortical neurons. Valproic acid (50, 100 and 200 µM) treatment caused a significant decrease in cellular viability, which was accompanied by increases in reactive oxygen species (ROS) generation, GSSG and GSH content, lipid peroxidation and lysosomal and mitochondrial damages. Sodium selenite (1 µM) and L-carnitine (1 mM) pretreatment attenuated valproic acid-induced decrease in cell viability. In addition, sodium selenite (1 µM) and L-carnitine (1 mM) pretreatment significantly protected against valproic acid-induced raise in oxidative stress, mitochondrial and lysosomal dysfunction, lipid peroxidation levels and depletion of GSH content. Our results in the current study provided insights into the protective mechanism by L-carnitine and sodium selenite, which is liked, to neuronal ROS generation and mitochondrial and lysosomal damages.

Mitochondrial Oxidative and Nitrosative Stress and Alzheimer Disease.

Oxidative and nitrosative stress are widely recognized as critical factors in the pathogenesis and progression of Alzheimer disease (AD) and its earlier stage, amnestic mild cognitive impairment (MCI). A major source of free radicals that lead to oxidative and nitrosative damage is mitochondria. This review paper discusses oxidative and nitrosative stress and markers thereof in the brain, along with redox proteomics, which are techniques that have been pioneered in the Butterfield laboratory. Selected biological alterations in—and oxidative and nitrosative modifications of—mitochondria in AD and MCI and systems of relevance thereof also are presented. The review article concludes with a section on the implications of mitochondrial oxidative and nitrosative stress in MCI and AD with respect to imaging studies in and targeted therapies toward these disorders. Taken together, this review provides support for the notion that brain mitochondrial alterations in AD and MCI are key components of oxidative and nitrosative stress observed in these two disorders, and as such, they provide potentially promising therapeutic targets to slow—and hopefully one day stop—the progression of AD, which is a devastating dementing disorder.

In vitro analysis of the activity of human monoamine oxidase type B (hMAOB), treated with the cyanotoxin anatoxin-a: supposed factor of neurodegenerative diseases

In this study, we investigated the hypothesis that an additional source of free radicals may be hydrogen peroxide formed by monoamino oxidase (MAO) -catalyzed deamination of catecholamines. Also, increased MAO-B activity in the brain has been linked to the development of some neurodegenerative diseases. The toxicant we used to treat recombinant human MAO-B enzyme is the cyanotoxin аnatoxin-a. For anatoxin-a is known that it’s an agonist of neuronal acetylcholine receptors with 20 times greater affinity to them compared to the natural neurotransmitter. In this study, we analyzed the effect of anatoxin at various selected concentrations on the activity of recombinant human MAO-B enzyme. The method we use is to analyze the activity of human MAO-B with the fluorimetric reagent Amplex UltraRed and the substrate tyramine hydrochloride. The aim of this study is to analyze the effect of anatoxin-a on the hMAO-B enzyme activity and its influence as a factor for the development and progression of neurodegenerative diseases.

Abstract 485: Mito-Targeted Antioxidant Superior to Non-Targeted Isoform in Modulating Energy Metabolism and Preventing Cardiovascular Remodelling in Spontaneously Hypertensive Rat

Hypertension induced left ventricular hypertrophy (LVH) augments the risk of cardiovascular anomalies. Oxidative stress leads to the activation of the hypertrophic program with a metabolic switch from fatty acid to glucose oxidation. Mitochondria, the major source of free radicals, exhibit alterations in hypertensive heart diseases. Targeted antioxidants are expected to reduce mitochondrial reactive oxygen species more effectively than general antioxidants. This study was designed to assess whether mito-targeted antioxidant, MitoTempol is more effective than general oxidant, Tempol on hypertension, hypertrophy and cardiac energy metabolism. Spontaneously Hypertensive Rat were administered either Tempol (20mg/kg/day) or Mito Tempol (2mg/kg/day) orally for 30 days. Post treatment, animals were subjected to 2D-echocardiography. The Myocardial lysates were subjected to Insolution digestion followed by RPLC - LTQ-Orbitrap-MS analysis. Mid-ventricular sections were probed for markers of energy metabolism and fibrosis. The beneficial effect on cardiovascular structure and function was significantly higher for Mito Tempol. Increase in mitochondrial antioxidants and stimulation of fatty acid metabolism with significant improvement in cardiovascular function was apparent in SHR treated with Mito Tempol. The study indicates that Mito Tempol is superior to its non- targeted isoform in preventing hypertension induced LVH, and the beneficial effects on heart are possibly mediated by reversal of metabolic remodelling.

Efficient Coupling of Reaction Pathways of Criegee Intermediates and Free Radicals in the Heterogeneous Ozonolysis of Alkenes.

In the gas phase, ozonolysis of olefins is known to be a significant source of free radicals. However, for heterogeneous and condensed phase ozone reactions, the importance of reaction pathways that couple Criegee intermediates (CI) with hydroxyl (OH), alkoxy, and peroxy free radicals remains uncertain. Here we report experimental evidence for substantial free radical oxidation during the heterogeneous reaction of O3 with cis-9-tricosene (Tri) aerosol. A kinetic model with three coupled submechanisms that include O3, CI, and free radical reactions is used to explain how the observed Tri reactivity and its product distributions depend upon [O3], [OH], and the presence of CI scavengers. During multiphase ozonolysis, the kinetic model predicts that only ∼30% of the alkene is actually consumed by O3, while the remaining ∼70% is consumed by free radicals that cycle through pathways involving CI. These results reveal the importance of free radical oxidation during heterogeneous ozonolysis, which has been previously difficult to isolate due to the complex coupling of CI and OH reaction pathways.