Increase In Free Radical Production Research Articles

Foliar treatment with melatonin modulates photosynthetic and antioxidant responses in Silybum marianum L. under salt stress

Salinity is a significant global environmental problem that alters the physiology and morphology of plants. Melatonin modulates several physiological activities in plants under various environmental stresses. However, the contribution of melatonin to stress tolerance in response to salinity remains yet unclear. Therefore, the present study was conducted to investigate the potential impact of melatonin on various physiological reactions and metabolic processes in milk thistle (Silybum marianum) exposed to salinity stress. Salinity causes a reduction in photosynthesis and an increase in free radical production, ultimately resulting in growth inhibition. To combat the adverse effects of salinity stress, milk thistle produced increased levels of antioxidant compounds compared with control group. However, this increase in antioxidant activity could not help the plant in tolerating salinity stress. Conversely, foliar treatment of 100 µM melatonin improved photosynthesis (Pn) 64 %, relative water contents RWC (30.8 %), photochemical efficiency 0.44, antioxidant activities, and seedling characteristics in salinity-exposed plants compared with those in the negative control. Moreover, treatment with 100 µM melatonin resulted in better salinity tolerance by enhancing physiological changes such as stomatal conductance, transpiration, CO2 concentration, photosynthesis, germination, and generation of reactive oxygen species and reducing the hydrogen peroxide concentration in milk thistle plants under salinity stress.

Oxidative metabolism of neutrophils in acute coronary syndrome.

Inflammation in acute coronary syndrome (ACS) involves neutrophil activation and oxidative stress. Here, we studied the production of reactive oxygen species (ROS) by neutrophils in ACS. The study included 42 patients, men and women aged 46-91 years with ischaemic heart disease (IHD), non-ST-segment elevation ACS and ST-segment elevation ACS. Neutrophil-derived ROS were quantified with double-step stimulated luminol-enhanced chemiluminometry. The specific indices of spontaneous and double-step stimulated chemiluminescence did not differ in the subgroups of IHD, non-ST-segment elevation ACS and ST-segment elevation ACS. The total double-step stimulated ROS production by neutrophils was significantly higher in ST-segment elevation ACS than in non-ST-segment elevation ACS and IHD. In ACS, special activation mechanisms of peripherical neutrophils were not triggered in our study. The significant increase in free radical production by neutrophils in acute myocardial infarction was presumably a consequence of an increase in their number.

Intranasal Nanotransferosomal Gel for Quercetin Brain Targeting: I. Optimization, Characterization, Brain Localization, and Cytotoxic Studies.

Numerous neurological disorders have a pathophysiology that involves an increase in free radical production in the brain. Quercetin (QER) is a nutraceutical compound that shields the brain against oxidative stress-induced neurodegeneration. Nonetheless, its low oral bioavailability diminishes brain delivery. Therefore, the current study aimed to formulate QER-loaded transferosomal nanovesicles (QER-TFS) in situ gel for QER brain delivery via the intranasal route. This study explored the impacts of lipid amount, edge activator (EA) amount, and EA type on vesicle diameter, entrapment, and cumulative amount permeated through nasal mucosa (24 h). The optimum formulation was then integrated into a thermosensitive gel after its physical and morphological characteristics were assessed. Assessments of the optimized QER-TFS showed nanometric vesicles (171.4 ± 3.4 nm) with spherical shapes and adequate entrapment efficiency (78.2 ± 2.8%). The results of short-term stability and high zeta potential value (-32.6 ± 1.4 mV) of QER-TFS confirmed their high stability. Compared with the QER solution, the optimized QER-TFS in situ gel formulation exhibited sustained release behavior and augmented nasal mucosa permeability. CT scanning of rat brains demonstrated the buildup of gold nanoparticles (GNPs) in the brains of all treatment groups, with a greater level of GNPs noted in the rats given the transferosomal gel. Additionally, in vitro studies on PCS-200-014 cells revealed minimal cytotoxicity of QER-TFS in situ gel. Based on these results, the developed transferosomal nanovesicles may be a suitable nanocarrier for QER brain targeting through the intranasal route.

Polyamine catabolism via spermine oxidase in the pathogenesis and treatment of hyperglycemia and diabetes mellitus-A short discussion

Diabetes mellitus can be described as chronic, endocrine dysfunction of pathophysiological regulation related to glucose and insulin. Hyperglycemia is the most common and intensely related complication of this dysfunction and has countless methods of pathogenicity. Hyperglycemia has the ability to exacerbate a degenerative positive feedback loop within critical tissues. Considering the fact that pancreatic hormonal regulation has played an increasingly considerable role in serum glucose homeostasis, here we begin a discussion into the implication of polyamine catabolism as a pathway with a mechanism that would contribute considerably to the necrosis and dysfunction of islet cells in the pancreas. The pathogenicity of this mechanism focuses on how the sustained increase in free radical production by hyperglycemic induction extenuates several complications in diabetes mellitus. The oxidation of spermine to spermidine produces hydrogen peroxide, as well as 3-aminopropanol (which spontaneously converts to acrolein) and spermidine (the precursor for the substrate of this reaction). This increase in reactive oxygen species exhibits the ability to inhibit autophagy and apoptosis as well as stimulate fat necrosis within the cells of the pancreas. Considering the islet cells of the pancreas play an extremely important role in glucose homeostasis, small changes in concentrations of these ROS are able to eliminate large regulatory factors while going undetected in the analysis of disease processes and therapeutics.

Redox imbalance in COVID-19 pathophysiology

BackgroundThe pathophysiologic significance of redox imbalance is unquestionable as numerous reports and topic reviews indicate alterations in redox parameters during corona virus disease 2019 (COVID-19). However, a more comprehensive understanding of redox-related parameters in the context of COVID-19-mediated inflammation and pathophysiology is required. MethodsCOVID-19 subjects (n = 64) and control subjects (n = 19) were enrolled, and blood was drawn within 72 h of diagnosis. Serum multiplex assays and peripheral blood mRNA sequencing was performed. Oxidant/free radical (electron paramagnetic resonance (EPR) spectroscopy, nitrite-nitrate assay) and antioxidant (ferrous reducing ability of serum assay and high-performance liquid chromatography) were performed. Multivariate analyses were performed to evaluate potential of indicated parameters to predict clinical outcome. ResultsSignificantly greater levels of multiple inflammatory and vascular markers were quantified in the subjects admitted to the ICU compared to non-ICU subjects. Gene set enrichment analyses indicated significant enhancement of oxidant related pathways and biochemical assays confirmed a significant increase in free radical production and uric acid reduction in COVID-19 subjects. Multivariate analyses confirmed a positive association between serum levels of VCAM-1, ICAM-1 and a negative association between the abundance of one electron oxidants (detected by ascorbate radical formation) and mortality in COVID subjects while IL-17c and TSLP levels predicted need for intensive care in COVID-19 subjects. ConclusionHerein we demonstrate a significant redox imbalance during COVID-19 infection affirming the potential for manipulation of oxidative stress pathways as a new therapeutic strategy COVID-19. However, further work is requisite for detailed identification of oxidants (O2•-, H2O2 and/or circulating transition metals such as Fe or Cu) contributing to this imbalance to avoid the repetition of failures using non-specific antioxidant supplementation.

Momordica charantia L. Fruit Fractions inhibit Malondialdehyde Level and Regenerate Hepatic Damage of Hyperglycemic Rats

BACKGROUND: Chronic hyperglycemia causes an increase of free radical production and in longterm, the hyperglycemia increases oxidative stress. Among medicinal plants, Momordica charantia L. fruit has been known to overcome hyperglycemia. However, role of M. charantia L. fruit on oxidative stress is not well understood. Therefore, current study was conducted to investigate the effect of M. charantia L. fruit extract on malondialdehyde (MDA) level and hepatic damage in hyperglicemic rat model.METHODS: Twenty five white rats (Rattus novergicus) were induced with Streptozotocin (STZ) and treated with/without glibenclamide, sodium carboxymethyl cellulose (Na-CMC), or M. charantia L. fruit ethanol/ethyl acetate/ n-hexane fraction. After the treatment, rat’s livers were collected and separated for histopathological examination and MDA analysis.RESULTS: The MDA level average of rats before the STZ induction was 1.37 μg/mL. MDA level average was markedly increased (23.85 μg/mL) in rats induced with STZ and treated with Na-CMC merely. The MDA level average of STZ-induced glibenclamide-treated rats was 3.12 μg/mL. Meanwhile, the MDA level averages of STZ-induced M. charantia L. fruit ethanol, ethyl acetate and n-hexane fractions-treated rats were 14.95, 8.98 and 5.37 μg/mL, respectively. The histopathology results of this study showed that adipocytes, dilated sinusoids and central vein thickening were mostly observed in STZ-induced Na-CMC-treated rats. Meanwhile, the STZ-induced ethanol/ethyl acetate/n-hexane fraction-treated rats did not exhibitthose expressions.CONCLUSION: M. charantia L. fruit fractions inhibit the MDA level average in liver tissue and regenerate hepatic damage of STZ-induced rats, especially the n-hexane fraction which could be a potential hepatic antioxidant and regenerative agent.KEYWORDS: Momordica charantia L., malondialdehyde, oxidative stress, hyperglycemia, diabetes mellitus

Possible Association of Smokeless Tobacco Dependent Impairment in the Erythrocytes and Platelets Membranes of Human Male Volunteers: An Observation.

Background:Smokeless tobacco (SLT) acts as a modifier of erythrocyte and platelet membranes by disrupting antioxidant system with the concomitant increase in free radical production and induction of apoptosis. Methods:The SLT users was that individuals used gutkha and khaini products (Khaleja/mahak chaini brand respectively) habitually, at least >20 times per week consists of 50-60 g during the last 2-4 years. Results:The gutkha and khaini users found to be significantly increased levels of iNOS (Inducible nitric oxide synthase) enzyme in plasma, erythrocytes, and platelet membranes when compared to normal controls. The gutkha and khaini users exhibited that the significant increase in the levels of gene expression of apoptotic proteins (Bcl2-B cell lymphoma gene 2, Bax, caspases 8, caspase 10, and caspase 12), IL-6 (Interleukin-6), and decreased levels of TNF-α (Tumor necrosis factor-alpha) and decreased expression of caspase 12 of khaini users were observed from blood samples. The significant increase in the concentrations of peroxynitrites (ONOO-), nitric oxide (NO) (Nitrates and nitrites), malondialdehyde (MDA), cholesterol, and phospholipids were reported in the smokeless tobacco users of erythrocytes and platelets. The experimental subjects showed that the increased osmotic fragility and decreased membrane fluidity of erythrocytes and platelets in comparison with non-tobacco users. The normal subjects had been exposed that the proper functioning of antioxidant enzymes and decreased enzyme activities of antioxidants were reported by SLT users. Conclusion:The smokeless tobacco products are exerted chronic damage to membranes of erythrocytes and platelets and elevation of apoptosis in the prolonged periods of human male volunteers.

Kemampuan Jus Jambu Biji Merah (Psidium Guajava L.) Dibanding Multivitamin 500 Mg Dalam Mempertahankan Antal Eritrosit Pasca Senam Aerobik High Impact Di Jurusan Jamu Politeknik Kementerian Kesehatan Surakarta

Background: One of important missions from American Collage of Sports Medicine (ASCM) is to support physical activity in community. During high impact physical activity, oxygen consumption in whole bodies are increasing 20 times. This increasing of oxygen consumption may lead to increase of free radical production that can cause cell damage. One of free radicals, Hydrogen peroxide causes damage in red blood cell (erythrocyte) membrane, with the result decreasing of red blood cell life time, moreover inducing anemia. Substance that can inhibit damage cell caused by free radical called antioxidant. Antioxidants are plentiful in fruit and vegetables, especially colorfull fruits and vegetables. One of fruit that well known as antioxidant source is red guava (Psidium guajava). Red guava containing lycopen which is has high antioxidant activity. The aim of this study is to understand effect of red guava juice treatment to red blood cell serum level in respondent who given physical activity. Standard of comparison in this study is vitamin C (zegavit 500 mg). Method: this study used quasi experiment, independent variable is vitamin C (zegavit 500 mg) and red guava juice treatment, dependent variable is red blood cell serum level. Results: The result of this study showed that there was no decreasing indication in red blood cells serum level of 3 groups. Conclusion: The conclusion in this study is there was no difference between red guava juice and vitamin C (zigavit 500 mg) treatment to avoid decreasing of red blood cells serum level after high impact physical activities.

In vitro cardiotoxicity evaluation of graphene oxide

Graphene is a two-dimensional (2D) monolayer of carbon atoms, tightly packed, forming a honey comb crystal lattice, with physical, chemical, and mechanical properties greatly used for energy storage, electrochemical devices, and in nanomedicine. Many studies showed that nanomaterials have side-effects on health. At present, there is a lack of information regarding graphene and its derivatives including their cardiotoxic properties. The aim of the present study was to evaluate the toxicity of nano-graphene oxide (nano-GO) in the rat cardiomyoblast cell line H9c2 and the involvement of oxidative processes. The cell viability was evaluated with the fluorescein diacetate (FDA)/propidium iodide (PI) and in the trypan blue exclusion assay, furthermore mitochondrial membrane potential and production of free radicals were measured. Genotoxicity was evaluated in comet assay and low molecular weight DNA experiment. Reduction of cell viability with 20, 40, 60, 80, and 100 μg/mL nano-GO was observed after 24 h incubation. Besides, nano-GO induced a mitochondrial hyperpolarization and a significant increase of free radicals production in the same concentrations. DNA breaks were observed at 40, 60, 80, and 100 μg/mL. This DNA damage was accompanied by a significant increase in LMW DNA only at 40 μg/mL. In conclusion, the nano-GO caused cardiotoxicity in our in vitro model, with mitochondrial disturbances, generation of reactive species and interactions with DNA, indicating the importance of the further evaluation of the safety of nanomaterials.

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.

Melatonin and human mitochondrial diseases.

Mitochondrial dysfunction is one of the main causative factors in a wide variety of complications such as neurodegenerative disorders, ischemia/reperfusion, aging process, and septic shock. Decrease in respiratory complex activity, increase in free radical production, increase in mitochondrial synthase activity, increase in nitric oxide production, and impair in electron transport system and/or mitochondrial permeability are considered as the main factors responsible for mitochondrial dysfunction. Melatonin, the pineal gland hormone, is selectively taken up by mitochondria and acts as a powerful antioxidant, regulating the mitochondrial bioenergetic function. Melatonin increases the permeability of membranes and is the stimulator of antioxidant enzymes including superoxide dismutase, glutathione peroxidase, glutathione reductase, and catalase. It also acts as an inhibitor of lipoxygenase. Melatonin can cause resistance to oxidation damage by fixing the microsomal membranes. Melatonin has been shown to retard aging and inhibit neurodegenerative disorders, ischemia/reperfusion, septic shock, diabetes, cancer, and other complications related to oxidative stress. The purpose of the current study, other than introducing melatonin, was to present the recent findings on clinical effects in diseases related to mitochondrial dysfunction including diabetes, cancer, gastrointestinal diseases, and diseases related to brain function.

Histopathological assessment of C57Bl/J mice organs exposed to tannery effluents

The effluent produced in tanneries can cause environmental damage and public health problems when disposed of improperly. However, few toxicological studies have evaluated the effects of the intake of tannery wastewater by mammals. The objective of this study is the histological assessment of organs of C57Bl/J mice exposed to the intake of different concentrations of raw tannery effluents, beginning with the hypothesis that these effluents can cause damage to the histological structure of the organs. The animals were divided into the following groups: control (0% effluent) and exposed to 0.1%, 1%, and 5% raw tannery effluent diluted in water, for a period of 120 days. For the histopathological evaluations, samples of the liver, kidney, spleen, heart, and lung were collected, fixed, and stained by the hematoxylin and eosin staining techniques. No anomalies were observed in kidney, spleen, heart, and lung fragments. Alterations were observed only in liver fragments. Moderate hydropic degeneration was detected in animals exposed to tannery effluents, mainly in the periportal space. A large number of necrotic hepatocytes (p<0.05) were detected, especially in animals exposed to higher tannery effluent concentrations. Further, the largest number of hepatocytes with karyomegaly (p<0.05) was observed in animals exposed to the highest effluent concentrations. Our study suggests that the observed alterations are related to the intake of tannery effluents and that these effluents cause changes that lead to an increase of free radical production and direct aggressions to hepatocyte membranes as well as to the appearance of hepatocellular karyomegaly.

Oxidative stress at different stages of two-step semen cryopreservation procedures in dogs

Sperm cryopreservation generates sperm damage and reduced fertilization capacity as a consequence of reactive oxygen species formation. Identifying the critical points of the process will contribute to the development of strategies for oxidative stress prevention. Therefore, the aim of this experiment was to verify the occurrence of oxidative stress during the two-step cryopreservation process in dogs. Six healthy mature dogs were used and submitted to the two-step sperm cryopreservation protocol. The sperm analysis was done at three time points: after refrigeration, after glycerolization, and after thawing by sperm motility, measurement of spontaneous and induced oxidative stress, sperm mitochondrial activity, plasma membrane integrity, flow cytometric evaluation of plasma and acrosome membrane integrity, mitochondrial membrane potential, and sperm chromatin structure assay. There was an increase in free radical production after glycerolization (87.4 ± 15.5 ng/mL of spontaneous thiobarbituric acid reactive substances (TBARS) after refrigeration and 1226.3 ± 256.0 ng/mL after glycerolization; P < 0.05), in association with loss of sperm mitochondrial activity. However, frozen-thawed samples had lower sperm motility, lower resistance to oxidative stress (448.7 ± 23.6 ng/mL of induced TBARS after glycerolization and 609.4 ± 35.9 ng/mL after thawing; P < 0.05) and increased lipid peroxidation (4815.2 ± 335.4 ng/mL of spontaneous TBARS after thawing; P < 0.05) as well as increased damage to plasma and acrosomal membranes, compared with refrigeration and glycerolization. In conclusion, the production of free radicals by sperm cells begins during glycerolization. However, sperm oxidative damage intensifies after thawing. Despite intracellular ice formation during cryopreservation, the increased production of reactive oxygen species can be the explanation of the decrease in sperm motility, reduced mitochondrial activity, and sperm plasma membrane and acrosomal damage.

Role of Mitochondrial Protein Quality Control in Oxidative Stress-induced Neurodegenerative Diseases.

Proteins are constantly exposed to environmental stressors such as free radicals and heat shock leading to their misfolding and later to aggregation. In particular mitochondrial proteins are challenged by reactive oxygen species (ROS) due to the oxidative metabolism of the organelle. Protein aggregation has been associated with a wide variety of pathological conditions called proteopathies. However, for the maintenance of protein and cellular homeostasis, mitochondria have developed an elaborate protein quality control system consisting of chaperones and ATP-dependent proteases, specifically employed to rescue this organelle from damage due to the accumulation of misfolded proteins and toxic aggregates. Aging is characterized by a general decline of mitochondrial functions, correlating with a decrease in mitochondrial protein quality control activity and an increase of free radical production. In particular in age-related diseases like neurodegeneration, a correlation between mitochondrial damage and disease onset has been established. In this review we summarize the current knowledge about mitochondrial protein quality control mechanisms in mammalian cells, with a special emphasis on the role in oxidative stress and in neurodegenerative diseases.

Effect of long-term intake of aspartame on serum biochemical parameters and erythrocyte oxidative stress biomarkers in rats

Aspartame is one of the most widely used artificial sweeteners globally. Data concerning acute toxicity of aspartame is controversial, and knowledge on its chronic effect is limited. The present study evaluates the effect of long-term intake of aspartame on serum biochemical parameters and erythrocyte antioxidant defence system in rats. Male Wistar rats, weighing 150–175 g, were randomly divided into one control group and three experimental groups. The control group received only drinking water, whereas the experimental groups were orally administered with aspartame at the concentrations of 50, 500 and 1000 mg/kg b.wt respectively for 180 days. Results showed that administration of aspartame (1000 mg/kg b.wt) caused a significant increase in the levels of serum total bilirubin (P < 0.05). The activity of glutathione peroxidase and glutathione reductase was significantly reduced in the erythrocytes of rats that had received aspartame (1000 mg/kg b.wt) (P < 0.05). Glutathione was significantly decreased in 500 mg/kg (P < 0.05) and 1000 mg/kg (P < 0.001) aspartame groups. It can be concluded from these observations that long-term consumption of aspartame leads to dose-dependent increase in free radical production and produces impairment in antioxidant status in erythrocytes mainly through alterations in glutathione-dependent system.

English

Aspartame (L- aspartyl- L-phenylalanine methyl ester) is one of the most widely artificial sweeteners consumed in so many products worldwide in various countries which added to a large variety of food, most commonly found in low calorie beverages. On metabolism in humans and experimental animals, aspartame is rapidly and completely metabolized to aspartic acid (40%), phenylalanine (50%) and methanol (10%). Methanol, a toxic metabolite is primarily metabolized by oxidation to formaldehyde and then to formate; these processes are accompanied by the formation of superoxide anion and hydrogen peroxide. This study focus is to understand whether the oral administration of aspartame (40 mg/kg b.w) for 15, 30 and 90 days have any effect on the antioxidant status (enzymatic and non-enzymatic) in immune organs such as the spleen, thymus, lymph nodes and bone marrow of rats. To mimic human methanol metabolism, folate deficient rats were used. After 15 days of aspartame administration, animals showed a significant increase in free radical production as indicated by the increase in both enzymatic (superoxide dismutase, catalase, glutathione peroxidase) and non-enzymatic (reduced glutathione and vitamin C) antioxidant level along with the marked increase in lipid peroxidation and nitric oxide level. However, after repeated long term administration (30 and 90 days), the generation of reactive free radicals overwhelmed the antioxidant defense as indicated by an increase in lipid peroxidation with the decrease in antioxidants level. This study concludes that administration of aspartame even at the Food and Drug Administration permitted level its repeated exposure causes oxidative stress by altering the oxidant/antioxidant balance in immune organs of the rats and its effects also reflected in the histology of the spleen and lymph nodes Key words: Aspartame, folate- deficient, immune organs, oxidative stress.

Antioxidant dynamics in the live animal and implications for ruminant health and product (meat/milk) quality: role of vitamin E and selenium

The global population is predicted to grow to over 9 billion by the middle of 21st century, with 70% of people living in urban areas, and food demand is projected to grow by 70% by 2050. Climate change presents a series of challenges for global animal agriculture. As a result of thermal challenges associated with climate variability, availability of quality pasture, animal behaviour, physiological and immunological functions are potentially impacted. Oxidative status plays an important role in the regulation and maintenance of several physiological and immunological functions of the body. Ruminants are exposed to several environmental and metabolic challenges that can trigger oxidative stress. In this scenario, it is possible for an increase in free radical production and a depletion of antioxidant reserves, resulting in damage to lipids, proteins and DNA. Since oxidative stress can affect animal health and the quality of their products (meat/milk), antioxidant supplementation of ruminant diets represents a useful tool to sustain redox homeostasis when the ruminants are exposed to oxidative stress. This paper will examine the roles that oxidative stress plays in some physiological functions, and it will discuss the implications of antioxidant supplementation on ruminant health and production. Physiological levels of dietary antioxidants underpin efficient energy utilisation, optimal antioxidant potential, and balanced mitochondrial function to enhance protein deposition without impacting animal health. The research conducted over the last decade has improved the understanding of physiological functions of antioxidants, with selenium and vitamin E receiving particular attention. There is evidence that the functions of selenium and vitamin E extend beyond the classical antioxidant properties to immunomodulation especially when administered at higher doses than recommended. Improving the oxidative status of ruminants will play an important role in delivering high-quality milk and meat products to consumers. Considering the growing awareness among consumers of the benefits of antioxidant-rich food, there is a great opportunity for the livestock industries to focus on producing antioxidant-enriched milk and meat products or functional foods. Therefore, the premise of this paper is to review the recent developments in understanding antioxidant dynamics in ruminants and their role in reducing the impact of environmental stress and metabolic diseases. In addition, the paper will explore the putative implications that antioxidant supplementation has on the quality animal products and how the improved understanding can be best utilised to achieve efficient and sustainable animal production systems to ensure quality animal products for human consumption.

The Effects of Levosimendan Exposure on Oxidant/Antioxidant Status and Trace Element Levels in the Pulmonary Artery of Rats

We investigated both the effect of levosimendan and the role of oxidant/antioxidant status and trace element levels in the pulmonary artery of rats. Fourteen male Wistar albino rats were randomly divided into two groups of seven animals each. Group 1 was not exposed to levosimendan and served as a control. Levosimendan (12 μg/kg) diluted in 10 ml 0.9 % NaCl was administered intraperitoneally to group 2. Animals of both groups were killed after 3 days, and their pulmonary arteries were harvested to determine changes in tissue oxidant/antioxidant status and trace element levels. The animals in both groups were killed 72 h after the levosimendan exposure treatment, and pulmonary arteries were harvested to determine levels of the lipid peroxidation product MDA and the antioxidant GSH as well as the decreased activity of antioxidant enzymes such as SOD, GSH-Px and CAT. It was found that MDA levels increased in pulmonary artery tissues of rats after levosimendan administration. The GSH level decreased in the pulmonary artery of rats after levosimendan treatment. Co, Mn, Fe, Cd and Pb levels were significantly higher (P < 0.001) and Mg, Zn and Cu levels significantly lower (P < 0.001) in the levosimendan group compared to the control group. These results suggest that levosimendan treatment caused an increase in free radical production and a decrease in antioxidant enzyme activity in the pulmonary artery of levosimendan-treated rats. It also caused a decrease or increase in the levels of many minerals in the pulmonary artery, which is an undesirable condition for normal pharmacological function.

Cell cycle arrest, extracellular matrix changes and intrinsic apoptosis in human melanoma cells are induced by Boron Neutron Capture Therapy

Boron Neutron Capture Therapy (BNCT) involves the selective accumulation of boron carriers in tumor tissue followed by irradiation with a thermal or epithermal neutron beam. This therapy is therefore a cellular irradiation suited to treat tumors that have infiltrated into healthy tissues. BNCT has been used clinically to treat patients with cutaneous melanomas which have a high mortality. Human normal melanocytes and melanoma cells were treated with BNCT at different boronophenylalanine concentrations for signaling pathways analysis. BNCT induced few morphological alterations in normal melanocytes, with a negligible increase in free radical production. Melanoma cells treated with BNCT showed significant extracellular matrix (ECM) changes and a significant cyclin D1 decrease, suggesting cell death by necrosis and apoptosis and cell cycle arrest, respectively. BNCT also induced a significant increase in cleaved caspase-3 and a decrease in the mitochondrial electrical potential with selectivity for melanoma cells. Normal melanocytes had no significant differences due to BNCT treatment, confirming the data from the literature regarding the selectivity of BNCT. The results from this study suggest that some signaling pathways are involved in human melanoma treatment by BNCT, such as cell cycle arrest, ECM changes and intrinsic apoptosis.

Juniperus communis Linn oil decreases oxidative stress and increases antioxidant enzymes in the heart of rats administered a diet rich in cholesterol

It has been asserted that consumption of dietary cholesterol (Chol) raises atherosclerotic cardiovascular diseases and that Chol causes an increase in free radical production. Hypercholesterolemic diet has also been reported to cause changes in the antioxidant system. In our study, different doses of Juniperus communis Linn (JCL) oil, a tree species growing in Mediterranean and Isparta regions and having aromatic characteristics, were administered to rats; and the levels of antioxidant enzymes superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), catalase (CAT), and thiobarbituric acid reactive substances assay (TBARS) were examined in the heart tissue of rats. In this study, 35 Wistar Albino male adult rats weighing approximately 250-300g were used. The rats were divided into five groups of seven each. The control group was administered normal pellet chow, and the Chol group was administered pellet chow including 2% Chol, while 50 JCL, 100 JCL, and 200 JCL groups were administered 50, 100, and 200mg/kg JCL oil dissolved in 0.5% sodium carboxy methyl cellulose, respectively, in addition to the pellet chow containing 2% Chol, by gavage. After 30days, the experiment was terminated and the antioxidant enzyme activities were examined in the heart tissue of rats. While consumption of dietary Chol decreases the activities of SOD, GSH-Px, and CAT in heart tissue of rats (not significant), administeration of 200mg/kg JCL oil in addition to Chol led to a significant increase in the activity of antioxidant enzymes. Administering Chol led to a significant increase in TBARS level. Administering 100 and 200mg/kg JCL oil together with Chol prevented significantly the increase in lipid peroxides. As a result of the study, JCL oil showed oxidant-antioxidant effect in the heart tissue of rats.