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Oxidative Stress in the Development of Genetic Generalised Epilepsy: An Observational Study in Southern Indian Population.

Oxidative stress resulting from excessive generation of Reactive Oxygen Species (ROS) plays a significant role in neurodegeneration associated with seizures/epilepsy.

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Deciphering the toxic effects of organochlorine pesticide, dicofol on human RBCs and lymphocytes.

Organochlorine pesticides have generated growing concern owing to their diverse toxicities. In this connection, we have evaluated toxic potential of an acaricide, dicofol (DCF) and its harmful effects on human RBCs and lymphocytes. DCF caused hemolysis and rupture of human erythrocytes as confirmed by scanning electron microscopy (SEM). Significant increase in protein oxidation, lipid peroxidation, ROS production, methemoglobin formation with enhanced activities of superoxide dismutase and catalase but decreased level of reduced glutathione were observed as a result of DCF exposure to human erythrocytes. SEM showed significant DCF induced alterations in RBCs from normal discoid shape to echinocytes. Similarly, lymphocytes showed membrane damage, formation of membrane blebs and distorted cell morphology. In vitro comet assay indicated a significant DNA fragmentation in human lymphocytes upon DCF exposure. These results strongly suggest that DCF induces oxidative stress in RBCs via generation of ROS and alters the cellular architecture directly and indirectly.

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In vivo assessment of polydatin, a natural polyphenol compound, on arsenic-induced free radical overproduction, gene expression, and genotoxicity.

Arsenic (As) is a well-known contaminant of global groundwater. Its exposure causes several hazardous effects on animals and human via oxidative stress. The present study examined the effect of polydatin (PD) on free radical overproduction in rats exposed to As. Thirty-five male rats randomly allocated into five equal groups. To the control group, physiological saline was given orally and to the second group only 100 mg/L As was given by drinking water for 60 days. The other groups were treated with As (100 mg/L) and PD orally at 50, 100, and 200 mg/kg/day, respectively. Treatment with As enhanced malondialdehyde level but decreased glutathione level in blood, liver, kidney, brain, lung, and heart of rats. Also, As decreased superoxide dismutase and catalase activities of erythrocyte, liver, kidney, brain, lung, and heart in rats. Furthermore, As treatment gave rise to increased DNA damage and gene expressions of interleukin 1 beta (IL-1β), nuclear factor kappa beta (NFκB), p53, and tumor necrosis factor-α (TNF-α) in the lung, brain, kidney, and liver. However, treatment of PD ameliorated As-exposed lipid peroxidation, antioxidant enzymes activities, DNA damage, gene expressions, and histopathological changes in tissues. In conclusion, PD has a dose-dependent protective effect on lipid peroxidation and antioxidant defense mechanism in rats against As exposure.

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DNA (cytosine 5) methyltr Anti AGO2 Human, Monoclon Anti AGO2 Mouse, Monoclon Anti AGO2 Human, Monoclon Anti AGO2 Mouse, Monoclon Human Epstein-Barr Virus Mouse Epstein-Barr Virus TGF beta induced factor 2 Anti CML Monoclonal Antib Directed In Vivo Angiogen PARP in vivo Pharmacodyna Gene Expression: Mouse N

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Glycogen-gold nanohybrid escalates the potency of silymarin.

In this study, a glycogen-gold nanohybrid was fabricated to enhance the potency of a promising hepatoprotective agent silymarin (Sly) by improving its solubility and gut permeation. By utilizing a facile green chemistry approach, biogenic gold nanoparticles were synthesized from Annona reticulata leaf phytoconstituents in combination with Sly (SGNPs). Further, the SGNPs were aggregated in glycogen biopolymer to yield the therapeutic nanohybrids (GSGNPs). Transmission electron microscopy, UV-Vis spectroscopy, X-ray diffraction, and Fourier transform infrared spectroscopy analysis confirmed the successful formation and conjugation of both SGNPs and GSGNPs. The fabricated nanohybrids showed significant protection against CCl4-induced hepatic injury in Wistar rats and maintained natural antioxidant (superoxide dismutase and catalase) levels. Animals treated with GSGNPs (10 mg/kg) and SGNPs (20 mg/kg) retained usual hepatic functions with routine levels of hepatobiliary enzymes (aspartate transferase, alanine transaminase, alkaline phosphatase, and lactate dehydrogenase) and inflammatory markers (interleukin-1β and tumor necrosis factor-α) with minimal lipid peroxidation, whereas those treated with 100 mg/kg of Sly showed the similar effect. These results were also supported by histopathology of the livers where pronounced hepatoprotection with normal hepatic physiology and negligible inflammatory infiltrate were observed. Significant higher plasma Cmax supported the enhanced bioavailability of Sly upon GSGNPs treatment compared to SGNPs and free Sly. Graphite furnace atomic absorption spectrophotometry analysis also substantiated the efficient delivery of GSGNPs over SGNPs. The fabricated therapeutic nanohybrids were also found to be biocompatible toward human erythrocytes and L929 mouse fibroblast cells. Overall, due to increased solubility, bioavailability and profuse gut absorption; GSGNPs demonstrated tenfold enhanced potency compared to free Sly.

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Antioxidant and Protective Effects of Schinus terebinthifolius Raddi Against Doxorubicin-Induced Toxicity.

Doxorubicin is an anticancer drug whose toxic effects on non-cancer cells are associated with increased oxidative stress. This study investigated the chemical composition, antioxidant activity of the methanolic extract of Schinus terebinthifolius Raddi leaves (MESL) as well as effects against doxorubicin-induced toxicity in human erythrocytes, K562 human erythroleukemia cells, and mouse hearts. The chemical composition indicated the presence of phenolic compounds, flavonoids, tannins, and ascorbic acid. MESL showed antioxidant activity by scavenging free radicals and inhibiting hemolysis and lipid peroxidation in human erythrocytes incubated with an oxidizing agent, and was able to increase the enzymatic activity of superoxide dismutase and glutathione peroxidase in human erythrocytes, without influencing the activity of enzyme catalase. The increase of oxidative hemolysis and malondialdehyde levels in erythrocytes incubated with doxorubicin was reduced by treatment with MESL. The cytotoxic activity of doxorubicin in erythroleukemia cells treated with MESL was unmodified. Additionally, the extract protected mice against the doxorubicin-induced cardiotoxicity. In conclusion, the MESL exhibits antioxidant activity, reducing doxorubicin-induced oxidative stress without changing the anticancer action of the drug, and protects against doxorubicin-induced cardiotoxicity. Hence, these findings suggest that these effects are via anti-oxidative by inhibiting free radicals, decreased oxidative stress, and increased antioxidant enzyme activity.

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Differences of lipid membrane modulation and oxidative stress by digoxin and 21-benzylidene digoxin.

Cardiotonic steroids (CTS) are compounds which bind to the Na,K-ATPase, leading to its inhibition and in some cases initiating signaling cascades. Long utilized as a treatment for congestive heart disease, CTS have more recently been observed to inhibit proliferation and cause apoptosis in several cancer cell lines. A synthetic derivative of the CTS digoxin, called 21-benzylidene digoxin (21-BD), activates the Na,K-ATPase rather than cause its inhibition, as its parent compound does. Here, the mechanism behind the unique effects of 21-BD are further explored. In HeLa cancer cells, low (5µM) and high (50µM) doses of 21-BD activated and inhibited the Na,K-ATPase, respectively, without altering the membrane expression of the Na,K-ATPase. While digoxin did not affect HeLa membrane cholesterol or phospholipid content, 50µM 21-BD increased both lipids via a mechanism reliant on an intact cell. Afterwards, the direct action of 21-BD was evaluated on erythrocyte membranes; however, no effect was observed. As CTS may generate reactive oxygen species (ROS) which can affect plasma membrane fluidity and therefore Na,K-ATPase activity, several markers involved in ROS generation were analyzed such as, lipid peroxidation (TBARS), reduced glutathione (GSH), catalase (CAT) and superoxide dismutase (SOD). GSH content and catalase activity were unaffected by digoxin or 21-BD. Surprisingly, TBARS and SOD activity was decreased with digoxin and with 50µM 21-BD. Thus, 21-BD and digoxin altered components involved in ROS generation and inhibition in a similar fashion. This study suggests alterations to the Na,K-ATPase and membrane lipids by 21-BD is not reliant on ROS generation.

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Oxidative stress and glutathione S-transferase genetic polymorphisms in medical staff professionally exposed to ionizing radiation.

Ionizing radiation (IR) is considered as a diagnostic and therapeutic tool in medicine. However, chronic occupational exposure of medical staff to IR may affect the antioxidant status and, as a result, DNA damage and cancers as well. The objective of our study was to evaluate the oxidative stress profile caused by IR in 29 Tunisian medical staff from radiology and radiotherapy departments, and to find an association between the GSTM1 null, GSTT1 null, and GSTP1 Ile105Val polymorphisms and oxidative stress biomarkers.

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Bisphenol A, bisphenol S, bisphenol F and bisphenol AF induce different oxidative stress and damage in human red blood cells (in vitro study).

Bisphenol A (BPA) and its analogs are widely used in the production of various everyday use products, which leads to a common exposure of humans to these substances. The effect of bisphenols on oxidative stress parameters has not been described in detail in non-nucleated cells, therefore, we have decided to evaluate the impact of BPA and its analogs, i.e. bisphenol S (BPS), bisphenol F (BPF) and bisphenol AF (BPAF) on reactive oxygen species (ROS) formation, lipid peroxidation, glutathione (GSH) level and the activities of superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GSH-Px) in human erythrocytes. The erythrocytes were incubated with the compounds studied in the concentrations ranging from 0.1 to 500μg/ml for 1, 4 or 24h. It has been found that bisphenols enhanced ROS (including •OH) formation, depleted GSH level, increased lipid peroxidation and changed the activities of SOD, CAT and GSH-Px. It has been noted that the strongest alterations in ROS formation, lipid peroxidation and the activity of antioxidant enzymes were induced by BPAF, which changed CAT and SOD activity even at 0.5μg/ml. It has also been shown that BPA caused the strongest changes in GSH level, while BPS, which is the main BPA substituent in the manufacture did not alter most parameters studied.

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Variations in Oxidative Stress Levels in 3 Days Follow-up in Ultramarathon Mountain Race Athletes.

Spanidis, Y, Stagos, D, Orfanou, M, Goutzourelas, N, Bar-or, D, Spandidos, D, and Kouretas, D. Variations in oxidative stress levels in 3 days follow-up in ultramarathon mountain race athletes. J Strength Cond Res 31(3): 582-594, 2017-The aim of the present study was the monitoring of the redox status of runners participating in a mountain ultramarathon race of 103 km. Blood samples from 12 runners were collected prerace and 24, 48, and 72 hours postrace. The samples were analyzed by using conventional oxidative stress markers, such as protein carbonyls (CARB), thiobarbituric acid reactive substances (TBARS), total antioxidant capacity (TAC) in plasma, as well as glutathione (GSH) levels and catalase (CAT) activity in erythrocytes. In addition, 2 novel markers, the static oxidation-reduction potential marker (sORP) and the capacity oxidation-reduction potential (cORP), were measured in plasma. The results showed significant increase in sORP levels and significant decrease in cORP and GSH levels postrace compared with prerace. The other markers did not exhibit significant changes postrace compared with prerace. Furthermore, an interindividual analysis showed that in all athletes but one sORP was increased, whereas cORP was decreased. Moreover, GSH levels were decreased in all athletes at least at 2 time points postrace compared with prerace. The other markers exhibited great variations between different athletes. In conclusion, ORP and GSH markers suggested that oxidative stress has existed even 3 days post ultramarathon race. The practical applications from these results would be that the most effective markers for short-term monitoring of ultramarathon mountain race-induced oxidative stress were sORP, cORP, and GSH. Also, administration of supplements enhancing especially GSH is recommended during ultramarathon mountain races to prevent manifestation of pathological conditions.

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