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The effect of high strain on the oxidative stress relaxation of several natural rubber vulcanizates has been investigated. In peroxide and CBS accelerated vulcanizates, the rate of stress relaxation increases with increasing strain, and this increase appears to be due to an increase in the rate of oxidation of the network. TMTD and MBT vulcanizates showed marked premature failure at high strains and no oxidative stress relaxation measurement could be made. The tensile strength of a TMTD vulcanizate was at least 20 per cent higher in vacuum than in oxygen, due, it is believed, to stress-induced oxidative degradation at the tip of surface flaws in the rubber.

The purpose of this present study was to differentiate transudates and exudates in pleural effusions. Oxidative stress has been associated with various respiratory disorders. Ninety patients of pleural effusions of diverse etiologies were participated in this study. Subjects underwent diagnostic thoracentesis and standard biochemical parameters (total protein, lactate dehydrogenase, glucose, MDA levels) were measured in pleural fluid and serum. MDA, total protein, lactate dehydrogenase (LDH), glucose levels in plural fluid were higher in exudates compared to transudates (p < 0.001). Total protein pleural fluid/ total protein serum ratio, LDH pleural fluid/LDH serum ratio and MDA pleural fluid/MDA serum ratio were raised in exudates compared to transudates (p < 0.001). The present study showed that oxidative stress was more in exudates compared to transudates, probably due to the production of reactive oxygen species and it may serve as a marker for differentiation between transudates and exudates in clinical practice. Key Words: Exudates, Melondialdehyde, Oxidative Stress, Pleural Effusion, Transudates   doi:10.3329/sjps.v1i1.1806 S. J. Pharm. Sci. 1(1&2): 38-43

The effect of elevated levels of UV-β radiation in the vegetation experiment was studied. The object of the study was barley Zazersky 85 varieties, changes in the content of ascorbic acid and glutathione were revealed. It is known that even a small increase in the intensity of UV-β radiation can have a significant impact on the plant growth, development, photosynthetic and biochemical reactions. UV rays induce various DNA damage, and also contribute to the formation of free radicals in cells that cause lipid peroxidation of biological membranes. The existence of a plant cell in oxidizing conditions is possible only through the development of antioxidant defense mechanisms system. Particular attention is paid in this regard to ascorbic acid - vitamin C and glutathione. Ascorbic acid and glutathione are not considered separately, but as a redox pair to ensure the redox tone of the cell. In some reactions they can act independently of each other participating in a signaling system to transmit information in response to stress. Plants were grown in vessels containing 4.5 kg of air-dry soil. The repetition is sixfold (six vessels in each variant). As a source of UV-β irradiation were used LER-40 luminescent erythemal lamps (Russia). Plants were irradiated from the seedling stage to full ripeness from 10 to 14 h. Additional to solar UV-β irradiation levels are expressed in terms of the daily biologically effective dose taking into account the generalized spectrum of action for higher plants. The differences in the activity of oxidative processes and antioxidant protection depending on the stress degree have been established. The dose-dependent UV-β irradiation increase in the MDA content in the leaves indicates a pronounced oxidative stress due to a decrease in the efficiency of the photoreactivation process and the repair of DNA damage, which is caused by the partial shielding of the low-intensity UV radiation of area A in the greenhouse, which resulted in a decrease in biomass.

Alpha-lipoic acid, a dithiol compound derived from octanoic acid, which acts as a coenzyme for several redox reactions in almost all the tissue of the body. It retains its protective functions in both oxidized and reduced forms. Alpha-lipoic acid reduces oxidative stress by redox generation of other antioxidants such as vitamin C, E and increasing the intracellular glutathione. Exogenous alpha-lipoic acid has been shown to increase ATP production due to its role in the oxidation of pyruvate and alpha-ketoglutarate in the mitochondria. Alpha-lipoic acid administration has been shown to be effective in preventing pathology in various experimental models in which reactive oxygen species have been implicated. Key words: Antioxidant, free radical, alpha-lipoic acid DOI: 10.3329/bjms.v8i3.3982 Bangladesh Journal of Medical Sciences Vol.8(3) 2009 p46-51

Back ground: Lycopene, 40 carbon acyclic carotenoid containing 11 conjugated double bonds, is a phytochemical found in tomatoes and other red fruits. Oxygen derived free radicals are the most reactive species and as an antioxidant lycopene has a singlet oxygen quenching ability twice as high as that of ?-carotene and 10 times higher that of ?-tocoferol, lycopene participate in a host of chemical reactions to protect critical cellular biomolecules including lipid, proteins and DNA. Materials and Methods: The present study include 30 subjects having oxidative stress, age between 40-60 years, nonsmoker, with no history of chronic systemic illness and no medication were taken as patients.30 patients matched healthy subjects were taken as control. All subjects were selected from outpatient department of NSCB Medical College Jabalpur M.P. After estimation of base line antioxidant enzyme and vitamins, we supplement 180 gm of tomato (products like soup, paste. ketchup) contain 12 mg of lycopene to the patient group. After 60 days of lycopene supplementation oxidative stress biomarkers like SOD, GPX, GR, GSH, lipid peroxidation product MDA and other antioxidant vitamins A, vitamin C, vitamin E were estimated in patient's blood sample. Results: The main result of the study revealed that lipid per oxidation product MDA was found to be decreased significantly but after lycopene supplementation levels were improved. The results of SOD , GPX, GR, GSH,Vitamin A ,Vitamin E and Vitamin C were significantly increased after lycopene supplementation, it indicates the improved antioxidant profile after the supplementation of lycopene. Conclusion: There was a significant decrease in oxidative stress after the supplementation of lycopene therefore the study suggest that body's internal production of antioxidant is not enough to neutralize all free radicals, so increased dietary intake of antioxidant lycopene in the form of tomato products is beneficial, which is easily available in developing country like India. Key Words: Oxidative stress; Lycopene; MDA; GSH; SOD; Vitamin C; Vitamin E DOI: http://dx.doi.org/10.3329/bjms.v10i4.9500 BJMS 2011; 10 (4): 275-279

Lycopene, a carotenoid rich in tomato fruit (ripe), is an effective antioxidant and free radical scavenger. In this study n-hexane extract of tomato was evaluated for its protective action against oxidative stress in experimental myocardial infarction induced by administration of adrenaline in rats. Adrenaline produced significant elevation of malondialdehyde content of heart, an indicator of lipid peroxidation, with a significant rise in serum aspartate aminotransferase (AST) level and different grades of necrotic changes in myocardium. Rats were treated with two doses of n-hexane extract of tomato, intragastrically daily for one month prior to administration of adrenaline on the 31 st and 32 nd day. Pretreatment of tomato extract (1 mg/kg, 2 mg/kg) and vitamin E (50 mg/kg) significantly reduced the malondialdehyde concentration in heart and significantly lowered the serum AST level in adrenaline treated rats. Myocardial necrosis was significantly prevented by pretreatment. These results suggest that n-hexane extract of tomato possesses antioxidative property that may protect heart against catecholamine induced myocardial infarction. Â Â Â Â Â Â Keywords: Adrenaline; Myocardial infarction; Rat; Tomato Online: 29-1-2009 DOI:Â 10.3329/bmrcb.v34i3.1974 Bangladesh Med Res Counc Bull 2008; 34: 104-108.

The study investigated the effects of various levels of isoflavone aglycone-enriched fermented soybean meal (FSBM) on the redox status, serum hormones and milk quality of ewes from late pregnancy to early lactation. Twenty Chongming White ewes were chosen and divided into four treatment groups (n = 5): basal diet without FSBM (CON); basal diet with 2% (FSBM2); 4% (FSBM4); and 6% FSBM (FSBM6) replacing equal amounts of soybean meal (SBM). At parturition, maternal serum, the placenta and colostrum were collected. At day 21 of lactation, maternal serum and milk were collected. Results showed that, compared with CON, feeding ewes with FSBM6 reduced the concentrations of hydrogen peroxide (H2O2) and 8-hydroxy-2-deoxyguanosine (8-OHdG), and increased the activity of superoxide dismutase (SOD) and total antioxidant capacity (T-AOC) concentration in the placenta. At parturition and day 21 of lactation, the serum SOD activity and T-AOC concentration in FSBM4 and FSBM6 were higher than those in CON. Furthermore, the concentration of serum 8-iso prostaglandin (8-ISO-PGF2α) was markedly lower in FSBM6 than in CON. Serum prolactin (PRL), insulin-like growth factor 1 (IGF-1) and epidermal growth factor (EGF) concentrations were increased in FSBM4 and FSBM6 compared with CON. PRL concentration was increased in FSBM2. FSBM4 increased the levels of fat, protein, lactose, IgA, IgG and IgM in colostrum and milk. In conclusion, feeding ewes with FSBM from late pregnancy to early lactation seemed to increase maternal and placental anti-oxidative capacity, and improve serum hormones and milk quality. Considered overall, the level of 4% supplementation is recommended.Keywords: Milk contents, oxidative stress, placenta, serum parameters

Introducción: En la actualidad casi todos los esfuerzos para prevenir las enfermedades crónicas no transmisibles (ECNT) a nivel poblacional, se han centrado en promover comportamientos saludables como el ejercicio, la actividad física, el consumo de frutas y verduras, y el desestimular el consumo de tabaco y alcohol en la población adulta, pero los resultados han sido poco alentadores. En los últimos años, múltiples estudios han señalado la relación entre alteraciones del crecimiento fetal y el desarrollo de ECNT en la edad adulta. Más recientemente, se ha propuesto que factores maternos (función endotelial, estrés oxidativo y alteraciones en adipoquinas) y placentarios (disfunción mitocondrial) pueden ser mecanismos precursores de alteraciones metabólicas fetales y del desarrollo posterior de ECNT y que intervenciones como el ejercicio físico y la complementación con micronutrientes durante la gestación podrían regular dichos factores maternos y placentarios. Objetivo: Realizar una revisión de la literatura para verificar el papel del ejercicio físico y los micronutrientes durante la gestación sobre factores maternos y placentarios relacionados con ECNT del adulto. Metododología: Se utilizaron las siguientes bases de datos: Medline, Scielo, EMBASE, Science Direct, Cochrane Central Register of Controlled Trials y The Cochrane Libraryp Pregnancy, fetal development, oxidative stress, vascular endothelium, mitochondrial, adipokines, micronutrients, exercise. Resultados: El estrés oxidativo, como mecanismo central de otros eventos fisiopatológicos (alteración en los niveles de adipoquinas, disfunción endotelial y mitocondrial), tiene un papel importante en la programación fetal de ECNT, factores como la complementación con micronutrientes y el ejercicio físico, durante la gestación, podrían modular este estado y contribuir posiblemente a la prevención temprana de ECNT. Conclusión: Se debe establecer si los mecanismos moleculares y fisiológicos propuestos están relacionados con alteraciones metabólicas fetales y si la complementación durante la gestación con micronutrientes y/o el ejercicio físico los pueden regular. Introduction: Currently, most efforts to prevent nontransmissible chronic diseases at population level have centered on promoting healthy behaviors like physical activity, consumption of fruits and vegetables, and discouraging from the consumption of tobacco and alcohol in the adult population, but the results have been less than hopeful. During recent years, a number of studies have indicated the relation between metabolic alterations and fetal growth with the development of nontransmissible chronic diseases in adult age. More recently, it has been proposed that maternal factors (endothelial function, oxidative stress, and alterations in adipokynes) and placental factors (mitochondrial dysfunction) are the precursory mechanisms of fetal metabolic alterations and of the later development of nontransmissible chronic diseases. Also, it has been suggested that possibly supplementation with micronutrients and physical exercise during gestation could regulate these maternal and placental factors. Aim: To conduct a literature review to verify the role of physical exercise and micronutrients during pregnancy on placental and maternal factors related to nontransmissible chronic diseases in adults. Methods: Medline, SciELO, Embase, Science Direct, Cochrane Central Register of Controlled Trials, and the Cochrane Library were used in the last 10 years (1998-2008). The following topics were reviewed: pregnancy, fetal development, oxidative stress, vascular endothelium, mitochondrial dysfunction, adipokines, micronutrients, and exercise. Results: Oxidative stress, as the central pathophysiological event, such as changes in levels of adipokynes, mitochondrial and endothelial dysfunction, plays an important role in fetal programming of chronic diseases and factors such as micronutrient supplementation and physical exercise during pregnancy could modulate this state in a charity institution aiding in the early prevention of chronic diseases. Conclusion: To clarify whether the proposed molecular and physiological mechanism items are related to metabolic abnormalities and fetal complementation with micronutrients during pregnancy and/or regular physical exercise.

Oksidatif stres kardiyovaskuler hastaliklarin pek coguyla iliskilidir ve reaktif oksijen turleri (ROS) damar endotel hucrelerinin sinyal transduksiyonunda onemli bir role sahiptir. Fluvastatinin dahil oldugu 3hidroksi-3 metil koenzim A (HMG-CoA) reduktaz inhibitorleri sadece plazma kolesterolunu dusurmekle kalmaz ayni zamanda da damar duvari uzerinde kardiyovaskuler komplikasyonlari azaltan kolesterol dusurucu etkiden bagimsiz direkt etkilere de sahiptir. Fluvastatinin dietiltiyokarbamik asit (DETCA) ile olusturulan oksidatif strese maruz kalmis izole tavsan karotid arterindeki etkileri ve yanitlar uzerinde Nωnitro L-arjinin (L-NA) ile nitrik oksit inhibisyonun iliskisi arastirilmistir. Her bir tavsandan dort arter segmenti kullanildi. Ringler, 3mM DETCA ile 30 dakika inkube edilmek suretiyle reaktif oksijen turlerine maruz birakildilar. Fluvastatin, DETCA inkubasyonundan 10 dakika once banyoya ilave edildi. Organ banyosunun birinde 10-4M L-NA kullanildi. Asetilkoline (ACh) karsi gevseme yanitlari ile fenilefrin (PE) ve serotonine (5-HT) kasilma yanitlari arastirildi. Damarlarda serotonine karsi kasilmalar ve duyarlilik DETCA’dan etkilenmedi. DETCA ile tedavi ACh gevsemeleri ve duyarligi azaltti. Bu etkiler fluvastatin ile engellendi. L-NA ile inkubasyon fluvastatin tarafindan olusturulan ACh gevsemelerindeki artisi geriye dondurdu. DETCA tedavisi goren ringlerde PE maksimum kasilma yanitlari ve duyarligi azaldi. Fluvastatin DETCA’nin neden oldugu PE kasilma yanitlarindaki azalmayi normalize etti. Sonuc olarak, fluvastatin izole karotid arterinde oksidatif stres altinda bozulan damar fonksiyonlarini lipid dusurucu etkisinden bagimsiz olarak iyilestirmektedir

Vitiligo is a common pigmentary disorder characterized by depigmented patches or macules caused by the destruction of melanocytes. The pathogenetic mechanisms involved in vitiligo have not been completely clarified. Oxidative stress and reduced circulating antioxidants could be important phenomena in the pathophysiology of vitiligo. We measured serum malondialdehyde (MDA) as an indicator of oxidative stress and serum zinc and vitamin C to check antioxidant status in thirty Vitiligo patients. Thirty healthy control subjects were also recruited by matching the socio-demographic status to that of the patients. Blood samples were analyzed for determining the serum levels of Zn (by atomic absorption spectroscopy), Vitamin C and MDA (by UV-VIS spectroscopy). Serum level of MDA increased in vitiligo patients significantly (p < 0.05) in the present study, where as serum level of Zn increased and serum Vit-C decreased in patients compared to control but the changes were not statistically significant (p > 0.05). Our study reveals the presence of an imbalance in the oxidant/antioxidant system in vitiligo patients which supports a free radical-mediated damage in the pathogenesis of vitiligo. Key words: Vitiligo; Oxidative stress; Antioxidant status; MDA; Vitamin C; Zinc DOI: http://dx.doi.org/10.3329/dujps.v9i2.7894 Dhaka Univ. J. Pharm. Sci. 9(2): 103-108, 2010 (December)

Context: Medicinal plants having diverse pharmacological properties including cytotoxic and cancer chemopreventive effects can be developed as novel drugs for cancer chemoprevention. One of the best approaches in search for anticancer agents from plant resources is the selection of plants based ethnomedical leads and testing the selected plants efficacy and safety in light of modern science. Objectives: The present study aims in assessing the hepatoprotective activity of protein fraction of Cynodon dactylon on CCl 4 induced mice. Materials and Methods: Fresh leaves were homogenized with phosphate buffered saline (PBS) at 4°C to obtain 20 % homogenate. The supernatant obtained was used for the ammonium sulphate fractionation. Hepatoprotective role was evaluated in the liver of mice administered with and without protein fraction. Paraffin oil and PBS serves as the vehicle control for Silymarin and protein fraction respectively. Silymarin was used as the standard antioxidant. CCl 4 acts as a hepatotoxin. The activity of enzymic antioxidants Catalase (CAT), Superoxide dismutase (SOD) and Peroxidase (Px) were determined in the liver homogenate of the control and experimental mice. The levels of these antioxidants were also assessed in the liver homogenate of the control and experimental mice. Results: The protein fraction of Cynodon dactylon had significant hepatoprotective potential by enhancing the activities of enzymic antioxidants, increasing the levels of non enzymic antioxidants, marker enzymes and antilipid peroxidative role by decreasing the lipid peroxide levels. These effects were found to be more significant than that of silymarin, the standard antioxidant and the CCl 4 the hepatotoxin. Administration of Cynodon dactylon plus CCl 4 significantly decreases the levels of liver marker enzymes, hepatic enzymic and non enzymic antioxidants. The observed increased levels of lipid peroxides and decreased levels of enzymic and non enzymic antioxidants are the indications of liver damage due to high oxidative stress in CCl 4 induced mice when compared to the respective vehicle controls. Conclusion: The findings of the present study revealed that the Cynodon dactylon had the potent hepatoprotective activity due to its antioxidant property against CCl 4 induced liver damage in mice. Key words: Protein fraction; Cynodon dactylon ; enzymic antioxidants; lipid peroxides; marker enzymes; CCl 4 . DOI: 10.3329/jbs.v17i0.7096 J. bio-sci. 17: 27-34, 2009

Oxidative stress is currently suggested as mechanism underlying diabetes and diabetic complications. The aim of the study was to evaluate the magnitude of oxidative stress in patients with diabetes by measuring the lipid peroxidation as well as the status of the antioxidant defense system, thyroid hormones status and other biochemical variables. The study population consisted of 100 subjects divided into two groups viz. diabetic (n=50) and healthy controls (n=50). Changes in the levels of lipid peroxidation and antioxidants and thyroid hormones status were determined in diabetic and non-diabetic subjects. The level of thiobarbituric acid reactive substances (TBARS) was found to be increased significantly in diabetic patients compared to healthy controls. On the other hand, the activities of superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), glutathione-S-transferase (GST), reduced glutathione (GSH), vitamin A, vitamin E and vitamin C were found to be decreased significantly in diabetics when compared to control subjects. We also noticed a marked increase in serum total cholesterol, triglyceride, low-density lipoprotein cholesterol (LDL-C), very low-density lipoprotein cholesterol (VLDL-C), and decrease in highdensity lipoprotein cholesterol (HDL-C), total protein and albumin in diabetic patients. The level of TSH was significantly decreased whereas the levels of T4 and FT4 were significantly increased in diabetic patients than the control subjects. However, the T3 and FT3 levels did not differ significantly between groups. Our findings indicate that changes in oxidant and antioxidant equilibrium will have biological and possibly pathological role in the development of secondary complications. It also demonstrate that detection of thyroid hormone status in the early stage of the disease will help the patients to improve quality of life and reduce the morbidity rate. Key Words: Diabetes mellitus, Oxidative stress, Lipid peroxidation, Antioxidant status, Thyroid hormones. doi: 10.3329/jom.v10i2.2816 J MEDICINE 2009; 10 : 60-66

Objective : An important mediator of testicular injury is oxidative stress; the implicating pathway has been pointed at a free radical mechanism by researchers. This article, investigates the effect of bitter melon (Momordica charantia) (MC) seed extract and antioxidant supplementation in the testes of Sprague-Dawley (S-D) rat. Methodology : Ninety male S-D rats, weighing between 110- 214 g, were assigned randomly into six main Groups A to F. Group A was administered 50 mg/100 g of MC extract orally, between 6 to 16 weeks. Group B were pre-treated with ascorbic acid (AA) 0.01mg/kg, three days/week, α-tocopherol (AT) 20 mg/kg, five days/week and both test solutions (TS) i.e. AA and AT; 0.01 and 20 mg/kg, three and five days/week for 8 weeks. This was followed by administration of the extract at dose and duration as in A. Group C received the extract for 8 weeks and afterwards post-treated for another 8 weeks with AA, AT and both TS (as above). Group D in addition to the extract administration were treated with AA, AT and both TS in dose and duration similar to B above. Group E had AA, AT and both TS alone for 8 weeks. Group F served as the control subjects. The animals testicular tissues were processed for malondialdehyde (MDA) and AA concentrations. Serum testosterone (TT) assay was done from left ventricular blood. Results : The extract administered for 6, 8 and 16 weeks produced significantly ( p < 0.05) increased testicular MDA (1.74 ± 1.15, 1.84 ± 0.38 and 2.38 ± 0.40) compared to control (0.38 ± 0.02, 0.38 ± 0.03 and 0.35 ± 0.02) and decreased AA (0.01± 0.02, 0.01± 0.01 and 0.00± 0.01) compared to control (0.15 ± 0.02, 0.12 ± 0.02 and 0.13 ± 0.02). There was also an associated significant decrease ( p < 0.05) in peripheral TT levels compared to control. The extract produced responses that showed no prophylactic rather modulatory effect with TS. Conclusion : These findings suggest that the extract resulted in changes in the testicular oxidative status. This may play a role in testicular dysfunction that may compromise fertility. Key words: Momordica charantia; malondialdehyde; ascorbic acid; testosterone. DOI: http://dx.doi.org/10.3329/bjms.v10i2.7805 Bangladesh Journal of Medical Science Vol.10 No.2 Apr’11 pp.104-111

Background: In the pathogenesis of CHF neurohormonal changes, in particular, changes of activity of sympathetic nervous system (SNS) occupies an important position. For this reason, researchers concentrated on the use β-blockers in therapy of patients with CHF. They reduce heart rate, improve diastolic function of the myocardium, reduce secretion of renin and restore the sensitivity of β- adrenoreceptors to its regulatory influences. We studied the influence of the 3rdgeneration betaadrenoblocker – Carvedilol in patients with CHF- including clinical efficacy and reduction of oxidative stress. Methods: The study was conducted in Saint-Petersburg State Medical University, from January 2000 to June 2000. 37 patients (33 male and 4 female) with CHF class III or IV despite receiving standard therapy of heart failure were enrolled in the study for the treatment with Carvedilol. All of the patients received Carvedilol for 6 months at a dose of 12.5-50mg/day with standard therapy of Heart Failure, which was not changed during next 6 months. Results: The average age of the patients was 56.8±2.3 years. The cause of CHF was IHD. 34 patients had chronic stable angina (CCS class II-IV). The majority of the patients had a history of myocardial infarction (91.8%); of these 73.5% of the patients had a history of repeated MI. Hypertension stage 2 and 3 was associated in 32.4% patients.Long-term therapy with Carvedilol led to improvement of the clinical status of the patients. After 6 months therapy with Carvedilol frequency of hospitalization was significantly reduced (1.36±0.23 vs. 0.33±0.1; p2 vs. 188.1±10.8 gm/m2, p

Context: Cisplatin, an effective antineoplastic agent, is the drug of choice in the treatment of germ cell tumours. It is one of the important nephrotoxic drugs. Oxidative stress is suggested to be a significant contributor to cisplatin-induced nephrotoxicity. So, vitamin C and spirulina having antioxidant properties are expected to deal with the situation. The study was designed to observe the effects of vitamin C and spirulina on cisplatin-induced interstitial nephritis in Long Evans rats. Study design: Experimental Place and period of study: Department of Anatomy, Sir Salimullah Medical College, Dhaka, from September, 2005 to December, 2006. Materials and Methods: Forty adult Long Evans rats, of either sex, weighing 220-300 gms each, were divided into four equal batches depending on the drug treatment they received: (a) 'normal control' – distilled water and normal saline, (b) 'experimental control' – cisplatin, (c) 'vitamin C treated' – cisplatin plus vitamin C, and (d) 'spirulina treated' – cisplatin plus spirulina. Histologically, nephrotoxicity was determined by the presence of inflammatory changes in the interstitium. Results: Nephrotoxic control rats showed marked interstitial nephritis as evidenced by histological features. Pretreatment with either vitamin C or spirulina reduced the cisplatin-induced interstitial nephritis (p

Oxidative embrittlement and stress cracking of high-density polyethylene has been studied by using fuming nitric acid at 60°C as the oxidative agent. Oxidative stress cracking was found to be insensitive to changes in molecular weight in contrast to environmental stress cracking in a surface-active medium. The oxidative attack was found to be influenced by the surface crystalline texture of the polyethylene. Oriented polyethylene showed an increased resistance to oxidative embrittlement and stress cracking, the mode of failure being dependent upon the prior annealing treatment.

The present study evaluated the hepatoprotective activity of ginger oleoresin against Carbontetrachloride induced liver toxic damage in rats. Rats were divided into six groups. Hepatotoxicity was induced by the administration of a single intraperitoneal dose (2ml/kg) of Carbontetrachloride in experimental rats. Post-treatment with Ginger oleoresin at 300 and 600mg/kg dose given by oral routewas carried out to find their protective effectsagainst carbontetrachloride induced hepatic injury. Biochemical parameterfor oxidative stress, inflammation and lipid profile along with genotoxicity and histological changes in rat serum and liver were studied. Silymarin was used as standard hepatoprotective agent. Extracted oleoresin dose dependently provided hepatoprotective effects.The hepatoprotective action of ginger oleoresin may be related to its free radical scavenging,anti-inflammatory and hypolipidemic activity and concluded to be partly mediated by its active constituent’s 6-gingerol, shogaol and zingerone. -phospate; CCl3 *, Trichloromethyl free radical; CCl3 OO*, Trichloromethyl peroxy radical; ROS, Reactive oxygen species; iNOS, inducible nitric oxide synthase; NO, Nitric oxide, VLDL, Very low density lipoprotein.

Turner has shown that irradiation of natural rubber results in the formation of carbon to carbon crosslinks by combination of allylic radicals; the same type of crosslinks are formed by heating rubber in presence of organic peroxides2. Since peroxide vulcanizates may be freed from excess vulcanizing ingredients and by products by extraction while radiation crosslinking may be effected without additive, it is expected that the two types of vulcanizate should age in an analogous manner. The present study was undertaken in order to see whether radiation vulcanizates did show the same aging behavior as peroxide vulcanizates according to measurements of oxidative stress relaxation, and, if so, to ascertain whether the efficiency of antioxidants of the dithiocarbamate type was affected by the irradiation and whether such materials had an adverse effect upon cure. It has been stated that radiation vulcanizates are resistant to aging even in the absence of antioxidant and their stability has been attributed to the presence of purely carbon-carbon crosslinks. However, it has recently been demonstrated that a carbon-carbon crosslink is not a sufficient condition for vulcanizate stability in the absence of antioxidant. Previous studies concerning the aging of radiation cures appear to have been made using materials containing carbon black, which is now known to act as an antioxidant; it is necessary, for work of fundamental significance, to use gum stocks based on very pure rubber.

Stress relaxation measurements of chlorosulfonated polyethylene vulcanizates show that curing with m-phenylene-bis-maleimide gives thermally more stable crosslinks than the conventional metal oxide/sulfur accelerator system. The superior thermal stability of the bis-maleimide cure is based on the covalent nature of the crosslinks. In conventionally cured vulcanizates interchange reactions of the metal sulfonate and polysulfide crosslinks occur at elevated temperatures. The interchange reactions of the crosslinks cause a rapid stress decline at the beginning of the stress relaxation process. Over longer aging periods stress relaxation due to oxidative degradation becomes apparent in vulcanizates of both types. The activation energies of oxidative stress relaxations are very similar for the bis-maleimide and the conventional cure. The similarity of the activation energies indicates that oxidative degradation follows the same path. The site of the oxidative attack is established for bis-maleimide cured vulcanizates. Oxidative degradation is found to occur in the polymer chains rather than in the crosslinks. The effects of fillers and stabilizers are investigated and their mode of action is explained on the basis of the stress relaxation results.

Spirulina, a naturally occurring micro algae, was suspended in water and administrated orally to streptozotocin induced diabetic and nondiabetic rats at a dose of 400 mg per kg body weight. The animal of the control group was administrated extract of Spinacea oleracea (locally known as Palong Shak). Thirty days after the oral administration all the rats were sacrificed for the determination of super oxide dismutase. Spirulina increased the level of oxidative stress responsive enzyme Super oxide dismutase (SOD) in erythrocyte by 17.5% (p

Summary. Experiments in rats with jejunal blind pouches and bacterial overgrowth demonstrate increased levels in red cells of reduced glutathione, suggesting oxidative stress on red cells, and decreased serum levels of vitamin E, a known anti-oxidant. The urine of such animals contains increased amounts of tryptophan metabolites, some of which demonstrate strong oxidant activity as measured by methaemoglobin production in vitro. It is felt that enterogenous cyanosis, or intestinal autointoxication, does exist in this experimental model. Whether the oxidative damage previously described is due to the presence of the tryptophan metabolites, the low levels of vitamin E or both, cannot be unequivocally ascertained.

Several mechanisms recently proposed for regulation of the hexose monophosphate shunt require the concentration of NADP to be low or that of NADPH to be high. The present study indicates that the first enzyme of the hexose monophosphate shunt of human erythrocytes is under severe restraint even when these conditions do not exist. In human erythrocytes containing low-activity variants of this enzyme, glucose-6-phosphate dehydrogenase (D-glucose-6-phosphate:NADP + 1-oxidoreductase; EC 1.1.1.49), measurements of the rate of oxidation of C-1 labeled glucose show that the enzyme is operating at a rate much closer to its maximum than in normal cells. This requires that the ratio of inhibitory NADPH to NADP be much lower in the variant cells than in normal cells. A small increase in oxidative rate, induced by naphthol, then causes a disappearance in reduced glutathione in the variant cells, presumably because a significant further decrease in NADPH occurs in these cells, whereas the same oxidative stress in normal cells would not lower the NADPH level appreciably. A low NADPH/NADP ratio in unstressed cells deficient in glucose-6-phosphate dehydrogenase is confirmed by direct measurement. The maximum activity of the variant enzyme in the cell, as measured with methylene blue to keep most of the NADP in the oxidized form, is only about 1/60 of that found in hemolysates, thus accounting for the failure to compensate for a relatively small oxidative stress in vivo in spite of an apparent sufficiency of enzyme. The reason for the limitation on maximum intracellular activity is unknown. A similar limitation is seen with normal cells incubated with methylene blue, where the maximum intracellular rate is also only about 1/60 of that found in hemolysates.

2007/2008 ABSTRACT: Human Hepatocellular Carcinoma (HCC) is the fifth most frequent neoplasm worldwide and its incidence is rising in Western countries. HCC is frequently diagnosed at advanced stage and, until today, there are no effective treatments of this late phase. Therefore, research focused on finding new markers of progression and new molecular targets for therapy for HCC is of the utmost importance. Unquestionably, HCC is the most serious complication of long-standing chronic disease representing generally the final event of a liver disease usually originated decades earlier. Any chronic liver disease that causes cirrhosis is considered a risk factor for HCC development and this disease is characterized by chronic inflammation involving repeated rounds of necrosis and regeneration associated with sustained oxidative stress. Apurinic apyrimidinic endonuclease/redox effector factor 1 (APE1/Ref-1) is a multifunctional protein involved in redox regulation of transcription factors and acting as an endonuclease of the base excision repair (BER) pathway of DNA lesions. APE1/Ref-1 has been found to be up-regulated and abnormally localized in the cytoplasmic compartment of several cancer cells. Of notice is the finding that cytoplasmic localization is associated with a poor prognosis. Since at the time I started my thesis no data were available about the possible involvement of APE1/Ref-1 in HCC, the aim of this work was to investigate the expression and sub-cellular localization of APE1/Ref-1 in HCC. In addition, my aim was also to analyze the correlation of these parameters with the progression of the disease. To accomplish these points I analyzed human samples of HCC and cirrhosis (in vivo model) and an in vitro model constituted by HCC cell lines at different degree of differentiation. I also assessed the protective role of APE1/Ref-1 to oxidative damage as a function of its sub-cellular localization over-expressing, in normal hepatocytes, wild type and mutated forms of the protein that force its distribution to different cellular compartments. Using these approaches, we found that HCC is characterized by increased APE1/Ref-1 mRNA and protein levels and, that this up-regulation increases accordingly with tumor differentiation grading showing an association between tumor progression and APE1/Ref-1 levels. The increased amount of APE1/Ref-1 induces its nuclear and cytoplasmic accumulation in HCC. The cytoplasmic localization is peculiar of HCC and more frequently observed in poorly-differentiated cancers. The fact that APE1/Ref-1 accumulates in the cytoplasm of poorly-differentiated tumors and correlates with a shorter survival time after HCC resection points to a possible role of the APE1/Ref-1 sub-cellular localization as a prognostic marker of HCC aggressiveness. Thereafter, I demonstrated that APE1/Ref-1 over-expression in the normal hepatocyte cell line (IHH) enhances survival after oxidative damage induced by exposure to H2O2 and UV radiation although the different forms of the protein behave in a different ways. Wild type and truncated forms of APE1/Ref-1, that localize mainly in the cytoplasm and mitochondria, confer protection to H2O2 damage while the non-cleavable form, localized in the nucleus, does not. Conversely, all the mutants protect IHH from UV induced apoptosis. These data demonstrate for the first time that APE1/Ref-1 expression is deregulated in HCC, that its over-expression has a protective role in vitro and that APE1/Ref-1 cytoplasmic localization has a prognostic significance in vivo. We favor the conclusion that APE1/Ref-1 may be considered as a new prognostic marker for HCC aggressiveness. Its possible involvement in HCC development offer a new molecular key to elucidate the role of this protein in oxidative stress related hepatocarcinogenesis. RIASSUNTO: Il carcinoma primitivo del fegato è la quinta neoplasia più frequente al mondo e rappresenta la terza causa di morte per cancro. La sua incidenza negli ultimi anni è significativamente aumentata nei paesi occidentali e, nonostante i miglioramenti delle metodiche diagnostiche, la diagnosi di epatocarcinoma è spesso effettuata solo nella fase avanzata di malattia quando, le terapie al momento disponibili sono esclusivamente palliative. L’incremento di nuovi casi e la mancanza di terapia medica efficace, sottolineano la necessità di individuare nuovi marcatori prognostici e nuovi target terapeutici. Dal punto di vista fisiopatologico, il carcinoma epatocellulare rappresenta la complicanza più grave di una malattia cronica di fegato, generalmente iniziata molti anni prima della diagnosi di HCC, evoluta in cirrosi. La cirrosi epatica si sviluppa come conseguenza di un flogosi cronica che causa, cicli di necrosi e rigenerazione con un danno epatocitario sostenuto dallo stress ossidativo ed è considerata il fattore di rischio principale per lo sviluppo di HCC. APE1/Ref-1 (Apurinic apyrimidinic endonuclease/redox effector factor 1) è una proteina coinvolta nella regolazione dello stato redox cellular e agisce come co-attivatore di fattori trascrizionali e nel meccanismo BER (base excission repair) di riparo dei danni ossidativi al DNA. In molti tumori è stato dimostrata una up-regolazione di APE1/Ref-1 e in diversi casi la localizzazione citoplasmatica della proteina si è dimostrata correlare con una cattiva prognosi. Nel momento in cui ho cominciato il lavoro di tesi non era disponibile alcun dato sul possibile coinvolgimento di una alterata espressione di APE1/Ref-1 nel carcinoma primitivo del fegato. Gli obbiettivi di questa tesi sono stati, pertanto, la valutazione dell’espressione e del pattern di localizzazione cellulare di APE1/Ref-1 nel HCC in correlazione alla progressione della malattia e alla prognosi. In questa ottica ho valutato sia campioni di pazienti, diagnosticati affetti da HCC su cirrosi e trattati chirurgicamente, che un modello in vitro di epatocarcinoma a diversi gradi di differenziazione. Un ulteriore obbiettivo è stato quello di valutare l’eventuale effetto protettivo della overespressione di APE1/Ref-1 in una linea cellulare derivata da epatociti umani da fegato sano. In questo caso sono state overespresse differenti forme della proteina in modo da valutare il ruolo protettivo in relazione alle diverse localizzazioni intracellulari. Sulla base di questi modelli noi abbiamo osservato che l’epatocarcinoma è caratterizzato da un incremento dei livelli di mRNA e proteina di APE1/Ref-1 che cresce in modo inversamente proporzionale rispetto al grado di differenziazione del cancro. L’aumentata produzione della proteina si associa ad un accumulo della stessa sia nei nuclei che nei citoplasmi di HCC con livelli maggiori rispetto alla SLC, la localizzazione citoplasmatica nel tessuto tumorale si è dimostrata peculiare del cancro e più frequente negli HCC poco differenziati. L’osservazione che associa la maggiore frequenza della localizzazione citoplasmatica nei tumori poco differenziati e la correlazione di tale localizzazione con una ridotta sopravvivenza individua in APE1/Ref-1 un marker di aggressività di HCC. I dati ottenuti hanno inoltre dimostrato che la overespressione di APE1/Ref-1, seppur con peculiarità legate alle diverse forme, conferisce alle IHH una resistenza allo stress ossidativo indotto da H2O2 e radiazioni UV. La forma wild type e la forma tronca della proteina, che localizzano nel citoplasma, proteggono le cellule dal danno da H2O2, mentre la forma non clivabile, a localizzazione nucleare, non conferisce la stessa protezione. Per quanto riguarda invece il danno indotto da UV tutte le forme della proteina sono in grado di proteggere le cellule epatiche dall’apoptosi. Tutti questi dati dimostrano per la prima volta che l’espressione di APE1/Ref-1 è deregolata nel carcinoma epatocelluare e che la sua overespressione ha un ruolo protettivo in vitro. La localizzazione citoplasmatica nel tessuto tumorale della proteina ha significato prognostico. Pertanto, APE1/Ref-1 può essere considerato come un possibile nuovo marker prognostico di aggressività dell’epatocarcinoma. Il suo possibile coinvolgimento nello sviluppo di HCC apre nuove possibili strade nella comprensione del ruolo di questa proteina nei meccanismi che associano lo stress ossidativo all’epatocarcinogenesi.

Xu M, Xie H, Zhong Y, Ma J, Liu S, Yang H. 2015. Treatment with MG-132 and TSA induced apoptosis in OS-RC-2 cells by increasing oxidative stress and decreasing the expression of NF-kappa B. Nusantara Bioscience 7: 20-25. Here we assessed the effect of the proteasome inhibitor MG-132 alone or in combination with the histone deacetylase inhibitor TSA on human renal cell on human renal cell carcinoma cells in vitro and we explored the underlying molecular mechanisms.OS-RC-2 cells were treated byMG-132 alone or in combination with TSA and/or NAc. The MTT assay and flow cytometry (FCM) were used to determine cell viability, ROS levels, and apoptosis. Expression of Bax and NF-kappa B p65 proteins was quantified by Western blotting. MG-132significantly increased the level of ROS, inhibited cell growth and induced apoptosis in a dose- and time-dependent manner. Both ROS and apoptosis were further increased following the combined addition of MG132 and TSA. In all cases, expression of p65 was down-regulated. MG-132 alone or in combination with TSA induced apoptosis in OS-RC-2 cells through the generation of ROS and the down-regulation of p65 expression.

2006/2007 The phatophysiology of muscle atrophy is a complex multifactor process, which occurs in response to environmental solicitations, injury, various disease states, disuse and normal aging. Persistent low-grade or acute activation of inflammatory/oxidative cascade, acute stress, altered energy intake, or reduced mechanical action, contribute to muscle decline, as well as to the progression of chronic and acute associated disease. Elevated concentrations of pro-inflammatory markers have also devastating effects on the vasculature and are implicated in the pathogenesis of atherosclerosis, which at peripheral level contributes to muscle suffering. A more understanding of the molecular relationships underpinning muscle atrophy, inflammation and cardiovascular risk in different human clinical models should be helpful to design new therapies to the recovery of muscle. Thus, we investigated the effect of some effectors of inflammatory/oxidative responses on muscle atrophy, inflammation and cardiovascular dysfunction, in chronic, acute or healthy conditions. We explored: a) the interaction between energy restriction and muscle unloading in the regulation of lean body mass, protein kinetics or inflammatory response in healthy subjects; b) the links among inflammation, organ failure, cardiovascular risk and cytokine genotypes, in models of chronic muscle atrophy; c) the cross-interaction connecting translational machinery, proteolysis and apoptotic response with skeletal muscle atrophy induced by acute stress. We highlighted a link between inflammatory process, cardiovascular risk and muscle unloading, likely involving leptin hormone and the long pentraxin PTX3; the latter may represent a novel key of reading of some bed-rest effect on vasculature or inflammatory system. Cytokine genotypes (interpheron-gamma), and the extent of renal functions on cytokine clearence, may account of intraindividual variability and vulnerability to the process. Finally, we gained knowledge about a novel catabolic mechanism, involving the eukariotic elongation factor EEF1A1 and the stress response protein p66(ShcA) in acute muscle atrophy. We suggest that, a more controlled energy intake combined with various exercise regimes might protect from the effects of unloading and may be a reasonable approach to maintain muscle mass in health but also in disease conditions. La patofisiologia dell’atrofia muscolare è un complesso processo multifattoriale, che avviene in risposta a sollecitazioni ambientali, ferite, vari stati di malattia, disuso e nel normale invecchiamento. La persistente lieve od acuta attivazione della cascata infiammatoria/ossidativa, lo stress acuto, un alterato apporto energetico o una ridotta azione meccanica, contribuiscono al declino muscolare ed alla progressione di malattie croniche o acute ad esso associate. Le elevate concentrazioni di markers pro-infiammatori hanno effetti devastanti anche sul sistema vascolare e sono implicate nella patogenesi dell’aterosclerosi, la quale a livello periferico contribuisce alla sofferenza muscolare. Una maggior comprensione delle relazioni molecolari che sostengono l’atrofia muscolare, l’infiammazione ed il rischio cardiovasolare in diversi modelli clinici umani, dovrebbe essere utile per disegnare nuove terapie dirette al recupero del muscolo. Perciò, abbiamo investigato gli effetti di alcuni effettori della risposta infiammatoria/ossidativa sull’atrofia muscolare, l’infiammazione e la disfunzione cardiovascolare, in condizioni croniche, acute o di salute. Abbiamo esplorato: a) l’effetto dell’interazione tra la restrizione energetica e l’inattività muscolare sulla regolazione della massa magra corporea, sulla cinetica delle proteine e sulla risposta infiammatoria in soggetti sani; b) i legami tra l’infiammazione, il danno d’organo, il rischio cardiovascolare e i genotipi delle citochine in modelli di atrofia muscolare cronica; c) l’interazione che connette il maccanismo traduzionale, la proteolisi e l’apoptosi, con l’atrofia del muscolo scheletrico indotta da stress acuto. Abbiamo evidenziato un legame tra processo infiammatorio, rischio cardiovascolare ed inattività muscolare, probabilmente legato all’ormone leptina e alla pentraxina lunga PTX3; quest’ultima potrebbe rappresentare una nuova chiave di lettura di alcuni effetti del bed-rest sulla vascolatura o il sistema infiammatorio. I genotipi delle citochine (interferon-gamma), e la portata della funzione renale sulla loro clearence, potrebbero esser causa della variabilità e vulnerabilità intraindividuale al processo. Per ultimo, abbiamo ottenuto conoscenza di un nuovo meccanismo catabolico, riguardante il fattore di elongazione eucariotico EEF1A1 e la proteina di risposta allo stress p66(ShcA) nell’atrofia muscolare acuta. Noi suggeriamo che, un maggior controllo dell’introito energetico combinato con vari regimi di esercizio, potrebbe proteggere dagli effetti dell’inattività muscolare e potrebbe essere un approccio ragionevole per mantenere la massa muscolare in salute, ma anche in condizioni di malattia.

Liver microsomes and mitochondria and heart sarcosomes from rats fed diets with varying α-tocopherol concentrations and lipid contents were peroxidized over a 6 hr time period. Lipid peroxidation was measured by absorption of oxygen, production of thiobarbituric acid (TBA) reactants and by development of fluorescence. The spectral characteristics of the fluorescent compounds were the same for all peroxidizing systems; the excitation maximum was 360 nm and the emission maximum was 430 nm. As time of peroxidation increased, uptake of oxygen and production of fluorescent compounds increased. These two parameters as well as production of TBA reactants were dependent upon dietary antioxidant and all three had an inverse relationship with the amount of dietary α-tocopherol. The relationship between absorption of oxygen and development of fluorescent compounds was also dependent upon dietary polyunsaturated fats (PUFA). Subcellular particles from animals fed higher levels of PUFA produced more fluorescent products per mole of oxygen absorbed than did those from animals on a diet with lower PUFA content. TBA reacting products increased with time during the initial phase of peroxidation: in the microsomal systems their production stabilized or decreased by 4–6 hr of peroxidation. Using the synthetic 1-amino-3-iminopropene derivative of glycine as standard for quantitation of fluorescence, the molar ratios of oxygen absorbed per fluorescent compound produced were calculated. This ratio for subcellular particles isolated from rats fed diets with PUFA ratios similar to those in the average American human diet was 393∶1. The fluorescent compounds had the same spectral characteristics as the lipofuscin pigment that accumulates in animal tissues as a function of age, oxidative stress or antioxidant deficiency. The fluorescent molecular damage represented by that accumulated in human heart age pigment by 50 years of age was calculated to have been caused by approximately 0.6 μmole of free radicals per gram of heart tissue.

Riboflavin deficiency results in diminished glutathione reductase activity of the red cells of human subjects and of rats. The effect of such glutathione reductase deficiency on the rate of hexose monophosphate shunt pathway metabolism has been studied by measuring the rate of 14CO2 production of red cells subjected to oxidative stress, measuring the rate of regeneration of GSH from GSSG, and by estimating the steady-state levels of GSSG and the rate of transport of GSSG from glutathione reductase-deficient red cells. No difference was observed between the red cells of normal subjects, of riboflavin-deficient (glutathione reductase-deficient) subjects, and the red cells of glutathione reductase-deficient subjects treated with riboflavin in vivo or in vitro to correct the glutathione reductase deficiency. These studies indicate that, in the red cell, glutathione reductase does not play limiting role in the rate of metabolism in the hexose monophosphate pathway.

Oxidative stress causes biological changes responsible for carcinogenesis and aging in human cells. The retinal pigmented epithelium is continuously exposed to oxidative stress. Therefore reactive oxygen species (ROS) and products of lipid peroxidation accumulate in RPE. Neutralization of ROS occurs in retina by the action of antioxidant defence systems. In the present study, the protective effect of caffeic acid (3,4-dihydroxy cinnamic acid), a dietary phenolic compound, has been examined in normal and in oxidative stress conditions (500 µM peroxide oxygen) in cultures human epithelial pigment retinal cells (Nowak, M. et al.). The cell viability, the antioxidant enzymes activity (CAT, GPx, SOD) and the level of intracellular reactive oxygen species (ROS) were determined. Exposure to l00 µM caffeic acid for 24 h induced cellular changes indicating the protective effect of caffeic acid in RPE cells. Caffeic acid did not show any cytotoxic effect at concentrations lower than 200 μM in culture medium. Treatment of RPE cells with caffeic acid causes an increase of catalase, glutathione peroxidase and superoxide dismutase activity, especially in cells treated with hydrogen peroxide. Caffeic acid causes a decrease of ROS level in cells treated with hydrogen peroxide. This study proved that caffeic acid or food that contain high levels of this phenolic acid may have beneficial effects in prevention of retinal diseases associated with oxidative stress by improving antioxidant defence systems.

Fractures are a serious health problem in Indonesia due to increasing prevalence. The healing process of fracture is disturbed by the oxidative stress that caused by imbalance quantity of free radical and antioxidant. An antioxidant such as polyphenol, which can be found in cocoa, is needed to suppress oxidative stress. The study aimed to investigate the effect of the ethanolic extract of cacao on fracture healing process in a rat model through MDA concentration and histopatological appearance. This study is in vivo experimental study with post-test only controlled group design. 30 male Wistar rats were randomized and divided into 5 groups. 1 group was rats without fractured. The negative control and three treatment groups were rats with fractured manually on left tibia under anesthesia and immobilized by bandage. The treatment groups treated with cocoa ethanolic extract in a dose of 125 mg/kgBW, 250 mg/kgBW, and 500 mg/kgBW orally for 21 days. The result showed that there was a significant different between the treatment groups and the negative control group on MDA concentration and histopatological appearance (p>0,05). The corelation between them were strong and had negative direction (R=-0,771). The study concluded that cocoa ethanolic extract had a positive effect to supress oxidation stress and increases the number of osteoblast on fracture healing process. Key words: cocoa ethanolic extract, polyphenol, fracture healing process, oxidative stress

Coronary heart disease is an important health problem. It is estimated that the death rate from coronary heart disease by 23,4 millions in 20130 (WHO, 2009). Excessive physical activity can cause oxidative stress which lead to atherosclerosis. Mung bean sprouts (Vigna radiata (L)) contain vitamin E, vitamin C, fenol, flavonoid, fitosterol, and other minerals. The aim of this study is to determine the effect of mung beans sprout extract on on the thicknes of the tunica intima-media on physical stress-induced atherosclerosis of male wistar rat. This research is true experimental study using 20 male wistar rat were divided into five groups: negative control, positive control and treatment groups P1, P2, P3 (physical stress + bean sprout extract 50 mg/day, 100 mg/day, 200 mg/day for 10 days). There is significant decrease of MDA serum level in the treatment groups.Keywords : Vigna radiata, physical stress, thicknes of tunica intima-media