Organic Peroxy Free Radicals and the Role of Superoxide Dismutase and Antioxidants

1988 ◽  
pp. 81-84
Author(s):  
R. L. Willson
Keyword(s):  
Superoxide Dismutase ◽  
Free Radicals

Superoxide Dismutase and Sulfite Oxidation

1992 ◽  
Vol 47 (5-6) ◽  
pp. 360-364 ◽  
Author(s):  
Z. Miszalski ◽  
H. Ziegler
Keyword(s):  
Superoxide Dismutase ◽  
Free Radicals ◽  
Resistance Mechanism ◽  
Sulfite Oxidation ◽  
Oxidation Effect

50 U SOD in 1 ml or 10 mᴍ DDTC do not much change sulfite oxidation due to the free radicals procuding system xanthin-xanthin oxidase. Sulfite oxidation due to the activity of this free radicals producing system proceeds probably as the univalent oxidation of sulfite. The role of SOD in SO, resistance mechanism in plants and the role of DDTCas SO2 oxidation effect stimulator is discussed.

scholarly journals SUPEROKSIDA DISMUTASE (SOD) DAN RADIKAL BEBAS

2020 ◽  
Vol 2 (2) ◽  
pp. 124-129
Author(s):  
Evirosa Juliartha Simanjuntak ◽  
Zulham Zulham
Keyword(s):  
Oxidative Stress ◽  
Superoxide Dismutase ◽  
Free Radicals ◽  
Cellular Tissue ◽  
The Body ◽  
Enzymatic Antioxidants ◽  
Superoxide Anions ◽  
Cell Components ◽  
Endogenous Antioxidant

Superoxide dismutase (SOD) is an endogenous antioxidant that works by regulating ROS levels. This group of enzymes functions to catalyze the efficient disposal of superoxide anions. Superoxide anions are produced enzymatically and non-enzymatically. In mammals there are 3 types of SOD, namely SOD1 (CuZnSOD), SOD2 (MnSOD), SOD3 (ECSOD). Oxidative stress caused by free radicals has been reported to be involved in several diseases. Various stressors trigger ROS production, also triggering the production of enzymatic antioxidants such as catalase (CAT), hydroperoxidase (HPx) and superoxide dismutase (SOD). Free radicals cause oxidative stress when the amount in the body is excessive, this situation will cause oxidative damage at the cellular, tissue to organ levels that will accelerate the aging process and the onset of disease. Free radicals are molecules that have one or more unpaired electrons and are therefore relatively unstable. Free radicals try to stabilize themselves by taking electrons from other molecules and will produce reactive oxygen species (ROS). If there is a disturbance in the balance of ROS products with antioxidants, oxidative stress will occur which results in damage to cell components. The higher levels of oxidative stress will increase the lipid peroxidation marker which is presented as malondialdehyde (MDA) and decrease the SOD enzyme activity. Thus the role of molecules that have antioxidant activity is very necessary to ward off oxidative stress.

scholarly journals The Role of Antioxidant to Prevent Free Radicals in The Body

Sains Medika ◽  
2017 ◽  
Vol 8 (1) ◽  
pp. 39 ◽  
Author(s):  
Siti Thomas Zulaikhah
Keyword(s):  
Superoxide Dismutase ◽  
Antioxidant Enzymes ◽  
Free Radicals ◽  
Negative Impact ◽  
Reduced Glutathione ◽  
The Body ◽  
Enzyme Superoxide Dismutase ◽  
Vegetables And Fruits ◽  
Β Carotene

AbstractAntioxidants are compounds that can counteract or reduce the negative impact oxidants in the body. Antioxidants work by donating an electron to compounds that are oxidant so that the oxidant compound activity can be inhibited. Antioxidants are classified into two, namely antioxidant enzymes and non-enzyme. Antioxidant enzymes as enzyme superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPx), a non-enzyme antioxidant found in many vegetables and fruits, which include reduced glutathione (GSH), vitamin C, E, β- carotene, flavonoids, isoflavones, flavones, antosionin, catechins, and isokatekin, and lipoic acid. Low antioxidant enzymes can be used as a marker of high levels of free radicals in the body. Following review aims to provide an overview of the role of antioxidants in preventing the formation of free radicals in the body.

Superoxide dismutase restores endothelium-dependent arteriolar dilatation during acute infusion of nicotine

1998 ◽  
Vol 85 (4) ◽  
pp. 1292-1298 ◽  
Author(s):  
William G. Mayhan ◽  
Glenda M. Sharpe
Keyword(s):  
Superoxide Dismutase ◽  
Free Radicals ◽  
Topical Application ◽  
Oxygen Radicals ◽  
Cheek Pouch ◽  
Oxygen Derived Free Radicals ◽  
Before And After

We previously showed [ Am. J. Physiol. 272 ( Heart Circ. Physiol. 41): H2337–H2342, 1997] that nicotine impairs endothelium-dependent arteriolar dilatation. However, mechanisms that accounted for the effect of nicotine on endothelium-dependent vasodilatation were not examined. Thus the goal of this study was to examine the role of oxygen radicals in nicotine-induced impairment of arteriolar reactivity. We measured diameter of cheek pouch resistance arterioles (∼50 μm diameter) in response to endothelium-dependent (ACh and ADP) and -independent (nitroglycerin) agonists before and after infusion of vehicle or nicotine in the absence or presence of superoxide dismutase. ACh, ADP, and nitroglycerin produced dose-related dilatation of cheek pouch arterioles before infusion of vehicle or nicotine. Infusion of vehicle, in the absence or presence of superoxide dismutase (150 U/ml), did not alter endothelium-dependent or -independent arteriolar dilatation. In contrast, infusion of nicotine (2 μg ⋅ kg−1 ⋅ min−1) impaired endothelium-dependent, but not -independent, arteriolar dilatation. In addition, the effect of nicotine on endothelium-dependent vasodilatation was reversed by topical application of superoxide dismutase. We suggest that nicotine impairs endothelium-dependent arteriolar dilatation via an increase in the synthesis/release of oxygen-derived free radicals.

scholarly journals THE ROLE OF SELENIUM MICRONUTRIENTS AS ANTIOXIDANTS IN EXPOSURE TO E-CIGARETTE SMOKE

2019 ◽  
pp. 265-268
Author(s):  
RIVAN VIRLANDO SURYADINATA ◽  
MERRYANA ADRIANI ◽  
SANTI MARTINI ◽  
SRI SUMARMI ◽  
BAMBANG WIRJATMADI
Keyword(s):  
Experimental Study ◽  
Superoxide Dismutase ◽  
Antioxidant Enzymes ◽  
Free Radicals ◽  
Cigarette Smoke ◽  
Wistar Rats ◽  
The Body ◽  
Preventive Actions ◽  
Male Wistar Rats

Objective: E-cigarette products have resulted in various controversies concerning their posed impacts on health. Some argue that exposure to e-cigarette smoke could improve free radicals in the body; thus, it causes harming impacts on health. Peroral selenium (Se) administration can increase superoxide dismutase (SOD) and glutathione peroxidase (GPx) serving as antioxidants in the body. Methods: This research is an experimental study aiming to analyze the effectiveness of Se to decrease free radical due to exposure to e-cigarette smoke as one of the preventive actions. The research was carried out to male Wistar rats with exposure to e-cigarette smoke and peroral Se intake with different time and duration of administration. Results: Research results showed a decrease of antioxidant SOD and GPx in the administration of exposure to e-cigarette smoke, and they gradually increased after Se administration (p=0.000). Meanwhile, the malondialdehyde level was inversely proportional compared to antioxidant SOD and GPx. Conclusion: Se is a micronutrient that can reduce free radicals due to exposure to e-cigarette smoke through enhancement of antioxidant enzymes such as SOD and GPx.

Endothelial dysfunction in mesenteric resistance arteries of diabetic rats: role of free radicals

1994 ◽  
Vol 266 (3) ◽  
pp. H1153-H1161 ◽  
Author(s):  
D. Diederich ◽  
J. Skopec ◽  
A. Diederich ◽  
F. X. Dai
Keyword(s):  
Nitric Oxide ◽  
Superoxide Dismutase ◽  
Free Radicals ◽  
Endothelial Dysfunction ◽  
Hydroxyl Radicals ◽  
Superoxide Anion ◽  
Diabetic Rats ◽  
Resistance Arteries ◽  
Luminal Diameter

Diabetes was induced in rats by an injection of streptozotocin (55 mg/kg). Endothelium-dependent relaxations in mesenteric resistance arteries (luminal diameter 210 +/- 20 microns) of control and diabetic rats were compared in myographs. Acetylcholine induced endothelium-dependent relaxations that were mediated by nitric oxide (EDNO). EDNO-mediated relaxations were impaired in diabetic arteries; concentrations of acetylcholine required to produce 50% relaxation (ED50) of activated arteries were 5 nM in control and 13.5 nM in arteries from diabetic rats studied after 6 wk (P < 0.05). The impairment in relaxation worsened with duration of the diabetes; ED50 for acetylcholine increased to 63 and 100 nM in diabetic arteries studied after 16 and 24 wk of diabetes, respectively. NG-nitro-L-arginine produced 5.5- and 16-fold decreases in sensitivity of control and diabetic arteries to acetylcholine. NG-nitro-L-arginine produced at least as much inhibition of acetylcholine relaxations in diabetic arteries, indicating that the impaired relaxation noted in diabetic arteries does not result from decreased production of EDNO. EDNO-mediated relaxations in diabetic arteries were impaired by increased production of endothelium-derived free radicals. Superoxide dismutase, a scavenger of superoxide anion, and dimethylthiourea, a scavenger of hydroxyl radicals, normalized EDNO-mediated relaxations in diabetic arteries. The ED50 values for acetylcholine were 13.5, 5.5, and 4 nM for untreated and SOD- and DMTU-treated diabetic arteries, respectively (P < 0.05 for treated vs. untreated arteries). Superoxide anion and hydroxyl radicals appear to block EDNO-mediated relaxation by inactivating EDNO.(ABSTRACT TRUNCATED AT 250 WORDS)

Adriamycin-induced myocardial dysfunction in vitro is mediated by free radicals

1991 ◽  
Vol 261 (4) ◽  
pp. H989-H995 ◽  
Author(s):  
V. Lee ◽  
A. K. Randhawa ◽  
P. K. Singal
Keyword(s):  
Lipid Peroxidation ◽  
Superoxide Dismutase ◽  
Free Radicals ◽  
Hydroxyl Radical ◽  
Myocardial Dysfunction ◽  
Ultrastructural Changes ◽  
Radical Scavenger ◽  
Hydrolysis Of

The role of free radicals in adriamycin (Adr)-induced acute myocardial changes was examined by using different antioxidants. Exposure of papillary muscles to Adr (100 microM) in a tissue bath for 60 min reduced developed force by 42%, increased lipid peroxidation by 200%, and resulted in characteristic ultrastructural changes. Catalase (4 x 10(4) U/l), an enzyme effective in the hydrolysis of hydrogen peroxide (H2O2), was more effective in maintaining the developed force than mannitol (20 mM), a hydroxyl radical scavenger. A small protection of developed force seen with superoxide dismutase (1.2 x 10(5) U/l), a quencher of superoxide radical, was evident for the first 15 min only. Only catalase and mannitol showed significant protection against Adr-induced increase in lipid peroxidation. Ultrastructural changes due to Adr alone included mitochondrial swelling, intramitochondrial granules, vacuolization, and disruption of sarcomeres. All of these changes were reduced in the presence of both catalase and mannitol, whereas superoxide dismutase was without any effect. Complete structural or functional protection was not seen with any of the antioxidants used in the study. Although both H2O2 and hydroxyl radical appear to be involved in Adr-induced deleterious effects, data on developed force also indicate that H2O2 may have a major role in mediating the acute effects of Adr in vitro.

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