• Clinical and Experimental Pediatrics
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• v.56 no.3
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• pp.107-111
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• 2013

Preterm infants are vulnerable to the oxidative stress due to the production of large amounts of free radicals, antioxidant system insufficiency, and immature oligodendroglial cells. Reactive oxygen species (ROS) play a pivotal role in the development of periventricular leukomalacia. The three most common ROS are superoxide ($O2^{\cdot-}$), hydroxyl radical ($OH^{\cdot}$), and hydrogen peroxide ($H_2O_2$). Under normal physiological conditions, a balance is maintained between the production of ROS and the capacity of the antioxidant enzyme system. However, if this balance breaks down, ROS can exert toxic effects. Superoxide dismutase, glutathione peroxidase, and catalase are considered the classical antioxidant enzymes. A recently discovered antioxidant enzyme family, peroxiredoxin (Prdx), is also an important scavenger of free radicals. Prdx1 expression is induced at birth, whereas Prdx2 is constitutively expressed, and Prdx6 expression is consistent with the classical antioxidant enzymes. Several antioxidant substances have been studied as potential therapeutic agents; however, further preclinical and clinical studies are required before allowing clinical application.

• Journal of Oriental Neuropsychiatry
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• v.24 no.3
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• pp.309-320
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• 2013

Objectives : There is a possibility LRE as remedy in Alzheimer disease (AD), but it's nerve protection effect and mechanism have to be elucidate. In this research, we applied LRE on $A{\beta}_{25-35}$ pre-treated SH-SY5Y cells, to find out the nerve protection effect and mechanism in AD cell model. Methods : We tried to confirm that effect by experimenting with 20, 50, and $100{\mu}g/ml$ concentration of LRE as a medicine. Next experiment, we assessed damage effect which induced $A{\beta}_{25-35}$, known to cause AD, on SH-SY5Y cell. In addition, cellular viability test is executed under $H_2O_2$ treatment condition in a SH-SY5Y cell. Results : 1. In $A{\beta}_{25-35}$ treated SH-SY5Y cell, LRE exhibited an anti-phosphorylation effect about tau protein, JNK, and IKB. 2. LRE prevent nerve cell apoptosis, which indued $A{\beta}_{25-35}$ and oxidative stress, modify JNK engaged synaptic structure and $NF{\kappa}B$ induced p75-neurotrophin receptor polymorphism. Conclusions : We found that LRE prevented oxidative stress-induced cellular destruction, for example, increased SOD activity of $A{\beta}_{25-35}$ treated SH-SY5Y cell and reduced toxicity of oxygen free radical. Consequently, the ingredients of LRE have a role as a catalyzer for $A{\beta}_{25-35}$ clearance and as scavenger for active oxygen free radical.

• Journal of Physiology & Pathology in Korean Medicine
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• v.24 no.6
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• pp.976-982
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• 2010

We studied to know the anti-inflammation effect on water extracts of Lophatheri Herba which was growing in every places in our country. We objected free radical scanvenger effect and nitrite eliminate effect of the Lophatheri Herba water extracts, and the cell viabillity, the effects of Lophatheri Herba water extracts on NO production, iNOS synthesis induced by LPS. Free radical scavenger effects were $27.91{\pm}0.12%$, $38.96{\pm}0.10%$, $46.22{\pm}0.15%$ depend on 0.5, 1.0, 2.0 mg/ml each dose of Lophatheri Herba water extracts. Nitrite eliminate effects were $9.86{\pm}0.3%$, $80.61{\pm}0.23%$, $97.62{\pm}0.56%$ in 0.1, 1.0, 2.0 mg/ml Lophatheri Herba water extracts on pH 1.2. NO production and iNOS synthesis induced by LPS were reduced in RAW 264.7 cell by Lophatheri Herba water extracts. As the above results, Lophatheri Herba water extracts have anti-inflammation effects via NO production decrease, iNOS synthesis decrease mechanism. So Lophatheri Herba water extracts will be used as the protection or treatment in chronic inflammation desease like a asthma, stomatitis etc.

• Archives of Reconstructive Microsurgery
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• v.14 no.2
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• pp.85-94
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• 2005

Purpose: This study was to evaluate the effect of ${\alpha}-lipoic$ acid, a potent free radical scavenger, on the expression of active form of extracellular signal-regulated kinase (pERK1/2) proteins from hindlimb muscles of rats following ischemia-reperfusion injury. Material and methods: 64 health, $280{\sim}350\;g$ weighted Sprague-Dawley male rats were used. In order to make a muscle flap, the gastrocnemius (GC) and soleus (SOL) muscles were dissected and elevated. The popliteal artery was occluded for 4hours and reperfused for 10 minutes, 30 minutes, 1 hour, 2 hours and 4 hours, respectively. Results: The ischemia by occlusion of the popliteal artery itself caused a minimal change in expression of phosphorylated form of proteins observed in hindlimb muscle. In contrast, after 4 hours of ischemia, immunoreactivity for pERK1/2 in the GC muscle showed dual peaks at 10 minutes and 4 hours after reperfusion. In ${\alpha}-lipoic$ acid treated group, the expression of pERK1/2 was increased significantly compared to I/R-only group. Conclusion: These results suggest that ${\alpha}-lipoic$ acid may protect I/R injury of the skeletal muscle through free radical scavening and activation of intracellular pERK1/2 expression.

• Environmental Engineering Research
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• v.10 no.3
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• pp.138-143
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• 2005

Laboratory batch experiments were conducted to evaluate the Fenton degradation rates of phenanthrene. Fenton reactions for the degradation of phenanthrene were carried out with aqueous and slurry phase, to investigate the effects of sorption of phenanthrene onto solid phase. Various types of surfactants and electrolyte solutions were used to evaluate the effects on the phenanthrene degradation rates by Fenton's reaction. A maximum 90% removal of phenanthrene was achieved in aqueous phase with 0.9% of $H_2O_2$ and 300 mg/L of $Fe^{2+}$ at pH 3. In aqueous phase reaction, inhibitory effects of synthetic surfactants on the removal of phenanthrene were observed, implying that surfactant molecules acted as strong scavenger of hydroxyl radicals. However, use of $carboxymethyl-{\beta}-cyclodextrin$ (CMCD), natural surfactant, showed a slight enhancement in the degradation of phenanthrene. It was considered that reactive radicals formed at ternary complex were located in close proximity to phenanthrene partitioned into CMCD cavities. It was also show that Fenton degradation of phenanthrene were greatly enhanced by addition of NaCl, indicating that potent radical ion ($OCI^-$) played an important role in the phenanthrene degradation, although chloride ion might be acted as scavenger of radicals at low concentrations. Phenanthrene in slurry phase was resistant to Fenton degradation. It might be due to the fact that free radicals were mostly reacting with dissolved species rather than with sorbed phenanthrene. Even though synthetic surfactants were added to increase the phenanthrene concentration in dissolved phase, low degradation efficiency was obtained because of the scavenging of radicals by surfactants molecules. However, use of CMCD in slurry phase, showed a slight enhancement in the phenanthrene degradation. As an alternative, use of Fenton reaction with CMCD could be considered to increase the degradation rates of phenanthrene desorbed from solid phase.

• Journal of the Korean Society of Food Science and Nutrition
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• v.35 no.8
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• pp.979-984
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• 2006

Although iron is essential for many physiological processes, excess iron can lead to tissue damage by promoting the generation of reactive oxygen species (ROS). There is increasing evidence that ROS might play an important role in the pathogenesis of cardiovascular disease. However, the effects of iron excess on platelet function and the thrombotic response to vascular injury are not well understood. We examined the effects of iron excess-induced oxidative stress and the antioxidants on platelet aggregation. Oxidative stress was accessed by either free iron $(Fe^{+2})$ or hydrogen peroxide $(H_2O_2)$, as well as their combination on washed rabbit platelets (WPs) in vitro. When WPs were stimulated with either $Fe^{+2}$ alone or a subthreshold concentration of collagen, which gave an aggregatory curve with a little effect, and a dose dependent increase in platelet aggregation was observed by increasing concentrations of $Fe^{+2}$ with $H_2O_2$. This aggregation was associated with the iron-catalyzed formation of hydroxyl radicals from $H_2O_2$, and were inhibited by NAD/NADP (proton acceptor), catalase $(H_2O_2\;scavenger)$, tiron (iron chelator), mannitol (hydroxyl radical scavenger), and indomethacin (cyclooxygenase inhibitor), but not by NADH/NADPH (proton donor), superoxide mutase, and aspirin. However, NADH/NADPH, an essential cofactor for the antioxidant capacity by the supply of reducing potentials, showed the effect of an enhanced radical formation, suggesting a role for NADH/NADPH-dependent oxidase. These results suggest that iron $(Fe^{+2})$ can directly interact with washed rabbit platelets and this aggregation be mediated by OH formation as in the Fenton reaction, inhibited by radical scavengers.

• Journal of Food Hygiene and Safety
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• v.13 no.2
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• pp.121-128
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• 1998

Ochratoxin A (OA) is a mycotoxin produced by Aspergillus ochraceus as well as other molds. It is a natural contaminant of mouldy food and feed. OA has a number of toxic effects, the most prominant being nephrotoxicity. Futhermore, OA is immunosuppressive, genotoxic, teratogenic and carcinogenic. OA inhibits protein synthesis by competition with phenylalanine in the phenylalanine-tRNA aminoacylation reaction. Recently, lipid peroxidation induced by OA has been reported, indicating that the lesion induced by this mycotoxin could be also related to oxidative pathway. Since it seems impossible to avoid contamination of foodstuffs by toxigenic fungi, detoxification and detoxication of OA are needed. In this study we investigated the protective effects of aspartame (Asp), phenylalanine (Phe), polyphenol 70S (PP) and aloe extract (AE) on the nephrotoxicity induced by subacute exposure to the OA. Asp and Phe are structural analogues of OA. PP, an ingredient of Green Tea and AE have been known as antioxidant and radical scavenger. Phe (40 mg/kg, i.p.) and Asp (25 mg/kg, p.o.) were administered to Sprague-Dawley rats simultaneously with OA (2.0 mg/kg, p.o.) for 2 weeks. PP (200 mg/kg, p.o.) and AE (50 mg/kg, i.v.) were pretreated before administration of OA, for 2 weeks and 3 days, respectively. Using enzymuria, BUN level, creatinemia and histophathologic examination as indices of renal damage, we observed that all of four compounds prevented the nephrotoxic effects induced by OA. It seems that structural analogues of OA such as Asp and Phe have better protective effect on the nephrotoxicity of OA than antioxidants. These results indicate that 1) formation of free radical and lipid peroxidation are likely to be involved in the nephrotoxicity of OA in vivo, 2) Asp, PP and AE might be used for prevention of renal lesions in cases of ochratoxicosis.

• Journal of Nutrition and Health
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• v.40 no.2
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• pp.111-117
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• 2007

This study was designed to investigate the effects of pyroligneous liquor on oxygen radicals and their scavenger enzymes in the liver of Cri/Bgi CD rats (7 rats per group). Male rats were fed a basic diet prepared in our Lab., PL-0 (Control), PL-1, PL-25, PL-50 and PL-75 groups were Prepared to be 0%, 1%, 25%, 50% and 75%with distilled water using pyroligneous liquor (35% of Choa Co. Ltd.), and were administrated orally for 8 weeks. Superoxide radical contents in liver mitochondria and microsomes were significantly decreased to 12-14%, 11-15%, respectively, in these PL-25 and PL-50groups compared with the control group. Hydroxyl radical content in mitochondria and microsomes were markedly decreased to 12-20% and 17%, respectively, in these PL-25 and PL-50% groups compared with the control group. Hydrogen peroxide content in mitochondria and microsomes were significantly decreased about 15-12% and 22-20% in liver of PL-25 and PL-50 groups compared with the control group. Mn-SOD and Cu/Zn-SOD activities in liver of PL-25 and PL-50 groups were remarkably increased to 15-25%, 11-16%, respectively, compared with the control group. GPx activities in mitochondria and microsomes were significantly increased in the liver of PL-25 and PL-50 groups compared with the control group. CAT activities in mitochondria and cytosol were significantly increased to 12-14%, 15-27%, respectively, in the liver of PL-25 and PL-50 groups compared with the control group. These results suggest that long term administration orally of 25 and 50% pyroligneous liquor may effectively inhibit the formation of oxygen free radicals, and also scavenger enzyme activities significantly increase through the administration orally.

• Biomolecules & Therapeutics
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• v.17 no.4
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• pp.395-402
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• 2009

Insulin appears to play a role in brain physiology, and disturbances of cerebral insulin signalling and glucose homeostasis are implicated in brain pathology. The objective of the present study was to investigate the protective effects of insulin under conditions of oxidative stress induced by hydrogen peroxide ($H_2O_2$) in C6 glial cells. Insulin at concentration of $10^{-7}$ M could prevent 12 h $H_2O_2$-induced cell death. The formation of reactive oxygen species (ROS), nitric oxide (NO) and 2-thiobarbituric acid-reactive substances (TBARS) were significantly scavenged by insulin pre-treatment in C6 glial cells after $H_2O_2$-induced oxidative stress. Insulin significantly stimulated the phosphorylation of Akt in the cells and the activation of Akt was maintained in response to insulin under $H_2O_2$ incubation for 12 h. In conclusion, these results provide evidence that insulin acts as a free radical scavenger and stimulating Akt activity. These data suggest that insulin may be effective in degenerative diseases with oxidative stress.

• Biomolecules & Therapeutics
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• v.10 no.2
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• pp.78-84
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• 2002

Taurine (2-ethaneaminosulfonic acid, $^+{NH}_3{CH_2}{CH_2}{SO_3^{-}}$) is endogenous amino acid with functions as modulator of osmoregulation, antioxidation, detoxification, transmembrane calcium transport, and a free radical scavenger in mammalian tissues. Taurine transporter(TAUT) contains 12 transmembrane helices, which are typical of the $Na^+$- and $Cl^-$-dependent transporter gene family, and has been cloned recently from several species and tissues. To analyze the expression of TAUT mRNA, one step RT-PCR was performed from human and mouse cultured cell lines and from various mouse tissues. The primers were designed to encode highly conserved amino acid sequences at the second transmembrane domain and at the fourth and fifth intracellular domains. RT-PCR analysis showed both of the human intestine HT-29 and mouse macrophage RAW264.7 cell lines expressed mRNA of TAUT. To define the expression patterns of the TAUT mRNA in the murine organs, RT-PCR was performed to detect cDNA representing TAUT mRNA from seven different mouse tissues. The TAUT was detected in all of the mouse tissues analyzed such as heart, lung, thymus, kidney, liver, spleen and brain. A large amount of transcript was fecund from heart, liver, spleen, kidney, and brain, while lung contained a very small amount of transcript.