• Journal of Environmental Science International
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• v.18 no.12
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• pp.1391-1398
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• 2009

In this study, we investigated the suppressive effects of ore minerals on the allergic cell damages and oxidative cell damages. The ore minerals significantly reduced the productions of tumor necrosis factor-alpha (TNF-${\alpha}$) and interleukin-4 (IL-4) in rat basophilic leukemia cells challenged with 2,4-dinitrophenol-bovine serum albumin (DNP-BSA). Lipoxygenase activity was also reduced by the ore minerals. Moreover, the ore minerals showed weak protective effects on the oxidative damage induced by hydrogen peroxide in pig kidney cells and retinal ganglion cells. Photohemolysis of erythrocytes in the presence of rose-bengal as a sensitizer was also inhibited by ore minerals. These results suggest that the ore minerals may be useful as the protectant for allergic and oxidative cell damages.

• Proceedings of the KSCN Conference
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• 2003.05a
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• pp.143-143
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• 2003

Reactive oxygen species are highly reactive oxidant molecules and react with cellular components, causing oxidative damages. These damages may play a significant role in the causation of several chronic diseases. Antioxidative defence systems are present in the body to protect cells from oxidative damages. The first line of defence include dietary antioxidants and enzymes such as superoxide dismutase. Cynanchum wilfordii Hemeseley has been used for centuries as a tonic nutraceutical in China and Korea. (omitted)

• Food Science and Biotechnology
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• v.15 no.4
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• pp.612-616
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• 2006

The protective effect of water extract of ash tree leaves (ALE) against oxidative damages was investigated in paracetamol-induced BALB/c mice. Biochemical analysis of anti-oxidative enzymes, immunoblot analyses of hepatic cytochrome P450 2El (CYP2E1), and the gene expression of tumor necrosis factor (TNF-${\alpha}$) were examined to determine the extract's protective effect and its possible mechanisms. BALB/c mice were divided into three groups: normal, paracetamol-administered, and ALE-pretreated groups. A single dose of paracetamol led to a marked increase in lipid peroxidation as measured by malondialdehyde (MDA). This was associated with a significant reduction in the hepatic antioxidant system, e.g., glutathione (GSH). Paracetamol administration also significantly elevated the expression of CYP2E1, according to immunoblot analysis, and of TNF-${\alpha}$ mRNA in liver. However, ALE pretreatment prior to the administration of paracetamol significantly decreased hepatic MDA levels. ALE restored hepatic glutathione and catalase levels and suppressed the expression of CYP2E1 and TNF-${\alpha}$ observed in inflammatory tissues. Moreover, ALE restored mitochondrial ATP content depleted by the drug administration. These results show that the extract of ash tree leaves protects against paracetamol-induced oxidative damages by blocking oxidative stress and CYP2E1-mediated paracetamol bioactivation.

• Environmental Mutagens and Carcinogens
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• v.22 no.4
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• pp.279-288
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• 2002

According to the epidemiological studies in chromium workers, hexavalent chromium is associated with the risk of lung cancer. Cellular oxidative damages by reactive oxygen species produced by hexavalent chromium exposure may play an important role in the carcinogenesis process. We investigated the availabilities of malondialdehyde measurement for the assessments of oxidative damages from chromium exposure with an experimental inhalation study in vivo. Lipid peroxidation, one kind of cellular oxidative damage, was measured in blood plasma of the rats which inhaled the hexavalent chromium mist for 1, 2 and 3 weeks. The concentrations of malondialdehyde (MDA), the metabolite of lipid peroxidation, in all exposed groups were higher than those of controls with dose-dependant manner. The levels of MDA were also correlated with urine chromium levels of the rats. Therefore, MDA as an indicator of lipid peroxidation could be proper biologic marker for the assessment of the oxidative damage from chromium exposure, which might be involved in carcinogenesis.

• Nutritional Sciences
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• v.8 no.4
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• pp.262-267
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• 2005

Reactive oxygen species can be generated in the skin by hair dyeing. The aim of this study was to find out the effects of the oxidative-type hair dye application in young women on the antioxidant systems. We investigated the lipid peroxide levels, glutathione (GSH) levels, and the antioxidant enzyme activities including superoxide dismutase (SOD), glutathione peroxidase (GSHPx) in plasma and erythrocytes and catalase (CAT) in erythrocytes, and DNA damages in lymphocytes. Also, plasma concentrations of antioxidant vitamins, vitamin A and E, were measured and the correlations between various antioxidant parameters and oxidative damages were evaluated The antioxidant enzyme activities in plasma (GSHPx) and in erythrocytes (SOD and CAT) were decreased significantly after hair dyeing. 1be lipid peroxide and GSH levels were not affected in both plasma and erythrocytes. No significant difference was found in the concentrations of both vitamin A and E between before and after hair dyeing. However, DNA damages expressed as the tail extent moment (TEM) and tail length (TL) were significantly (p<0.001) increased. The plasma vitamin E concentration was correlated with DNA damages (TEM: r=-0.590, p<0.01 and TL: r=-0.533. p<0.01) and RBC SOD activity (r=0.570, p<0.05). In turn, RBC SOD activity was significantly correlated with both plasma MDA levels (r=-0.412, p<0.05) and DNA damages (TM: r=-0.546, p<0.01, TL: r=-0.493, p<0.01). Our results demonstrated that the exposure to hair dyeing produced lymphocyte DNA damage and modification of the antioxidant enzyme activities. Also, there were very strong associations between plasma vitamin E concentration, RBC SOD activity and DNA damage induced by hair dyeing. It suggests that the antioxidant status of a subject is likely to be related to the extent of the harmful effects caused by hair dyeing.

• Biomedical Science Letters
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• v.17 no.1
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• pp.69-77
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• 2011

In this study, we evaluated the protective effects of supercritical extracts and two step ethanol extracts after supercritical extraction from Schizandra chinensis on antioxidant activities and oxidative DNA and cell damages. Supercritical extracts removed DPPH (1,1-diphenyl-2-picryldrazyl) radical by 85.5% at 200 ${\mu}g$/ml, but showed low activities of scavenging and chelating the hydroxyl radical and ferrous iron. However, two step ethanol extracts showed low activities of scavenging the DPPH radical, but removed the hydroxyl radical by 86% at 200 ${\mu}g$/ml. In addition, we tested the activities of extracts for reducing hydroxyl radical-induced DNA and cell damage. Two step ethanol extracts showed protective effect against the oxidative DNA damage by reducing DNA segmentation, inhibiting DNA migration and decreasing the expression of phospho-H2AX. Also, two step ethanol extracts showed protective effect against the oxidative cell damage by inhibiting lipid peroxidation and increasing the expression of p21 protein. Taken together, we suggest that two step ethanol extracts from S. chinensis have a role as useful inhibitors against oxidative damages.

• Biomolecules & Therapeutics
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• v.6 no.2
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• pp.111-118
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• 1998

Ambroxol is thought to have antioxidant ability and some antiinflammatory effect. Effect of ambroxol on the oxidative damages of lipid, collagen and hyaluronic acid was examined. F $e_{2+}$(10 $\mu$M) and 100$\mu$Mascorbate-induced lipid peroxidation of liver microsomes was inhibited by 10 and 100$\mu$M ambroxol, 30$\mu$g/ml catalase and 10 mM DABCO but was not affected by 30$\mu$g/ml SOD and 10 mM DMSO. A 10 and 100$\mu$M ambroxol and 10 mM DABCO inhibited the peroxidative action of 10$\mu$M F $e_{3+}$, 160$\mu$M ADP and 100$\mu$M NADPH on microsomal lipids, whereas inhibitory effects of 30$\mu$g/ml SOD,30$\mu$g/ml catalase and 10 mM DMSO were not detected. The degradation of hyaluronic acid caused by 107M Fe2\\`,5007M H2O2 and 100$\mu$M ascorbate was inhibited by 10 and 100$\mu$M ambroxol,30$\mu$g/ml catalase,10 mM DMSO and 10 mM DABCO, while 30$\mu$g/ml SOD did not show any effect. The cartilage collagen degradation caused by 307$\mu$ F $e_{2+}$,500$\mu$M $H_2O$$_2$ and 200$\mu$M ascorbate was prevented by 100$\mu$M ambroxol. $H_2O$$_2$ and OH . were scavenged by ambroxol, whereas $O_2$, was not removed by it. Ambroxol (100$\mu$M) and 1 mM cysteine reduced DPPH to 1,1-diphenyl-2-picrylhydrazine. In conclusion, ambroxol may inhibit the oxidative damages of lipid, hyaluronic acid and collagen by its scavenging action on oxidants, such as OH . and probably iron-oxygen complexes and exert antioxidant ability.

• The Korea Journal of Herbology
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• v.28 no.6
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• pp.79-86
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• 2013

Objectives : The purpose of this study is to investigate neuroprotective effects and molecular mechanisms of luteolin against ${\beta}$-amyloid ($A{\beta}_{25-35}$)-induced oxidative cell death in BV-2 cells. Methods : The protective effects of luteolin against $A{\beta}_{25-35}$-induced cytotoxicity and apoptotic cell death were determined by MTT dye reduction assay and TUNEL staining, respectively. The apoptotic cell death was further analyzed by measuring mitochondrial transmembrane potential and expression of pro- and/or anti-apoptotic proteins. To elucidate the molecular mechanisms underlying the protective effects of luteolin, intracellular accumulation of reactive oxygen species, oxidative damages, and expression of antioxidant enzymes were examined. Results : Luteolin pretreatment effectively attenuated $A{\beta}_{25-35}$-induced apoptotic cell death indices such as DNA fragmentation, dissipation of mitochondrial transmembrane potential, increased Bax/Bcl-2 ratio, and activation of c-Jun N-terminal kinase and caspase-3 in BV-2 cells. Furthermore, $A{\beta}_{25-35}$-induced intracellular formation of reactive oxygen species and subsequent oxidative damages such as lipid peroxidation and depletion of endogenous antioxidant glutathione were suppressed by luteolin treatment. The neuroprotective effects of luteolin might be mediated by up-regulation of cellular antioxidant defense system via up-regulation of ${\gamma}$-glutamylcysteine ligase, a rate-limiting enzyme in the glutathione biosynthesis and superoxide dismutase, an enzyme involved in dismutation of superoxide anion into oxygen and hydrogen peroxide. Conclusions : These findings suggest that luteolin has a potential to protect against $A{\beta}_{25-35}$-induced neuronal cell death and damages thereby exhibiting therapeutic utilization for the prevention and/or treatment of Alzheimer's disease.

• Biomolecules & Therapeutics
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• v.18 no.1
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• pp.24-31
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• 2010

Taurine, 2-aminoethanesulfonic acid, is an abundant free amino acid present in brain cells and exerts many important biological functions such as anti-convulsant, modulation of neuronal excitability, regulation of learning and memory, anti-aggressiveness and anti-alcoholic effects. In the present study, we investigated to explore whether taurine has any protective actions against oxidative stress-induced damages in neuronal cells. ERK I/II regulates signaling pathways involved in nitric oxide (NO) and reactive oxygen species (ROS) production and plays a role in the regulation of cell growth, and apoptosis. We have found that taurine significantly inhibited AMPA induced cortical depolarization in the Grease Gap assays using rat cortical slices. Taurine also inhibited AMPA-induced neuronal cell damage in MTT assays in the differentiated SH-SY5Y cells. When the neuronal cells were treated with $H_2O_2$, levels of NO were increased; however, taurine pretreatment decreased the NO production induced by $H_2O_2$ to approximately normal levels. Interestingly, taurine treatment stimulated ERK I/II activity in the presence of AMPA or $H_2O_2$, suggesting the potential role of ERK I/II in the neuroprotection of taurine. Taken together, taurine has significant neuroprotective actions against AMPA or $H_2O_2$ induced damages in neuronal cells, possibly via activation of ERK I/II.

• Clinical and Experimental Pediatrics
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• v.48 no.12
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• pp.1295-1309
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• 2005

Nowadays, the nutritional deficits are rarely seen in Korea. However, an increased availability of the highly palatable energy dense, nutrient-poor foods increases the risks of obesity and deficits of vitamins and minerals in the general population. Also, optimum intake of vitamins and minerals, which varies with age and genetic back ground, might not suffice the poor, young, obese, and elderly people. Young girls and individuals participating in weight reductions and aesthetic components are prone to micronutrient deficiencies because they restrict food intake and specific micronutrient rich foods. An inadequate intake of vitamins or minerals is associated with reduced physical performance and exercise capacity, increased obesity, decreased cognitive function, increased DNA damages such as single- and double-stranded breaks or oxidative DNA lesions, and accelerated aging process and increased neuronal damages with mitochondrial oxidative decay. Most of these deleterious effects of the deficit could be prevented by a one tablet of multivitamins with a good balanced diet. High dose B vitamins are frequently administered to overcome the metabolic inadequacy to the people with the less functional enzymes with increased Km values for their coenzymes due to the single gene mutation or due to the single nucleotide polymorphisms. And some certain antioxidant vitamins are also used in large quantities to overcome the oxidative stress and to repair the damages. In this review, new nutritional concepts of some vitamins and minerals, which are widely used and useful for the children, will be discussed.