• 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.

• The Journal of Internal Korean Medicine
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• v.20 no.1
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• pp.167-180
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• 1999

Cervus elaphus, being known to reinforce Kidney, have tested to study the effects concerning damages of brain tissue induced by lipid peroxidation. In vitro, the level of lipid peroxide in brain tissue was decreased proportinally according to dose by Cervus elaphus extract solution for aqua-acupuncture (CESAA). It was much more decreased, when lipid peroxidation was induced with Fe(II). And, it was seen proportinally decrease according to the dose of CESAA on xanthine oxidase activities and type conversion ratio. However, I can not find special changes about aldehyde oxidase activities. And, I had observed the effects of CESAA on damages of rat's brain following ischemia and reflow. Before ischemia was caused, CESAA was applied 0.2 ml per 250 g through femoral vein in ischemia and reflow group and normal sailine was applied in normal group. Ischemia was caused by cervical artery's clamp for 30 min and reflowed by clamp remove after 15 min. It was increased on the content of lipid peroxidation, activies and type conversion ratio of xanthine oxidase following ischemia and reflow. However, they were decreased when CESAA was pre-appllied. However, it could not seen special changes on aldehyde oxidase activities, either. In conclusion. CESAA recovers the damage of brain due to ischemia and reflow by decreasing the lipid peroxidation through decreasing of xanthine oxidase activies and type conversion ratio.

• 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.

• 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.

• The Journal of Internal Korean Medicine
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• v.35 no.2
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• pp.208-221
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• 2014

Purpose : Banhasasim-tang (BHSST) has been applied for treating the symptom of gastric stuffiness, which is similar to dyspepsia. The object of this study was to observe the healing effect of BHSST on the indomethacin (IND)-induced gastric ulcer in rats. Methods : Three different dosages of BHSST (400, 200 and 100 mg/kg) were orally administered 30 min before IND treatment; 6 hrs after IND treatment, the changes on the gross lesion scores, fundic histopathology, myeloperoxidase (MPO) activity, lipid peroxidation and antioxidant defense system (glutathione contents, catalase (CAT) and superoxide dismutase (SOD) activities) were observed, and compared with the activity of the synthetic anti-ulcer drug, a representative proton pump inhibitor omeprazole (OME) 10 mg/kg. Results : All three different dosages of BHSST treatment in the IND-induced gastric ulcer rats, significant and dose dependent decreased gastric damages - hemorrhagic gross lesions, gastric mucosa MPO levels and histopathological gastric ulcerative lesions - were detected as compared with the IND treated control rats. BHSST also strengthened the antioxidant defense systems - decreased the level of lipid peroxidation and CAT activity but increased the level of GSH and SOD activity, and BHSST 200 mg/kg showed similar anti-ulcerative effect as compared with OME 10 mg/kg. Conclusions : The results obtained in this study suggest that BHSST has favorable effects against IND-induced gastric damages, through significant and dose-dependent decreasing gastric damages and the strengthening of the body's antioxidant defense systems with direct anti-inflammatory effects.

• Toxicological Research
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• v.27 no.1
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• pp.1-6
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• 2011

Lipid peroxidation is a free radical oxidation of polyunsaturated fatty acids such as linoleic acid or arachidonic acid. This process has been related with various pathologies and disease status mainly because of the oxidation products formed during the process. The oxidation products include reactive aldehydes such as malondialdehyde and 4-hydroxynonenal. These reactive aldehydes can form adducts with DNAs and proteins, leading to the alterations in their functions to cause various diseases. This review will provide a short summary on the implication of lipid peroxidation on cancer, atherosclerosis, and neurodegeneration as well as chemical and biochemical mechanisms by which these adducts affect the pathological conditions. In addition, select examples will be presented where antioxidants were used to counteract oxidative damage caused by lipid peroxidation. At the end, isoprostanes are discussed as a gold standard for the assessment of oxidative damages.

• The Journal of Korean Medicine
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• v.19 no.1
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• pp.49-65
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• 1998

Holotrichia was tested for the effects on damages of liver tissue induced by bromobenzene. Holotrichia was treated firstly into samples, and then bromobenzene intoxicated animal models were set with them. In vitro, the level of lipid peroxide in tissue of liver proportinally decreased with the level of concentration of extract prepared from Holotrichia It was much more decreased, when lipid peroxidation was induced with ferrous iron ($Fe&{+2}$). In vivo, after the extract was administered to the animal model for twenty days, the level of lipid peroxide in liver decreased compared to that of bromobenzene-treated group. The enzyme activities of epoxide hydrolase and glutathione S-transferase in liver highly increased in Holotrichia pre-medicating group compare with the group treated with only bromobenzene. And we can get the same results in the enzyme activities of superoxide dismutase, catalase and glutathione peroxidase. The level of glutathione followed by Holotrichia pre-medicationg administration, increased as highly as normal group in compare with the group treated with only bromobenzene. Also, the enzyme activities of AL T, AST and $\{gammer}-GTP$ in liver considerably decreased. In conclusion, Holotrichia recovers the damage of liver due to bromobenzene intoxication by the increased activities of lipid peroxidation and bromobenzene scavenging enzymes.

• Nutrition Research and Practice
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• v.7 no.1
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• pp.34-42
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• 2013

This study investigated the effects of magnetized water supplementation on blood glucose, DNA damage, antioxidant status, and lipid profiles in streptozotocin (STZ)-induced diabetic rats. There were three groups of 4-week-old male Sprague-Dawley rats used in the study: control group (normal control group without diabetes); diabetes group (STZ-induced diabetes control); and magnetized water group (magnetized water supplemented after the induction of diabetes using STZ). Before initiating the study, diabetes was confirmed by measuring fasting blood glucose (FBS > 200 dl), and the magnetized water group received magnetized water for 8 weeks instead of general water. After 8 weeks, rats were sacrificed to measure the fasting blood glucose, insulin concentration, glycated hemoglobin level, degree of DNA damage, antioxidant status, and lipid profiles. From the fourth week of magnetized water supplementation, blood glucose was decreased in the magnetized water group compared to the diabetes group, and such effect continued to the 8th week. The glycated hemoglobin content in the blood was increased in the diabetes group compared to the control group, but decreased significantly in the magnetized water group. However, decreased plasma insulin level due to induced diabetes was not increased by magnetized water supplementation. Increased blood and liver DNA damages in diabetes rats did significantly decrease after the administration of magnetized water. In addition, antioxidant enzyme activities and plasma lipid profiles were not different among the three groups. In conclusion, the supplementation of magnetized water not only decreased the blood glucose and glycated hemoglobin levels but also reduced blood and liver DNA damages in STZ-induced diabetic rats. From the above results, it is suggested that the long-term intake of the magnetized water over 8 weeks may be beneficial in both prevention and treatment of complications in diabetic patients.

• Journal of the Korean Society of Food Science and Nutrition
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• v.20 no.2
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• pp.187-196
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• 1991

Aging is the progressive accumulation of changes with time associated with responsible for the ever-increasing susceptibility to disease and death which accompanies advancing age. Lipid peroxides easily produced in the membrane system by the chain reaction of free radicals which occurred from various environmental factors. The amount of lipid peroxides produced in biological system increased with aging process, and lipid peroxidation damages involved in aging process and pathological disorders. Although lipid peroxides have such deleterious effects on the organisms, there are numerous substances and mechanisms which prevent the reaction of peroxide formation and protect the subject from its toxicity. This review provides an overview of how does lipid peroxidation of unsaturated lipids take place by free radical, and what is the intervention of lipid peroxides in pathogenesis of some human diseases, and also how does food restriction influences the aging process and various pathological disorders. The major focus of this paper is to review the evidence indicating that food restriction retards the aging process, and possible mechanisms of its actions. Therefore, it discussed the effects of age and food restriction on life-span, membrane yield, lipid peroxidation, fatty acid composition and peroxidizability, cholesterol and triglyceride levels, prostaglasndin and thromboxane synthesis, which may be concerned with blood flow, membrane fluidity, homeostasis and glomerular filtration rate in living body.

• Journal of Nutrition and Health
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• v.29 no.2
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• pp.159-165
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• 1996

This study was performed to investigate the effects of concentration and degree of unsaturation of fatty acids on cellular proliferation and lipid peroxide production, using primary skin fibroblasts from neonate rats Fibroblasts (CPD : 2.8-5.4). Cells were cultured either in control medium (Dulbecco's modified Eagle's medium supplement with 10% fetal bovine serum) or in media supplemented with various kinds (stearic, oleic, linoleic, arachidonic, linolenic, eicosapentaenoic acid) and amounts (5, 10, 25, 50, 100, 150uM)of fatty acids. Cellular proliferation ratio and lipid peroxice production were measured and morphological changes were observed. Cellular proliferation was inhibited and morphological changes were observed. Cellular proliferation was inhibited and morphological changes were observed in cells grown in stearic containing media. Oleic, arachidonic, and eicosapentaenoic aicd tend to stimulate cellualar proliferation, and linolenic acid had no effects. Lipid peroxide concentrations in fibroblasts increased in proportion to the contents and unsaturation of fatty acids in media. Especially supplementation of arachidonic acid accelerated cellualr lipid peroxidation. Free radicals may cause severs damage to biological molecules, so lipid peroxidation probably contributes cellular membrane damages. However there were little relationship between lipid peroxide production and cellular proliferation in this study. (Korean J Nutrition 29(2) : 159~165, 1996)