• 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)

• Archives of Pharmacal Research
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• v.19 no.3
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• pp.178-182
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• 1996

Using superoxide dismutase (SOD)-deficient mutants of Saccharomyces cerevisiae, the oxidative stresses induced by 0.1 mM of copper ion $(Cu^{++})$ was studied. In aerobic culture condition, yeasts lacking MnSOD (mitochondrial SOD) showed more significant growth retardation than CuZnSOD (cytoplasmic SOD)-deficient yeasts. However, not so big differences in growth pattern of those mutants compared withwild type were observed under anaerobic condition. It was found that, under aerobic condition, the supplementation of 0.1 mM copper ioh:(Cu") into culture medium caused the remarkable increase of CuZnSOD but not so significant change in MnSOD. It was also observed that catalase activities appeared to be relatively high in the presence of copper ion in spite of the remarkable reduction of glutathion peroxidase in CuZnSOD-deficient yeasts, but the slight increments of catalase and glutathion peroxidase were detected in MnSOD-deficient strains. It implies that the lack of cytoplasmic SOD could be compensated mainly by catalase. However, these phenomena resulted in the significantincrease of cellular lipid peroxides content in CuZnSOD-deficient yeasts and the slight increment of lipid peroxides in MNSOD-deficient cells. In anaerobic cultivation supplementing copper ion, the cellular enzyme activities of catalase and glutathion peroxidase in SOD-deficient yeasts were slightly increased without any significant changes of lipid peroxides in cell membrane. It suggests that a little amount of free radicals generated by copper ion under anaerobic condition could be sufficiently overcome by catalase as well as glutathion peroxidase.dase.

• Journal of Nutrition and Health
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• v.37 no.9
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• pp.771-779
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• 2004

This study was performed to investigate the effect of dietary $\beta$-carotene supplementation on lipid metabolism and antioxidant enzyme activities in hyperlipidemic rats. Fifty Sprague-Dawley male rats aging 7 weeks were fed the control diet (CD,5% corn oil) and the high fat diet (HFD,15% beef tallow +1% cholesterol) for 4 weeks and then 0.02% $\beta$-carotene was supplemented to CD and HFD group for 8 more weeks. Serum lipid compositions, lipid peroxides and antioxidative enzymes in liver were analyzed at 4, 8 and 12week of the experiment. Serum levels of total lipid, total cholesterol, triglyceride, LDL-cholesterol, VLDL-cholesterol were higher in HFD groups than in CD groups (p < 0.001), Serum levels of HDL-cholesterol were higher in CD groups than in HFD groups (p < 0.01) . The effect of $\beta$-carotene supplementation was not significant in all groups but tended to be lower in total lipid, total cholesterol and Triglyceride. Thiobarbituric acid reactive substances (TBARS) levels in plasma and liver were showed significantly higher in HFD groups (p < 0.001, p < 0.05). The effects of $\beta$-carotene supplementation on the level of plasma and liver TBARS were not found except HFD groups at 12 week. Liver conjugated diene levels in HFD groups were higher than in CD groups (p < 0.01), but the effect of $\beta$-carotene supplementation did not show any differences. Liver lipofuscin levels were not significantly different among all groups. The activities of superoxide dismutase (SOD) and catalase were significantly lower in HFD groups at 8 week (p < 0.001) but were not significantly different at 4 and 12week. The activity of SOD in $\beta$-carotene supplemented HFD group was significantly higher at 8 week (p < 0.01). Glutathione peroxidase (GSH-Px) activity was significantly lower in HFD groups (p < 0.01) and was significantly increased in groups supplemented $\beta$-carotene (p < 0.05). It is suggested that $\beta$-carotene supplementation partly decreases the serum lipid and lipid peroxide levels and increases the activities of antioxidant enzymes in hyperlipidemic rats.

• The Korean Journal of Physiology and Pharmacology
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• v.25 no.5
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• pp.403-411
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• 2021

This study was designed to evaluate the gastroprotective activity of cirsilineol in hydrochloric acid (HCl)/ethanol-induced gastric ulcer model. Cirsilineol was administered at the doses of 20 and 40 mg/kg in HCl/ethanol-induced rats. The gastroprotective ability was verified by determining the ulcer score, total acidity, hemoglobin, inflammatory cytokines, lipid peroxides, and enzymatic antioxidants superoxide dismutase (SOD) and catalase (CAT) in gastric tissue and serum biochemical analysis. The results showed a favorable increase in the hemoglobin level, antioxidant enzymes (SOD and CAT), restored electrochemical balance (carbon dioxide & anion gap) while a noticeable decrease in ulcer index, total acidity, lipid peroxides, inflammatory cytokines (interleukin-1 beta [IL-1β], IL-6, and tumor necrosis factor alpha) in rats treated with the cirsilineol. The serum biochemical analysis on liver markers (alkaline phosphatases, alanine aminotransferase, and aspartate aminotransferase), kidney markers (urea, creatinine, albumin, globulin, total protein), and lipid profile (triglyceride, high-density lipoprotein, total cholesterol) were attenuated by cirsilineol treatment in rats. Histopathology showed enhanced gastric protection and preserved the integrity of gastric mucosa upon cirsilineol administration. These results ultimately suggest that cirsilineol has gastroprotective effects that prevent the development of gastric ulcer.

• The Korean Journal of Pharmacology
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• v.31 no.3
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• pp.323-331
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• 1995

Monocyte/macrophage infiltration is the well known initial features associated with the development of glomerular disease including non-immune mediated nephropathy. Tumor necrosis factor ${\alpha}(TNF{\alpha})$, a cytokine produced primarily by monocyte/macrophage, exhibits similar effects as observed at the initial stages and during the progression of glomerular injury. Because the mesangial cells are target cells for glomerular injury, the present study examined the effect of $TNF{\alpha}$ on glomerular mesangial cell membrane lipid peroxidation as an index of cytotoxicity attributing to $TNF{\alpha}$. Primary culture of rat mesangial cell was established by incubation of glomeruli isolated from male Sprague-Dawley rat kidneys utilizing a standard sieving method. The levels of lipid peroxides in the mesangial cells were quantitated by malondialdehyde- thiobarbituric acid adduct formation. During an 8 hour incubation at $37^{\circ}C$, $TNF{\alpha}$ at 10 to 10,000 units/ml increased the levels of lipid peroxides dose dependently. Western blot analysis demonstrated that a short thermal stress induced heat shock response and the synthesis of heat shock protein 70(hsp70) in this mesangial cells. Further, this induction of hsp 70 prevented increase of lipid peroxides in the mesangial cells exposed to $TNF{\alpha}$. These data suggest that $TNF{\alpha}-induced$ lipid peroxidation in the mesangial cells may have pathophysiological relevance to glomerular injury and prior induction of heat shock response may play a role in the cellular resistance against $TNF{\alpha}-induced$ glomerular injury.

• Archives of Pharmacal Research
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• v.17 no.2
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• pp.109-114
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• 1994

The role of sex homones in hepatic lipid peroxidation, and in hepatic adehyde odidase and xanthine oxidase activites were investigated using rat liver homogenates. It was observed that male rt had a significantly greater content of malondialdehyde in liver than female. Among the sex hormones tested, estradiol, one of female hormones, markedly inhibited the formation of lipid peroxides in liver tissues in vitro. Especially, the inhibitory effect of estradiol appeared more remarkably in Fe-induced lipid peroxidation. The hepatic xanthine oxidase activity was decreased about 15% by $10\;^6\;M$ estradiol, wherease, the adehyde oxidase activity was almost completely disappeared at the same concentration of estradiol. It implies that sex differences in lipid peroxidation is attributed to the suppression of radical generating system by estradiol.

• Journal of Nutrition and Health
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• v.29 no.1
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• pp.97-103
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• 1996

This study was performed to investigate the effects of lipid on cellular senescence, lipid peroxide production, and morphological changes. For this study we used primary skin fibroblasts from neonate rats grown in media various lipid contents. Fibroblasts were cultured until they lost their proliferation potential either in control medium (Dulbecco's modified Eagle's medium supplement with 10% fetal bovine serum) or in media supplemented with various concentrations of lipid-cholesterol rice component from bovine serum. Cumulative population doublings(CPD, as an index of cellular life span), and cellular thiobarbituric acid reactive substances (TBARS, as an index of lipid peroxide) concentrations were measured and morphological changes were observed. CPD were shortened with increasing lipid concentration in media ; 28.12 for cells grown in control medium and 13.42, 11.42, and 6.19 for those grown in 0.1%, 1% and 5% lipid rich components containing media, respectively. Cellular proliferation ratios were those grown in 5% lipid rich components containing media were delayed and they were degenerated soon. TBARS concentrations were increased with increasing concentration of lipid in media. Morphological changes were observed in cells grown in control medium by cellular senescence. Especially lipid droplets were observed in cells grown in 5% lipid rich components containing media. Therefore it seems that lipid contents in media had an effect on cellular proliferation and cellular life span, possibly via lipid peroxide production.

• Journal of Environmental Health Sciences
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• v.12 no.1
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• pp.25-38
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• 1986

This paper was intented to charily the cause of an increase of serum guanase activity in rats following injection of $CCI_4$. The cause of increasing serum guanase was focused on the change of guanase activities in both serum and liver, and additionally, these results were compared with the previously known alanine aminotransferase (ALT). Concomitantly the microscopic investigation on the histologic changes, and the determination of lipid peroxides of liver were combined in this experiment for a correlation to observe that the activity of guanase would be effected by the various degree of hepatic injury induced by $CCI_4$. The serum levels of guanase were increased about 2 fold in the fatty change stage (3-12 days), 5.2 fold representing the peak value in necrosis stage (21days), 4.5 fold in early cirrhosis stage (48 days), and 2 fold in severe cirrhosis stage (92 days). These changes of serum guanase activity showed similar patterns to those of ALT activity and lipid peroxides in liver cell. The changes of liver guanase activities showed an increase, whereas ALT activities in liver were markedly decreased. It is likely that the increase of serum guanase activity is based on the excess leaking of guanase into blood by the result of accelerated enzyme synthesis in liver cell of $CCI_4$ intoxicated rats. In addition, the possibility could not be ruled out, however, that the increase of serum guanase activity would be caused by the alteration of membrane permeability.

• Asian-Australasian Journal of Animal Sciences
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• v.23 no.2
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• pp.234-239
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• 2010

Effects of polyunsaturated fatty acid (PUFA) and vitamin E (VE) supplementation in the diet of breeder hens on the egg quality and hatchability, lipid peroxides of the egg yolk, and development of the newly-hatched offspring chicks were investigated. A total of 800 Avian 48, 28 wk-old broiler breeders were assigned randomly to 4 groups with 4 replicates of 45 females and 5 males. Each group was fed one of the following four diets with different oil sources and levels of VE: corn oil (CO), fish oil (FO), CO+VE and FO+VE. The results showed that: i) Addition of FO in the breeder diet reduced the whole egg weight, yolk weight, albumen weight, yolk color score and neonatal offspring chick body weight without affecting the hatchability as compared to the CO treatment. ii) Addition of VE efficiently reduced the lipid peroxides of egg yolk from hens fed diets containing FO. iii) VE in the breeder diet significantly promoted the development of liver and heart of the chick offspring.

• Biomolecules & Therapeutics
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• v.22 no.1
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• pp.47-54
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• 2014

The present study was aimed to evaluate the antioxidant defense system of cinnamaldehyde in normal, diabetic rats and its possible protection of pancreatic ${\beta}$-cells against its gradual loss under diabetic conditions. In vitro free radical scavenging effect of cinnamaldehyde was determined using DPPH (1,1-diphenyl-2-dipicrylhydrazyl), superoxide radical, and nitric oxide radical. Streptozotocin (STZ) diabetic rats were orally administered with cinnamaldehyde at concentrations of 5, 10 and 20 mg/kg body weight for 45 days. At the end of the experiment, the levels of plasma lipid peroxides and antioxidants such as vitamin C, vitamin E, ceruloplasmin, catalase, superoxide dismutase, reduced glutathione and glutathione peroxidase were determined. A significant increase in the levels of plasma glucose, vitamin E, ceruloplasmin, and lipid peroxides and significant decrease in the levels of plasma insulin and reduced glutathione were observed in the diabetic rats. Also the activities of pancreatic antioxidant enzymes were altered in the STZ-induced diabetic rats. The altered enzyme activities were reverted to near-normal levels after treatment with cinnamaldehyde and glibenclamide. Histopathological studies also revealed a protective effect of cinnamaldehyde on pancreatic ${\beta}$-cells. Cinnamaldehyde enhances the antioxidant defense against reactive oxygen species produced under hyperglycemic conditions and thus protects pancreatic ${\beta}$-cells against their loss and exhibits antidiabetic properties.