• Journal of the Korean Society of Food Science and Nutrition
• /
• v.27 no.6
• /
• pp.1262-1266
• /
• 1998

The purpose of this study was to investigate peroxidative damage and antioxidative defense systems such as superoxide dismutase(SOD), glutathione peroxidase(GSH Px), glutathione S transferase (GST) and vitamin E of liver in rat exposed microwave. Sprague Dawley male rats 200$\pm$10gm were randomly assigned to normal and microwave(MW) groups. After rats were irradiated with microwave at frequency of 2.45GHz for 15min, the change patterns of antioxidative defense system and peroxidative damage of liver tissue in MW group were investigated for 16 days(the 2nd, 4th, 6th, 8th and 16th days) compared with those of normal group. The activity of superoxide dismutase(SOD) in MW group was increased at the 2nd day compared with that of normal group, but not significantly. The glutathione peroxidase(GSH Px) in MW group was decreased to 24% and 25% at the 4th and 6th days, respectively, compoared with that of normal group, but GSH Px was increased to level of normal group at the 16th day. The activity of glutathione S transferase(GST) in MW group was decreased at the 2nd day after irradiated with microwave, but GST showed to that of normal group at the 16th day. The content of vitamin E in MW group was lower than that of normal group at the 6th and 8th days after the irradiation, but was recovered to the level of normal group at the 16th days. The content of thi obarbituric acid reactive substances(TBARS) of liver in MW group was increased to 28.9%, 53.8%, 69.7% and 30.2% of normal group at the 2nd, 4th, 6th and 8th days after the irradiation, respectively, but recovered to the level of normal group at the 16th day. The present results indicated that antiox idative defense systems of rats irradiated microwave was weaken more than that of normal group, which lead to acceleration of lipid peroxidation.

• Journal of the Korean Society of Food Science and Nutrition
• /
• v.20 no.2
• /
• pp.111-120
• /
• 1991

In order to investigate the cellular peroxidative damage due to heated oil intake and the preventive effect of vitamin E on it rats were fed heated corn oil with acid value of 4.02 at the level of 10 Cal% and three different levels of vitamin E that were 0, 40 and 200 mg/kg diet. Control group was fed fresh corn oil and 40mg/kg diet of vitamin E. After ech feeding period of 0, 3 and 6 weeks, liver superoxide dismutase (SOD), glutathione peroxidase (GPX) activities and microsomal content of vitamin E and lipid peroxide (LPO) were measured as well as cellular morphology was examined. SOD activities and LPO contents were higher, while GPX activities and vitamin e contents were lower in heated oil groups than control group. Electromicroscopic observation revealed the loss of inner mitochondrial membrane and cristae and irregular arrangement of nuclear membrane and chromatin in heated oil groups. As dietary vitamin e level was increased, SOD activity and LPO content were decreased, but GPX activity and vitamin E content in the liver increased and cellular peroxidative damage reduced progressively. This phenomena was more remarkable in 6 weeks of feeding than 3 weeks.

• Journal of Nutrition and Health
• /
• v.27 no.10
• /
• pp.1007-1017
• /
• 1994

In order to investigate the effect of Korean green tea, oolong tea and black tea beverage on the antioxidative detoxification in cadmium(Cd) poisoned rat liver, male Sprague-Dawley rat weighing 143$\pm$3.2g were divided into control and experimental groups. The experimental groups were fed standard diet containing 40ppm Cd and were given distilled water(CD), 5% black tea(BT), oolong tea(OT) and green tea(GT), respectively. Tea beverages were extracted from 5G dry leaves of teas in 100ml hot distilled water by the treatment at 85$^{\circ}C$ for 3 min. Liver xanthine oxidase(XOD) activity was increased by the administration of Cd except GT group. Liver superoxide dismutase(SOD), glutathione peroxidase(GSH-px), glutathione S-transferase(GST) activities were decreased by te administration of Cd but did not decreased by the administration of green tea(in GT group). Vitamin E and reduced glutathione contents were significantly decreased in Cd administered groups. Liver lipid peroxide value in Cd administered groups were increased compared to control group, but was not increased in GT group. Serum glutamic oxaloacetic transaminase(GOT) activities in CD, OT, BT groups were higher than control, but that in GT group was similar to control group. Serum glutamic pyruvic transaminase(GPT) activity was not significantly different among various groups. It was concluded that green tea might alleviate peroxidative damage in Cd-administered rat liver by reinforcing antioxidative detoxification system.

• Journal of the Korean Society of Food Science and Nutrition
• /
• v.26 no.5
• /
• pp.901-907
• /
• 1997

The purpose of this study was to investigate the effects of green tea catechin o n free radical generation system and peroxidative damage in the liver of streptozotocin(STZ)-induced diabetic rats. Spragu-Dawley male rats weighing 150$\pm$10gm were randomly assigned to one normal and three STZ-induced diabetic groups; diabetic groups were classified to catechin free diet(DM-oC group), 0.5% catechin diet(DM-0.5C group) and 1% catechin diet(DM-1C group) according to the levels of dietary catechin supplementation. Diabetes was experimentally induced by intravenous injection of 55mg/kg of body wt of STZ in citrate buffer(pH 4.3) after feeding of three experimental diet for 4 weeks. Animals were sacrificed at the 6th day of diabetic states. Activities of serum glutamic oxaloacetic transaminase(GPT) in DM-oC groups were higher than those of the normal group, and those in catechin supplementation group were similar to those of the normal group. Liver lipid peroxide values increased by 153%, 49%, and 27% in Dm-oC, DM-0.5C and DM-0C and Dm-1C but was not significantly different in catechin supplementation groups compared with the normal group, and liver cytochrome $P_{450}$ contents was similar to result of XOD activity. In electron microscopic examination of liver, lysosome was relatively scattered in Dm-oC and Dm-0.5C group and preserved normal shapes in DM-1C group. The present results indicate that STZ-induced diabetic rats are more sensitive to oxidative stress, leading to the acceleration of lipid peroxidation process, but this was reduced by anti-oxidative effect of high level of dietary catechin. It is concluded that dietary catechin serves as powerful antioxidant against lipid peroxidation in diabetic rats.

• 대한생식의학회:학술대회논문집
• /
• 2000.06a
• /
• pp.13-28
• /
• 2000

Human spermatozoa exhibit a capacity to generate ROS and initiate peroxidation of the unsaturated fatty acids in the sperm plasma membrane, which plays a key role in the etiology of male infertility. The short half-life and limited diffusion of these molecules is consistent with their physiologic role in key biological events such as acrosome reaction and hyperactivation. The intrinsic reactivity of these metabolites in peroxidative damage induced by ROS, particularly $H_2O_2$ and the superoxide anion, has been proposed as a major cause of defective sperm function in cases of male infertility. The number of antioxidants known to attack different stages of peroxidative damage is growing, and it will be of interest to compare alpha-tocopherol and ascorbic acid with these for their therapeutic potential in vitro and in vivo. Both spermatozoa and leukocytes generate ROS, although leukocytes produce much higher levels. The clinical significance of leukocyte presence in semen is controversial. Seminal plasma confers some protection against ROS damage because it contains enzymes that scavenge ROS, such as catalase and superoxide dismutase. A variety of defense mechanisms comprising a number of antioxidants can be employed to reduce or overcome oxidative stress caused by excessive ROS. Determination of male infertility etiology is important, as it will help us develop effective therapies to overcome excessive ROS generation. ROS can have both beneficial and detrimental effects on the spermatozoa and the balancing between the amounts of ROS produced and the amounts scavenged at any moment will determine whether a given sperm function will be promoted or jeopardized. Accurate assessment of ROS levels and, subsequently, OS is Vital, as this will help clinicians both elucidate the fertility status and identify the subgroups of patients that respond or do not respond to these therapeutic strategies. The overt commercial claims of antioxidant benefits and supplements for fertility purposes must be cautiously looked into, until proper multicentered clinical trials are studied. From the current data it appears that no Single adjuvant will be able to enhance the fertilizing capacity of sperm in infertile men, and a combination of the possible strategies that are not toxic at the dosage used would be a feasible approach.

• Proceedings of the Korean Society of Fisheries Technology Conference
• /
• 2001.05a
• /
• pp.97-98
• /
• 2001

Alpha-tocopherol (alpha-Toc) is a classical lipophilic antioxidant well known as a scavenger of free radicals in a hydrophobic milieu. The primary function of alpha-Toc is to stabilize cellular and subcellar membrane by preventing peroxidative damage of structural polyunsaturated fatty acids (PUFA). The characteristic aroma of sweet smelt Precoglossun altivelis is known as oxida breakdown products of PUFA ironically. (omitted)

• Journal of the Korean Society of Food Science and Nutrition
• /
• v.21 no.6
• /
• pp.601-607
• /
• 1992

In order to investigate the liver damage and hepatic protective systems in cadmium(Dd) administered rats, five different levels of Cd were injected intraperitoneally to male rats of sprague-Dawley strains weighing $250{\pm}15g.$ Levels of daily Cd administration were 0(control), 0.625(A), 1.25(B), 2.5(C) and 5mg(D)/kg of body weight and single inhection per day was done for consecutive two days. With increasing Cd dosed, serum glutamic oxaloacetic transaminase, glutamic pyruvic transaminase and alkaline phosphatase activities were increased. And at the same time, hepatic reduced glutathione contents were decreased, whereas the levels of oxidized form were increased. Liver lipid peroxide levels of A, B, C and D groups were 1.1, 1.5, 1.8 activities and vitamin E contents were progressively reduced in accordance with the increase in Cd dose. However, liver superoxide dismutase activities were not different between control and A group although it was higher in B and lower in C and D groups compared with control.

• Journal of Nutrition and Health
• /
• v.26 no.3
• /
• pp.286-298
• /
• 1993

In order to investigate the effect of selenium (Se) on the liver damage, metallothionein synthesis and hepatic antioxidative detoxification system in cadmium(Cd) administered rats. Sprague-Dawley male rats(60\\5g) were divided into two diet groups, depending on with (CdS groups) or without (Cd groups) 0.5ppm Se supplementation and fed experimental diets ad libidum for 4 weeks. And then each group was again subdivided into five groups, depending on injection number of Cd, i.e., 0, 1, 2, 3, and 4 times of 2.5mg Cd/kg of body wt once a day. Hemoglobin concentration, hematocrit values, superoxide dismutase, glutathione peroxidase and glutathione S-transferase activite were decreased progressively with increasing number of Cd injection, but increased by the supplementation of Se. The reduced form of glutathione (GSH) contents in blood and liver and vitamin E content were decreased and oxidized form (GSSG) increased in Cd groups, but these of Se supplemented groups were not very different from controls. Cd reduced liver vitamin E content which was not restored by Se supplementation. Liver lipid peroxide values were elevated with increasing doses of Cd, but Se supplementation reduced these elevated levels. Accumulation of metallothionein in liver and kidney was increased with increasing number of Cd injection, but Se did not affect on them. Histological examination revealed that lysosomes were significantly increased and mitochondria and Golgi apparatus were enlarged by Cd, however, these changes were reduced by Se. It was concluded that Se administration promoted antioxidative detoxification and alleviated peroxidative damage in rat liver by Cd.

• Journal of Nutrition and Health
• /
• v.33 no.6
• /
• pp.625-631
• /
• 2000

The purpose of this study was to investigate the effects of vitamin E on the oxidative damage and glomerular filteration rates(GFR) of kidney in streptozotocin(STZ) induced diabetic rats. Sprague-Dawley male rats weihing 100$\pm$10gm were randomly assigned to one normal and three STZ-induced diabetic groups which were subdivided into vitamin E free diet(DM-0E group)40mg vitamin E per kg diet(DM-40E group) and 400mg vitamin E per kg diet (DM-400E group), Vitamin E level of normal group was 40mg per kg diet. diabetes was experimentally induced by intravenous injection of 55mg/kg of body weight of STZ in citrate buffer(pH 4.3) after 4 weeks feeding of experimental diets. Animals were sacrificed at the 6th day of diabetic states. Activities of xanthine oxidase(XOD) in DM-0E DM-40 and DM-400E groups were significantly increased by 133%, 110%, and 74% respectively compared to normal group. The contents of microsomal superoxide radical(O2) in kidney were 106% and 119% higher of DM-0E and DM-40E groups than normal group respectively but that of DM-400E group was similar to normal group. The level of urnary microalbumin in DM-0E group was increased as 5 times much as normal group at the 6th day. Those of DM-40E and DM-400E groups were decreased to 16% and 36% respectively compared to DM-0E group. The content of urinary $\beta$2-microglobulin in DM-0E DM-40E and DM-400E group were increased by 268%, 181% and 163% respectively compared to normal group. GFR in DM-0E and DM-40E were significantly increased but was nor significantly different from DM-400E groups compared to normal group. In conclusion the supplementation of dietary vitamin E reduced peroxidative damage of renal glomerular and renal dysfunction in diabetic rats.

• The Korean Journal of Physiology and Pharmacology
• /
• v.3 no.6
• /
• pp.631-640
• /
• 1999

The present study investigated the stimulatory effects of iron (or ascorbate) on cyclosporine-induced kidney mitochondrial damage. Damaging effect of $50\;{\mu}M$ cyclosporine plus $20\;{\mu}M\;Fe^{2+}$ on mitochondrial lipids and proteins of rat kidney and hyaluronic acid was greater than the summation of oxidizing action of each compound alone, except sulfhydryl oxidation. Cyclosporine and $100\;{\mu}M$ ascorbate showed an enhanced damaging effect on lipids but not on proteins. The peroxidative action of cyclosporine on lipids was enhanced with increasing concentrations of $Fe^{2+}.$ Ferric ion $(20\;{\mu}M)$ also interacted with cyclosporine to stimulate lipid peroxidation. Damaging action of cyclosporine on mitochondrial lipids was enhanced by ascorbate $(100\;{\mu}M\;and\;1\;mM)$. Iron chelators, DTPA and EDTA, attenuated carbonyl formation induced by cyclosporine plus ascorbate. Cyclosporine $(100\;{\mu}M)$ and $50\;{\mu}M\;Fe^{2+}$ $(or\;100\;{\mu}M\;ascorbate)$ synergistically stimulated degradation of $2-{\alpha}$ deoxyribose. Cyclosporine $(1\;to\;100\;{\mu}M)$ reduced ferric ion in a dose dependent manner, which is much less than ascorbate action. Addition of $Fe^{2+}$ caused a change in absorbance spectrum of cyclosporine in $230{\sim}350$ nm of wavelengths. The results show that cyclosporine plus iron (or ascorbate) exerts an enhanced damaging effect on kidney mitochondria. Iron and ascorbate appear to promote the nephrotoxicity induced by cyclosporine.