• Journal of Nutrition and Health
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• 제38권4호
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• pp.297-306
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• 2005

It is known that dehydroepiandrosterone (DHEA) shows a dual effect, prooxidant or antioxidant, depending on the do-sage or physiological status of animals. The purpose of this study was to determine the effects of DHEA administration at low dose on lipid peroxidation, protein carbonylation and fatty acid composition in liver. Sprague Dawley male rats were fed either com oil diet containing $15\%$ com oil or fish oil diet containing $2\%$ corn oil + $13\%$ sardine oil, with or without $0.2\%$ DHEA for 9 weeks. Atherogenic index and hepatic triglyceride and cholesterol levels were significantly reduced by DHEA administration in rats fed with fish oil diet. Hepatic lipid peroxide product (TBARS) and protein carbonyl levels were significantly higher in rats fed with fish oil diet than in rats fed with corn oil diet. However, DHEA administration significantly reduced the hepatic thiobarbituric acid-reactive substance (TBARS) and conjugated diene levels in rats fed with fish oil diet. Contents of C16 : 0, C16 : 1, C20 : 5 and C22 : 6 in hepatic microsome were higher in rats fed with fish oil diet than in rats fed with corn oil diet, and contents of C18 : 2 and C20 : 4 were lower than in rats fed with com oil diet. DHEA administration significantly increased C16 : 0 and C18 : 3 contents and reduced C18 : 2 content in rats fed with com oil diet, while it increased C16 : 0 and C18 : 1 and reduced C20 : 5 and C22 : 6 in rats fed with fish oil diet. On overall, DHEA administration increased saturated fatty acid (SFA) and reduced polyunsaturated fatty acid (PUFA) in hepatic microsome, thereby PUFA/SFA ratio was significantly (p < 0.0001) reduced without the change of n-3/n-6 ratio. Taken together, low dose of DHEA administration lowered PUFA/SFA ratio in hepatic microsomal membranes and also showed antioxidative effect especially in fish oil-induced highly oxidative stress condition through blocking increases of C20 : 5 and C22 : 6 contents.

• Asian-Australasian Journal of Animal Sciences
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• 제18권4호
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• pp.497-501
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• 2005

An experiment was conducted on crossbred male calves to study the effect of arsenic (As) on immunity status and certain hematological parameters. Ten crossbred male calves of 3-4 months of age were distributed into two equal groups. Group I was kept as control, whereas, group II was supplemented daily with 50 ppm As (as $As_sO_3$) up to 90 days, in the diet. Calves of both groups were fed as per ICAR standards and their requirements were fulfilled by feeding concentrate mixture and green oats. All calves were kept under similar managemental conditions. Blood samples were collected at fortnightly intervals to estimate various haematological parameters and superoxide dismutase (SOD) enzyme activity. Serum Ig and serum glutamic pyruvate transaminase (SGPT) were also measured. Cell-mediated immune responses of the calves were monitored at 0, 45 and 90 of experimental feeding, through lymphocyte proliferation. No change in blood total leukocyte counts (TLC), differential leukocyte counts (DLC), packed cell volume (PCV), haemoglobin (Hb) and SGPT was observed with As supplementation. A decrease in SOD activity was noticed in group II calves. Stimulation index (SI) for lymphocyte proliferation decreased from 1.14 to 0.79 in group II calves during 90 days experimental feeding, whereas, there was no change in SI values in group I indicating significant decrease in immune response of As supplemented calves. Blood As concentration increased in group II calves with the decrease in immune response. Short term supplementation of As to growing calves suggested suppressive effects on cell-mediated immunity. However, long term experiments are required to demonstrate clearly the efects of this toxic metal in calves.

• Toxicological Research
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• 제34권3호
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• pp.249-257
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• 2018

The purpose of the present study was to evaluate the effects of different dietary concentrations of T-2 toxin on blood plasma protein content, lipid peroxidation and glutathione redox system of pheasant (Phasianus colchicus). A total of 320 one-day-old female pheasants were randomly assigned to four treatment groups fed with a diet contaminated with different concentrations of T-2 toxin (control, 4 mg/kg, 8 mg/kg and 16 mg/kg). Birds were sacrificed at early (12, 24 and 72 hr) and late (1, 2 and 3 weeks) stages of the experiment to demonstrate the effect of T-2 toxin on lipid peroxidation and glutathione redox status in different tissues. Feed refusal and impaired growth were observed with dose dependent manner. Lipid-peroxidation was not induced in the liver, while the glutathione redox system was activated partly in the liver, but primarily in the blood plasma. Glutathione peroxidase activity has changed parallel with reduced glutathione concentration in all tissues. Based on our results, pheasants seem to have higher tolerance to T-2 toxin than other avian species, and glutathione redox system might contribute in some extent to this higher tolerance, in particular against free-radical mediated oxidative damage of tissues, such as liver.

• Journal of the Korean Wood Science and Technology
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• 제8권3호
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• pp.64-76
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• 1980

Fig. 8 summarizes the present status of high yield pulp production and the directions of research on modification. A thick line indicates pulping process presently in use. As mentioned previously, one kind of modification is to introduce hydrophilic groups onto the pulp. Still unsolved is whether or not the introduction of hydrophilic groups should be restricted to lignin only. Goring (28) reported that middle lamella lignin has fewer phenolic hydroxyl groups than cell wall lignin and suggested that such a difference in the lignin may be useful in the removal of middle lamella lignin. The introduction of hydrophilic groups onto pulp may not be enough to modify high yield pulp. The removal of some portion of carbohydrate may be also necessary from the standpoint of softening of pulp fibers. There is no information at what lignin and carbohydrate, and how much should be removed. The combination with synthetic high polymers may also be important in modifying high yield pulp. Prof. C. Schuerch of the State University of New York who was a visiting professor at the University of Tokyo in 1974, mentioned that the hydrophilicity of lignin would be promoted, if phenolic hydroxyl or carboxyl groups could be introduced into the aromatic nucleus of lignin. If this were possible. this process would also mean a pulp yield of more than 100%. This idea is just one example of the expectation made possible through lignin chemistry. Instead of the introduction of hydrophilic group, the oxidative degradation of aromatic nucleus of lignin may also be useful in promoting the hydrophilicity of pulp. In this case, ozone may be an excellent chemical. However, there are a lot of problems to be solved such as homogeneity of reaction and selectivity of ozone for lignin. The above ideas are summarized in Fig. 9. There are many problems to be solved in the production of an excellent high yield pulp which is comparable to chemical pulp. The information from wood chemistry hopefully will elucidate some of the problems mentioned above.

• Molecules and Cells
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• 제38권5호
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• pp.452-456
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• 2015

Obesity is the fifth leading risk for death globally, and a significant challenge to global health. It is a common, complex, non-malignant disease and develops due to interactions between the genes and the environment. DNA methylation can act as a downstream effector of environmental signals; analysis of this process therefore holds substantial promise for identifying mechanisms through which genetic and environmental factors jointly contribute to disease risk. To assess the effects of excessive weight and obesity on gene-specific methylation levels of promoter regions, we determined the methylation status of four genes involved in inflammation and oxidative stress [interleukin 6 (IL6), tumor necrosis factor ${\alpha}$ ($TNF{\alpha}$), mitochondrial transcription factor A (TFAM), and glucose transport 4 (GLUT4)] in blood cell-derived DNA from healthy women volunteers with a range of body mass indices (BMIs) by methylation-specific PCR. Interestingly, the samples from obese individuals ($BMI{\geq}30kg/m^2$) showed significantly increased hypermethylation for IL6 gene compared to normal weight ($BMI<23kg/m^2$) and overweight sample ($23kg/m^2{\leq}BMI<30kg/m^2$) (P = 0.034 and P = 0.026). However there was no statistically significant difference in promoter methylation of the other 3 genes between each group. These findings suggest that aberrant DNA methylation of IL6 gene promoter may play an important role in the etiology and pathogenesis of obesity and IL6 methylation could be used as molecular biomarker for obesity risk assessment. Further studies are required to elucidate the potential mechanisms underlying this relationship.

• 한국임상수의학회지
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• 제26권3호
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• pp.200-204
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• 2009

This study was performed to evaluate the effects of reduced L-glutathione on the oxidant/antioxidant status(superoxide dismutase(SOD), catalase(CAT), glutathione peroxidase(GPx), protein carbonyl and lipid hydroperoxide(LPO) concentration), renal function(blood urea nitrogen(BUN) and serum creatinine levels), and microscopy of renal tissues in pigs undergoing unilateral renal ischemia-reperfusion(I/R). Sixteen Landrace and Yorkshire mixed-breed pigs were divided randomly into two groups: untreated control group and reduced L-glutathione-treated group(4 mg/kg IV). Each group had 8 pigs. Pigs were unilaterally nephrectomized and the kidney was subject to 30 min of renal pedicle occlusion. Blood samples for biochemical assay were collected on days 1, 3, 5, 7, and 14 post nephrectomy. Renal I/R injury were evaluated histopathologically by the microscopic observation of renal tissue sections and biochemically by the measurement of the plasma creatinine and urea levels. Parameters of oxidative stress such as SOD, GPx, CAT, protein carbonyl and LPO were measured. The elevation of creatine and BUN levels was lower in the treated group, compared with the control group. The activities of antioxidant-enzyme were higher in the treated group, compared with the control group. In histological findings, the severity of damage in the reduced L-glutathione treated group was less when compared to the control group.

• Annals of Clinical Neurophysiology
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• 제15권2호
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• pp.53-58
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• 2013

Background: The autophagy is the major route for lysosomal degradation of misfolded protein aggregates and oxidative cell components. We hypothesized that rapamycin (autophagy enhancer) would prolong the survival of motor neuron and suppress the disease progression in amyotrophic lateral sclerosis (ALS). Methods: A total of 24 transgenic mice harboring the human G93A mutated SOD1 gene were used. The clinical status involving rotarod test and survival, and biochemical study of ALS mice model were evaluated. Results: The onset of symptoms was significantly delayed in the rapamycin administration group compared with the control group. However, after the clinical symptom developed, the rapamycin exacerbated the disease progression and shortened the survival of ALS mice model, and apoptosis signals were up-regulated compared with control group. Conclusions: Even though further detailed studies on the relevancy between autophagy and ALS will be needed, our results revealed that the rapamycin administration was not effective for being novel promising therapeutic strategy in ALS transgenic mice and exacerbated the apoptosis.

• 대한생식의학회:학술대회논문집
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• 대한불임학회 2000년도 제39차 춘계 학술대회
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• pp.13-28
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• 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.

• Environmental Analysis Health and Toxicology
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• 제26권
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• pp.6.1-6.8
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• 2011

Objectives: The present study investigated the potential adverse effects of multi-wall carbon nanotubes (MWCNTs) on pregnant dams and embryonic development following maternal exposure in rats. Methods: MWCNTs were orally administered to pregnant rats from gestational day (GD) 6 through 19 at dose levels of 0, 8, 40, 200, and 1000 mg/kg/day. During the test period, clinical signs, mortality, body weights, food consumption, serum biochemistry, oxidant-antioxidant status, gross findings, organ weights, and Caesarean section findings were examined. Results: All animals survived to the end of the study. A decrease in thymus weight was observed in the highest dose group. However, maternal body weight, food consumption, serum biochemical parameters, and oxidant-antioxidant balance in the kidneys were not affected by treatment with MWCNTs. No treatment-related differences in gestational index, embryo-fetal mortality, or fetal and placental weights were observed between treated and control groups. Conclusions: The results show that 14-day repeated oral dosing of MWCNTs during pregnancy induces minimal maternal toxicity at 1000 mg/kg/day in rats. Under these experimental conditions, the no-observed-adverse-effect level of MWCNTs is considered to be 200 mg/kg/day for dams and 1000 mg/kg/day for embryonic development.

• The Korean Journal of Physiology and Pharmacology
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• 제24권5호
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• pp.403-412
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• 2020

Diabetic nephropathy (DN) is a hyperglycemia-induced progressive development of renal insufficiency. Excessive glucose can increase mitochondrial reactive oxygen species (ROS) and induce cell damage, causing mitochondrial dysfunction. Our previous study indicated that cilostazol (CTZ) can reduce ROS levels and decelerate DN progression in streptozotocin (STZ)-induced type 1 diabetes. This study investigated the potential mechanisms of CTZ in rats with DN and in high glucose-treated mesangial cells. Male Sprague-Dawley rats were fed 5 mg/kg/day of CTZ after developing STZ-induced diabetes mellitus. Electron microscopy revealed that CTZ reduced the thickness of the glomerular basement membrane and improved mitochondrial morphology in mesangial cells of diabetic kidney. CTZ treatment reduced excessive kidney mitochondrial DNA copy numbers induced by hyperglycemia and interacted with the intrinsic pathway for regulating cell apoptosis as an antiapoptotic mechanism. In high-glucose-treated mesangial cells, CTZ reduced ROS production, altered the apoptotic status, and down-regulated transforming growth factor beta (TGF-β) and nuclear factor kappa light chain enhancer of activated B cells (NF-κB). Base on the results of our previous and current studies, CTZ deceleration of hyperglycemia-induced DN is attributable to ROS reduction and thereby maintenance of the mitochondrial function and reduction in TGF-β and NF-κB levels.