• Environmental Analysis Health and Toxicology
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• v.20 no.1
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• pp.75-85
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• 2005

This study was aimed to know the effect of cadmium chloride (CdCl₂) on glucose transport in L6 myotube and its action mechanism. CdCl₂ increased the 2-deoxy- (l-3H)-D-glucose (2-DOG) uptake 1.9 and 2.4 fold at 10 and 25 μM respectively. To investigate the stimulating-mechanism of glucose transport induced by CdCl₂, the wortmannin and PD98059 were used as PI3K (phosphatidylinositol 3-kinase) inhibitor and MAPK inhibitor respectively, which did not affect 2-DOG uptake. This fact suggests that CdCl₂ induced 2-DOG uptake may not be concerned to the insulin signalling pathway. Whereas nifedipine, a calcium channel blocker, and trifluoperazine, a calmodulin inhibitor, were found to inhibit the 2-DOG uptake stimulted by CdCl₂. In addition, we also measured the ROS (reactive oxygen species) production and GSH level in L6 myotube to investigate the correlation between the glucose uptake and ROS. CdCl₂(25 μM) increased ROS generation approximately 1.5 fold and changed the cellular GSH level, but GSSG/GSH ratio remained unchanged. CdCl₂ stimulated 2-DOG uptake and ROS generation were inhibited by N-acetylcystein. And BSO pretreatment, a potent inhibitor of γ-GCS, resulted in the dramatic decrease of 2-DOG uptake and also the increase of the sensitivity to cadmium cytotoxicity. The obtained results suggest that CdCl₂-stimulated glucose uptake might be based on the activation of HMP shunt as an antioxidant defense mechanism of the cells.

• Preventive Nutrition and Food Science
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• v.13 no.2
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• pp.84-89
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• 2008

This study was designed to investigate the protective effect of a methanol extract of Chungkookjang (CKJ) on high glucose induced oxidative stress in LLC-$PK_1$ cells (renal tubular epithelial cells), which are susceptible to oxidative stress. Freeze dried CKJ powder was extracted with methanol, and the extract solution was concentrated, and then used in this study. To determine the protective effect of CKJ extract, oxidative stress was induced by exposing of LLC-$PK_1$ cells to high glucose (30 mM) or normal glucose (5 mM) for 24 hr. Exposure of LLC-$PK_1$ cells to high glucose for 24 hr resulted in a significant (p<0.05) decrease in cell viability, catalase, SOD and GSH-px activity and a significant (p<0.05) increase in intracellular ROS level and thiobarbituric acid reactive substances (TBARS) formation in comparison to the cells treated with 5 mM glucose. CKJ extract treatment decreased intracellular ROS level and TBARS formation, and increased cell viability and activities of antioxidant enzymes including catalase, SOD and GSH-px in high glucose pretreated LLC-$PK_1$ cells. These results suggest that CKJ extract may be able to protect LLC-$PK_1$ cells from high glucose-induced oxidative stress, partially through the antioxidative defense systems.

• 대한생식의학회:학술대회논문집
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• 2000.06a
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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.

• Journal of the Society of Cosmetic Scientists of Korea
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• v.37 no.2
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• pp.171-176
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• 2011

N-feruloylserotonin (FS) and N-(pcoumaroyl) serotonin (CS), serotonin derivatives, which have been isolated as major and unique phenolics of safflower seed extract (SSE), are member of hydroxycinnamic acid amides and are implicated in the defense against pathogen infection and insect feeding. In this study, we evaluate inhibitory effects of N-(p-Coumaroyl)serotonin and N-Feruloylserotonin on adipogenesis using oil-red O staining, triglyceride and GPDH activity. we found that while serotonin itself did not suppress differentiation of preadipocytes into adipocytes, N-(p-Coumaroyl)serotonin and N-Feruloylserotonin inhibited the differentiation of preadipocytes into adipocytes in a concentration-dependent manner. In addition, they showed antioxidant effects in DPPH assay. Taken together, these results show that N-feruloylserotonin (FS) and N-(pcoumaroyl) serotonin (CS) suppress differentiation of preadipocytes, suggesting the possibility that these serotonin derivatives can be utilized as an anti-obesity agent.

• Journal of Ginseng Research
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• v.41 no.3
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• pp.316-325
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• 2017

Background: Ginseng essence (GE) is a formulation comprising four medicinal and edible herbs including ginseng (Panax ginseng), American ginseng (Panax quinquefolius), lotus seed (Nelumbo nucifera), and lily bulb (Lilium longiflorum). This study was aimed at investigating the hepatoprotective effect of GE against carbon tetrachloride ($CCl_4$)-induced liver injury in rats. Methods: We treated Wistar rats daily with low, medium, and high [0.625 g/kg body weight (bw), 1.25 g/kg bw, and 3.125 g/kg bw, respectively] doses of GE for 9 wk. After the 1st wk of treatment, rats were administered 20% $CCl_4$ (1.5 mL/kg bw) two times a week to induce liver damage until the treatment ended. Results: Serum biochemical analysis indicated that GE ameliorated the elevation of aspartate aminotransferase and alanine aminotransferase and albumin decline in $CCl_4$-treated rats. Moreover, $CCl_4$-induced accumulation of hepatic total cholesterol and triglyceride was inhibited. The hepatoprotective effects of GE involved enhancing the hepatic antioxidant defense system including glutathione, glutathione peroxidase, glutathione reductase, glutathione S-transferase, superoxide dismutase, and catalase. In addition, histological analysis using hematoxylin and eosin and Masson's trichrome staining showed that GE inhibited $CCl_4$-induced hepatic inflammation and fibrosis. Furthermore, immunohistochemical staining of alpha-smooth muscle actin indicated that $CCl_4$-triggered activation of hepatic stellate cells was reduced. Conclusion: These findings demonstrate that GE improves $CCl_4$-induced liver inflammation and fibrosis by attenuating oxidative stress. Therefore, GE could be a promising hepatoprotective herbal formulation for future development of phytotherapy.

• Journal of Sasang Constitutional Medicine
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• v.27 no.2
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• pp.254-269
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• 2015

Objectives This study aimed to observe the effect of Taeumjowi-tang on the cisplatin-induced gastrointestinal dysfunctions in rats. Methods Four groups, each of 8 rats per group, were used in this study. Saline and distilled water treated control rats were intact vehicle control group. Delayed gastrointestinal motility was induced by intraperitoneal treatment of cisplatin 2mg/kg, once a week for 5 weeks(Cisplatin control group). Taeumjowi-tang aqueous extracts(TJ) were orally administered in a volume of 5ml/kg, once a day for 14 days from 4th cisplatin treatment(TJ group). Ondansetron 1mg/kg was subcutaneously treated, in a volume of 1ml/kg, as same as TJ(ondansetron group). We measured the body weights, intestinal charcoal transit ratio, fecal parameters, fundus MDA(malondialdehyde), GSH(glutathione) contents and SOD(superoxide dismutase), CAT(catalase) activities, TPH(tryptophanhydroxylase) and MAO(monoamine oxidase) activities, pyloric gastrin and serotonin contents with their immunoreactive cells, colonic serotonin-immunoreactive cells, the histopathology of pylorus, fundus mucosa and colon. Results 1) The body weight gains, the small intestinal charcoal transfer rates, the fecal parameters(numbers, weights and water contents) were increased in TJ, ondansetron group. 2) The inhibit of fundus antioxidant defense systems by cisplatin were decreased in TJ, ondansetron group. 3) The pyloric TPH activities were increased and the pyloric MAO activities were decreased in TJ group. 4) The pyloric gastric contents and the gastrin-immunoreactive cells were increased and the pyloric serotonin contents and the pyloric and colonic serotonin-immunoreactive cells were decreased in TJ group. 5) The pylorus atrophic changes and the gastric surface erosive damage regions by cisplatin were favorably inhibited by treatment of TJ group. Conclusions The results obtained in this study suggest that TJ favorably retarded the cisplatin related GI(gastrointestinal) dysfunctions and constipation through modulations of GI enterochromaffin cells, serotonin and gastrin-producing cells and antioxidative systems.

• Safety and Health at Work
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• v.12 no.1
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• pp.127-132
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• 2021

Background: Herbicides such as glyphosate, paraquat, and 2,4-dichlorophenoxyacetic acid have been reported to cause adverse side effects through production of reactive oxygen species. However, there were no data representing the adverse effects of a mixture herbicide usage in farmers, especially the changes in oxidative marker and antioxidant defense. This study aimed to determine the urinary malondialdehyde (MDA) and glutathione (GSH) level in farmers using mixed herbicides. Methods: Ninety-three farmers were recruited, and two spot urine samples (before and after work) were collected. The urinary MDA level was evaluated by thiobarbituric acid reactive substance assay, and the urinary GSH level was determined using the enzymatic recycling method. Results: Sixty-two percent of the participants were men, and 59% of the participants worked in a farm for 20-40 years. The common combinations of herbicide usage were glyphosate with 2,4-dichlorophenoxyacetic acid (36.5%). There was no significant difference between pre- and post-work urinary MDA and GSH levels among the 3 groups of herbicides. However, the urinary MDA levels in farmers using the combination of glyphosate and paraquat were significantly higher than those found in farmers using glyphosate alone. The associated factors with changes in MDA levels found that the exposure intensity index (B = 0.154), the cumulative exposure intensity index (B = 0.023), and wearing gloves while working (B = -2.347) were found to be significantly associated with MDA level. Conclusion: The results suggest that the combined use of glyphosate and paraquat caused a significant increase in urinary MDA levels. Moreover, intensity of exposure to herbicide and wearing gloves were associated with the level of MDA.

• Journal of Life Science
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• v.33 no.7
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• pp.586-592
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• 2023

Oxidative stress is a critical factor affecting the quality and viability of sperm during boar semen storage. Oxidative stress is also a significant concern during the process of freezing semen. The process of semen storage involves exposing the sperm to various stressors, including temperature changes, cryoprotectants, and extended periods of incubation. In addition, oxidative stress can lead to the production of reactive oxygen species (ROS) within the sperm, resulting in oxidative damage to cellular components, such as lipids, proteins, and DNA. Striking a balance between ROS production and the antioxidant defense system is crucial for maintaining sperm viability and functionality during semen storage. Moreover, the prolonged storage of boar semen leads to an increase in ROS levels, which can impair sperm motility, membrane integrity, and DNA integrity. ROS-induced lipid peroxidation affects the fluidity and stability of sperm membranes, leading to decreased sperm motility. Moreover, oxidative damage to the DNA can result in DNA fragmentation, compromising the genetic integrity of the sperm. In conclusion, oxidative stress is a significant challenge in maintaining sperm quality during boar semen storage. Understanding the mechanisms underlying oxidative stress and their impacts on sperm function is crucial for developing effective strategies to minimize oxidative damage and improve sperm storage outcomes.

• The Korea Journal of Herbology
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• v.39 no.3
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• pp.97-105
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• 2024

Objective : This study examined the effects of yaksun recipe on the anti-fatigue and endurance enhancement properties in the forced swimming test (FST). Methods : The treatment groups were divided randomly into three groups: water-treated FST (control), 200 mg/kg of red ginseng-treated FST (RG200), 200 mg/kg of water extract of yaksun recipe-treated FST (YS200). After FST, an autopsy was performed, and the tissue and serum were collected. Results : The swimming exhaustion time in the RG200 and YG200 groups were significantly increased compared to the control group. The YG200 group fatigue indicators, D-Lactate, LDH(lactate dehydrogenase), creatine kinase, and ammonia content, significantly decreased compared to the control group. In addition, liver glycogen content significantly increased in the YG200 and tended to increase in RG200. Likewise, the glucose contents were significantly increased compared to the control group. The muscle damage indicators GPT (glutamic pyruvic transaminase) and BUN (blood urea nitrogen), a protein metabolite, in the YG200 group significantly decreased compared to the control group. Furthermore the concentration of liver lipid peroxidation, MDA(malondialdehyde) levels significantly decreased in the RG200 and YG200 compared to control group. Conclusions : These results suggest that YG200 can increase the endurance exercise capacity by decreasing the fatigue indicators, saving glycogen, and elevating the antioxidant defense system.

• Biomolecules & Therapeutics
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• v.32 no.1
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• pp.77-83
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• 2024

Alzheimer's disease (AD) is a neurodegenerative disease characterized by neuronal cell death and memory impairment. Corticosterone (CORT) is a glucocorticoid hormone produced by the hypothalamic-pituitary-adrenal axis in response to a stressful condition. Excessive stress and high CORT levels are known to cause neurotoxicity and aggravate various diseases, whereas mild stress and low CORT levels exert beneficial actions under pathophysiological conditions. However, the effects of mild stress on AD have not been clearly elucidated yet. In this study, the effects of low (3 and 30 nM) CORT concentration on Aβ_25-35-induced neurotoxicity in SH-SY5Y cells and underlying molecular mechanisms have been investigated. Cytotoxicity caused by Aβ_25-35 was significantly inhibited by the low concentration of CORT treatment in the cells. Furthermore, CORT pretreatment significantly reduced Aβ_25-35-mediated pro-apoptotic signals, such as increased Bim/Bcl-2 ratio and caspase-3 cleavage. Moreover, low concentration of CORT treatment inhibited the Aβ_25-35-induced cyclooxygenase-2 and pro-inflammatory cytokine expressions, including tumor necrosis factor-α and interleukin-1β. Aβ_25-35 resulted in intracellular accumulation of reactive oxygen species and lipid peroxidation, which were effectively reduced by the low CORT concentration. As a molecular mechanism, low CORT concentration activated the nuclear factor-erythroid 2-related factor 2, a redox-sensitive transcription factor mediating cellular defense and upregulating the expression of antioxidant enzymes, such as NAD(P)H:quinone oxidoreductase, glutamylcysteine synthetase, and manganese superoxide dismutase. These findings suggest that low CORT concentration exerts protective actions against Aβ_25-35-induced neurotoxicity and might be used to treat and/or prevent AD.