• Korean Journal of Environmental Biology
• /
• v.22 no.4
• /
• pp.559-564
• /
• 2004

The effects of intra-peritoneal injection of inorganic mercury on haemato-logical parameters and hepatic oxidative stress enzyme activities were studied in common carp, Cyprinus carpio. The fish were injected thrice intra-peritoneally with mercuric chloride TEX>$(5,\;10mg\;Hg\;kg\;b.W.^{-1})$. After exposure of three different mercury concentrations a physiological stress response was exerted on C. carpio by causing changes in the blood status such as erythropenia in blood and oxidative stress in liver. Red blood cell counts, hemoglobin concentration and hematocrit level were reduced in most cases by inorganic mercury. Remarkable low level of serum chloride, calcium and osmolality were also observed in the mercury- exposed fish. However, serum magnesium and phosphate were not altered by exposure to mercury. An increased activity of hepatic glutathione peroxidase was observed in the lowest treatment group of carp $(1mg\;Hg\;mg\;b.w.^{-1})$, hence, hepatic catalase and glutathione peroxidase of carp exposed to higher concentration of mercury $(5,\;10mg\;Hg\;kg\;b.W.^{-1})$ showed significant reduction in such activities.

• ALGAE
• /
• v.27 no.1
• /
• pp.21-32
• /
• 2012

We report an oxidative burst triggered by prostaglandin $A_2(PGA_2)$ in the brown algal kelp Laminaria digitata, constituting the first such discovery in an alga and the second finding of an oxidative burst triggered by a prostaglandin in a living organism. The response is more powerful than the oxidative burst triggered by most other chemical elicitors in Laminaria. Also, it is dose-dependent and cannot be inhibited by diphenylene iodonium, suggesting that another source than NAD(P)H oxidase is operational in the production of reactive oxygen species. Despite the very strong oxidative response, rather few effects at other levels of signal transduction pathways could be identified. $PGA_2$ does not increase lipolysis (free fatty acids) in Laminaria, and only one oxylipin (15-hydroxyeicosatetraenoic acid; 15-HETE) was found to be upregulated in Laminaria. In a subsequent set of experiments in the genome model Ectocarpus siliculosus, none of 5 selected candidate genes, all established participants in various stress responses, showed any significant differences in their expression profiles.

• Korean Journal of Environmental Biology
• /
• v.28 no.2
• /
• pp.101-107
• /
• 2010

Metal ions are essential to life. However, some metals such as mercury are harmful, even when present at trace amounts. Toxicity of mercury arises mainly from its oxidizing properties. Ionizing radiation (IR) is an active tool for destruction of cancer cells and diagnosis of diseases, etc. IR induces DNA double strand breaks in the nucleus, In addition, it causes lipid peroxidation, ceramide generation, and protein oxidation in the membrane, cytoplasm and nucleus. Yeasts have been a commonly used material in biological research. In yeasts, the physiological response to changing environmental conditions is controlled by the cell types. Growth rate, mutation and environmental conditions affect cell size and shape distributions. In this work, the effect of IR and mercury chloride (II) on the morphology of yeast cells were investigated. Saccharomyces cerevisiae cells were treated with IR, mercury chloride (II) and IR combined with mercury chloride (II). Non-treated cells were used as a control group. Morphological changes were observed by a scanning electron microscope (SEM). The half-lethal condition from the previous experimental results was used to the IR combined with mercury. Yeast cells were exposed to 400 and 800 Gy at dose rates of 400Gy $hr^{-1}$ or 800 Gy $hr^{-1}$, respectively. Yeast cells were treated with 0.05 to 0.15 mM mercury chloride (II). Oxidative stress can damage cellular membranes through a lipidic peroxidation. This effect was detected in this work, after treatment of IR and mercury chloride (II). The cell morphology was modified more at high doses of IR and high concentrations of mercury chloride(II). IR and mercury chloride (II) were of the oxidative stress. Cell morphology was modified differently according to the way of oxidative stress treatment. Moreover, morphological changes in the cell membrane were more observable in the frequently stress treated cells than the temporarily stress treated cells.

• Journal of Nutrition and Health
• /
• v.55 no.4
• /
• pp.450-461
• /
• 2022

Purpose: DNA damage and repair responses are induced by metabolic diseases and environmental stress. The balance of DNA repair response and the antioxidant system play a role in modulating the entire body's health. This study uses a high-fat and high-calorie (HFC) drink to examine the new roles of a plant-based multivitamin/mineral supplement with phytonutrients (PMP) for regulating the antioxidant system and cellular DNA repair signaling in the body resulting from metabolic stress. Methods: In a double-blind, randomized, parallel-arm, and placebo-controlled trial, healthy adults received a capsule containing either a PMP supplement (n = 12) or a placebo control (n = 12) for 8 weeks. Fasting blood samples were collected at 0, 1, and 3 hours after consuming a HFC drink (900 kcal). The blood samples were analyzed for the following oxidative stress makers: areas under the curve reactive oxygen species (ROS) levels, plasma malondialdehyde (MDA), erythrocytes MDA, urinary MDA, oxidized low-density lipoprotein, and the glutathione:oxidized glutathione ratio at the time points. We further examined the related protein levels of DNA repair signaling (pCHK1 (Serine 345), p-P53 (Serine 15), and 𝛄H2AX expression) in the plasma of subjects to evaluate the time-dependent effects of a HFC drink. Results: In a previous study, we showed that PMP supplementation for eight weeks reduces the ROS and endogenous DNA damage in human blood plasma. Results of the current study further show that PMP supplementation is significantly correlated with antioxidant defense. Compared to the placebo samples, the blood plasma obtained after PMP supplementation showed enhanced DNA damage response genes such as pCHK1(Serine 345) (a transducer of DNA response) and 𝛄H2AX (a hallmark of DNA damage) during the 8 weeks trial on metabolic challenges. Conclusion: Our results indicate that PMP supplementation for 8 weeks enhances the antioxidant system against oxidative stress and prevents DNA damage signaling in humans.

• Journal of Life Science
• /
• v.25 no.3
• /
• pp.263-268
• /
• 2015

Coelomocytes are specialized cells that continually and nonspecifically scavenge fluid from the body cavity through endocytosis in Caenorhabditis elegans. Our previous study revealed that coelmocytes were specifically required for dietary-restriction-induced longevity in C. elegans. In the present study, we examined the effect of coelomocyte ablation on the response to environmental stressors and reproduction in C. elegans. Coelomocytes were ablated using diphtheria toxin specifically expressed in coelomocytes. After exposing worms to 20 J/cm²/min of ultraviolet irradiation in vivo, the survival of the worms was monitored daily. To examine their response to heat stress, their survival after 10 h of 35℃ heat shock was measured. Oxidative stress was induced using paraquat, and the susceptibility to oxidative stress was compared between wild-type control and coelomocyte-ablated worms. The total number of progeny produced was counted, and the time-course distribution of the progeny was determined. The worms with ablated coelomocytes showed reduced resistance to ultraviolet irradiation, but the ablation of coelomocytes had no effect on their response to heat or oxidative stress. The number of progeny produced during the gravid period was significantly decreased in the coelomocyte-ablated worms. These findings suggest that coelomocytes specifically modulate the response to ultraviolet irradiation and are required for normal reproduction in C. elegans. The findings could contribute to understanding of the mechanisms underlying dietary-restriction-induced longevity.

• Proceedings of the Korean Society of Developmental Biology Conference
• /
• 2003.10a
• /
• pp.97-97
• /
• 2003

Embryonic stem (ES) cells, derived from preimplantation embryos, are able to differentiate into various types of cells consisting the whole body, or pluripotency. In addition to the plasticity, ES cells are expected to be different from terminally differentiated cells in very many ways, such as patterns of gene expressions, ability and response of the cells in confronting environmental stimulations, metabolism, and growth rate. As a model system to differentiate these two types of cells, human ES (hES, MB03) cells and terminally differentiated cells (HeLa), we examined the ability of these two types of cells in confronting a severe oxidative insult, that is $H_2 O_2$. Ratio of dying cells as determined by the relative amount of dye neutral red entrapped within the cells after the exposures. Cell death rates were not significantly different when either MB03 or HeLa were exposed up to 0.4 mM $H_2 O_2$. However, relative amount of dye entrapped within the cells sharply decreased down to 0.12% in HeLa cells when the cells were exposed to 0.8 mM $H_2 O_2$, while it was approximately 54% in MB03. Pretreatment of cells with BSO (GSH chelator) and measurement of GSH content results suggest that cellular GSH is the major defensive mechanism of hES cells. Induction of apoptosis in hES cell was confirmed by DNA laddering, induction of Bax, and chromatin condensation. In summary, hES cells 1) are extremely resistant to oxidative stress, 2) utilize GSH as a major defensive mechanism. and 3) experience apoptosis upon exposure to oxidative stress.

• The Korean Journal of Physiology and Pharmacology
• /
• v.2 no.4
• /
• pp.479-491
• /
• 1998

In order to know the pathogenesis of adult respiratory distress syndrome (ARDS) in association with the oxidative stress by neutrophils, the role of platelet activating factor (1-0-alkyl-2-acetyl-snglycero-3-phosphocholine, PAF) was investigated during acute lung injury induced by interleukin- $1{\alpha}$ (IL-1) in rats. An insufflation of IL-1 into the rat's trachea increased the acetyltransferase activity in the lung and the increase of PAF content was followed. As evidences of acute lung injury by neutrophilic respiratory burst, lung leak index, myeloperoxidase activity, numbers of neutrophils in the bronchoalveolar lavage fluid, neutrophilic adhesions to endothelial cells and NBT positive neutrophils were increased after IL-1 treatment. In addition, a direct instillation of PAF into the trachea caused acute lung leak and the experimental results showed a similar pattern in comparison with IL-1 induced acute lung injury. For the confirmation of oxidative stress during acute lung leak by IL-1 and PAF, a histochemical electron microscopy was performed. In IL-1 and PAF treated lungs of rats, the deposits of cerrous perhydroxide were found. To elucidate the role of PAF, an intravenous injection of PAF receptor antagonist, WEB 2086 was given immediately after IL-1 or PAF treatment. WEB 2086 decreased the production of hydrogen peroxide and the acute lung leak. In ultrastructural study, WEB 2086 mitigated the pathological changes induced by IL-1 or PAF. The nuclear factor kappa B (NFkB) was activated by PAF and this activation was inhibited by WEB 2086 almost completely. Based on these experimental results, it is suggested that the PAF produced in response to IL-1 through the remodeling pathway has the major role for acute lung injury by neutrophilic respiratory burst. In an additional experiment, we can also come to conclude that the activation of the NFkB by PAF is thought to be the fundamental mechanism to initiate the oxidative stress by neutrophils causing release of proinflammatory cytokines and activation of phospholipase $A_2$.

• Proceedings of the Korea Environmental Mutagen Society Conference
• /
• 2002.05a
• /
• pp.25-35
• /
• 2002

Transcription factor Nrf2 is essential for the antioxidant responsive element (ARE)-mediated induction of phase II detoxifying and oxidative stress enzyme genes. Detailed analysis of differential Nrf2 activity displayed in transfected cell lines ultimately led to the identification of a new protein, which we named Keap1, that suppresses Nrf2 transcriptional activity by specific binding to its evolutionarily conserved amino-terminal regulatory domain. The closest homolog of Keap1 is a Drosophila actin-binding protein called Kelch, implying that Keap1 might be a Nrf2 cytoplasmic effector. We then showed that electrophilic agents antagonize Keap1 inhibition of Nrf2 activity in vivo, allowing Nrf2 to traverse from the cytoplasm to the nucleus and potentiate the ARE response. We postulate that Keap1 and Nrf2 constitute a crucial cellular sensor for oxidative stress, and together mediate a key step in the signaling pathway that leads to transcriptional activation by this novel Nrf2 nuclear shuttling mechanism. The activation of Nrf2 leads in turn to the induction of phase II enzyme and antioxidative stress genes in response to electrophiles and reactive oxygen species.

• Korean Journal of Food Science and Technology
• /
• v.30 no.5
• /
• pp.1222-1228
• /
• 1998

Stress will induce various changes in human metabolism. The remarkable phenomenon of these changes is increased energy metabolism that can induce many reactive oxygen species (ROS) production. ROS can peroxidize cellular macromolecules including lipid and protein. The object of this study was to investigate that stress may induce cellular damage by producing ROS and that Rooibos tea can protect cells against reactive oxygen species by immobilization stress in SD rat. The stress group significantly increased in 5-hydroxyindole acetic acid (5-HIAA), one of the stress hormone. Rooibos tea treatment had no effects on 5-HIAA contents, but body weight of Rooibos tea treated rat more increased than that of only the stress group. It was suggested that Rooibos tea colud not affect stress response itself, but protect against the another mechanism. We thought that the oxidative damage was caused by increased energy metabolism. Protein degradation level and lipid peroxide formation on index of oxidative damage significantly increased in the stress group. But the stress-induced activity change could not be observed in antioxidative enzymes such as superoxide dismutase, glutathione peroxidase and glutathione reductase. But the catalase activity of the brain significantly was inhibited by the stress. From these results, it was suggested that the immobilization stress induce the brain oxidative damage. However the oxidative damage was inhibited by feeding Rooibos tea containing various antioxidants, such as polyphenol, flavonoid and so on. Therefore, Rooibos tea have the protective effects against the stress caused by the ROS mediated cellular damage.

• Journal of Korean Society of Occupational and Environmental Hygiene
• /
• v.29 no.2
• /
• pp.251-258
• /
• 2019

Objective: Chronic obstructive pulmonary disease(COPD) is characterized by persistent airflow limitations associated with chronic inflammatory response due to noxious particles or gases in the lung. Inflammation and oxidative stress are associated with COPD. The aim of this study was to evaluate the relationship among inflammation, oxidative stress, and airflow limitation severity in retired miners with COPD. Methods: The levels of serum high-sensitivity C-reactive protein(hsCRP) as a biomarker for inflammation, degree of reactive oxygen metabolites(dROMs) and biological antioxidants potential(BAP) in plasma as biomarkers for oxidative stress were measured in 211 male subjects with COPD. Degree of airflow limitation severity as determined by spirometry was divided into three grades grouped according to the classification of the Global Initiatives for Obstructive Lung Disease(GOLD)(1, mild; 2, moderate; $3{\leq}$, severe or more) using a fixed ratio, post- bronchodilator $FEV_1/FVC$ < 0.7. Results: Mean levels of dROMs significantly increased in relation to airflow limitation severity(GOLD 1, 317.8 U.CARR vs. GOLD 2, 320.3 U.CARR vs. GOLD $3{\leq}$, 350.9 U.CARR, p=0.047) and dROMs levels were correlated with serum hsCRP levels(r=0.514, p<0.001). Mean levels of hsCRP were higher in current smokers(non-smoker, 1.47 mg/L vs. smoker, 2.34 mg/L, p=0.006), and tended to increase with degree of airflow limitation severity(p=0.071). Mean levels of BAP were lower in current smokers(non-smoker, $1873{\mu}mol/L$ vs. smoker, $1754{\mu}mol/L$, p=0.006). Conclusions: These results suggest that inflammation and oxidative stress are related to airflow limitation severity in retired miners with COPD, and there was a correlation between inflammation and oxidative stress.