Peroxiredoxins (Prx's) are a superfamily of peroxidases that are ubiquitous in all super-kingdoms. Previous biochemical and structural studies have suggested that Prx's could be divided into five subfamilies (1-Cys, Typical 2-Cys, Atypical 2-Cys C-, L- and R- types). In this work, we have developed a set of regular expression patterns describing subfamily-specific spatial constraints of the key catalytic residues. Using these patterns, 1,016 Prx's available in public databases were classified into the five subfamilies. Our method performed well for most of the types except for Atypical 2 Cys R type.
Classification* ; Peroxidases ; Peroxiredoxins*

OBJECTIVE: To assess the expression pattern of all six Prxs in normal ovarian tissue and epithelial ovarian tumor cell using immunohistochemical staining. METHODS: Patients were retrieved from those who had undertaken operation in Obstetrics and Gynecology of our hospital from January 1995 to June 2005. According to the pathologic result, five patients were allocated randomly in each group of malignant serous, malignant mucinous, benign serous and benign mucinous ovarian tumor. And another five with normal ovarian epithelial cell were included for the comparison. Immunohistochemical staining was performed with Prx I to VI antibodies. Using microscopy, we evaluated the immunoreactivities of nucleus and cytoplasm semiquantitatively by dividing into four categories : -; no immunoactivity present, +; weak, ++; moderate, +++; strong staining. RESULTS: The immunopositivity of Prx III in cytoplasm shows weak to moderate and Prx VI moderate to strong in normal ovarian tissue. In mucinous epithelial ovarian tumor cell, cytoplasmic Prx IV shows stronger activity than in normal epithelial cell or serous tumor cell. In malignant epithelial cell, Prx V shows stronger activity in cytoplasm than normal epithelial cell. It shows characteristically granular pattern. Prx VI shows stronger activity in the nucleus of malignant epithelial cell compared to normal epithelial cell or benign tumor epithelial cell. CONCLUSION: Normal ovarian tissue showed higher affinity for Prx III and VI. In epithelial ovarian tumor, cytosolic Prx IV in mucinous tumor, cytosolic Prx V and nuclear Prx VI in malignant tumor were overexpressed.
Antibodies ; Cytoplasm ; Cytosol ; Epithelial Cells ; Female ; Gynecology ; Humans ; Microscopy ; Mucins ; Obstetrics ; Ovary* ; Peroxiredoxins* ; Protein Isoforms*

PURPOSE: Peroxiredoxins(PRDXs) are antioxidant enzymes that play an important role on cell differentiation, proliferation and apoptosis. In this study, we investigated if the expression levels of PRDX I were related to bladder cancer. MATERIALS AND METHODS: The mRNA level of PRDX I was examined via real time polymerase chain reaction(PCR) in 186 cancer specimens from patients with primary bladder cancer, 73 corresponding samples of normal looking bladder mucosae surrounding the cancer and 21 samples of normal bladder mucosae. We investigated the correlation between the expression levels of PRDX I and the clinico-pathological parameters of the 154 patients who could be followed up more than three years. RESULTS: The expression levels of PRDX I in bladder cancer(0.73pg/ml) were significantly higher that that in the normal bladder mucosae (0.04 pg/ml)(p<0.01) or that in the corresponding normal bladder mucosae surrounding the cancer(0.38pg/ml)(p<0.01). The expression level of PRDX I was not significantly enhanced in the non-recurred(0.87pg/ml) superficial bladder tumor patients compared with the recurred superficial bladder tumor patients(0.63pg/ml), but it was significantly enhanced in the non-progressed(0.82pg/ml) patients compared with the progressed (0.50pg/ml) patients(p<0.05 for each). CONCLUSIONS: An enhanced expression of PRDX I is strongly associated with the development of bladder cancer. Moreover, enhanced expressions of PRDX I are also positively associated with a low rate of progression of bladder cancer, and this might be useful as a marker for assessing progression in human bladder cancers.
Apoptosis ; Cell Differentiation ; Humans ; Mucous Membrane ; Peroxiredoxins ; RNA, Messenger ; Urinary Bladder ; Urinary Bladder Neoplasms

Oxidative stress plays a critical role in the pathogenesis of asthma. To effectively control oxidative stress in asthmatics, it is important to investigate the precise intracellular mechanism by which the development of immunity, rather than immune tolerance and progression of airway inflammation, is induced. In this article, we suggest that protein tyrosine phosphatases, as intracellular negative regulators, and intracellular antioxidant enzymes such as peroxiredoxins can be regulated by oxidative stress during intracellular signaling.
Antioxidants ; Asthma ; Hypersensitivity ; Immune Tolerance ; Inflammation ; Oxidative Stress ; Peroxiredoxins ; Protein Tyrosine Phosphatases

Peroxiredoxins (Prxs) are antioxidant enzymes that protect cells from oxidative stress by reducing intracellular accumulation of reactive oxygen species (ROS). In mammalian cells, the six Prx isoforms are ubiquitously expressed in diverse intracellular locations. They are involved in the regulation of various physiological processes including cell growth, differentiation, apoptosis, immune response and metabolism as well as intracellular ROS homeostasis. Although there are increasing evidences that Prxs are involved in carcinogenesis of many cancers, their role in cancer is controversial. The ROS levels in cancer cells are increased compared to normal cells, thus promoting cancer development. Nevertheless, for various cancer types, an overexpression of Prxs has been found to be associated with poor patient prognosis, and an increasing number of studies have reported that tumorigenesis is either facilitated or inhibited by regulation of cancer-associated signaling pathways. This review summarizes Prx isoforms and their basic functions, the relationship between the expression level and the physiological role of Prxs in cancer cells, and their roles in regulating cancer-associated signaling pathways.
Apoptosis ; Carcinogenesis ; Homeostasis ; Humans ; Metabolism ; Oxidative Stress ; Peroxiredoxins ; Physiological Processes ; Prognosis ; Protein Isoforms ; Reactive Oxygen Species

BACKGROUND: Peroxiredoxin I (Prx I) is part of an oxidative stress defense system with thioredoxin peroxidase activity to eliminate hydrogen peroxide (H2O2). UV irradiation is one of the major sources to produce H2O2, which should then be scavenged by antioxidant systems to maintain functional integrity of the skin. OBJECTIVE: This study aimed to evaluate the modulation of Prx I by ultraviolet B (UVB) irradiation in human epidermal keratinocytes. The modulation of Prx I expression by H2O2 was also evaluated. METHOD: Primary culture of epidermal keratinocytes was performed, and sub-confluent cells were irradiated with UVB irradiation (20mJ/cm(2)). Western blot and Northern blot analysis were performed after the cells were harvested at different time-points after UVB irradiation. Prx I expression and intracellular levels of H2O2 were evaluated in the cells which had been irradiated with different doses of UVB. The localization of Prx I expression was identified by immunocytochemical staining. RESULTS: UVB irradiation induced Prx I mRNA and protein expressions from 3 h and 6 h after irradiation, respectively, indicating that UVB induced Prx I expression at a transcription level. Intracellular H2O2 levels were steadily increased as keratinocytes were irradiated with increasing doses of UVB. Next, when keratinocytes were treated with 0.1-10.0mM of H2O2, the marked induction of Prx I protein expression was observed above 1 mM H2O2 at a time-dependent manner (after 6 h). The H2O2-induced Prx I expression was abolished by N-acetyl-L-cysteine, a H2O2 scavenger, pre-treatment. In 2D-gel electrophoresis, the active reduced form of Prx I was rapidly transformed into the oxidized, inactive form, and then it restored to the reduced form by H2O2 treatment, suggesting that Prx I was active in responding to the H2O2-induced oxidative stress. CONCLUSION: UVB irradiation up-regulates Prx I by the mediation of H2O2 in the keratinocytes.
Acetylcysteine ; Blotting, Northern ; Blotting, Western ; Electrophoresis ; Humans* ; Hydrogen Peroxide ; Keratinocytes* ; Negotiating ; Oxidative Stress ; Peroxiredoxins* ; RNA, Messenger ; Skin

PURPOSE: This study investigated the influence of irradiation and cisplatin on PrxI & PrxII expression and on their survival rates (SR) in SK-N-BE2C and Rat2 cell lines. MATERIALS AND METHODS: The amount of PrxI & PrxII production with or without N-acetyl-L-cysteine (NAC) pretreatment was studied using a western blot after 20 Gy irradiation to determine the degree of inhibition of ROS accumulation. In addition, the amount of PrxI & PrxII production after cisplatin and after combination with cisplatin and 20 Gy irradiation was studied. The SRs of the cell lines in SK-N-BE2C and Rat 2 cells, applied with 20 Gy irradiation only, with various concentrations of cisplatin and with the combination of both, were studied. The 20 Gy irradiation-only group and the combination group were each subdivided according to NAC pretreatment, and corresponding SRs were observed at 2, 6, 12 and 48 hours after treatment. RESULTS: Compared with the control group, the amount of PrxI in SK-N-BE2C increased up to 60 minutes after irradiation and slightly increased after irradiation with NAC pretreatment 60 minutes. It did not increase in Rat2 after irradiation regardless of NAC pretreatment. PrxII in SK-N-BE2C and Rat2 was not increased after irradiation regardless of NAC pretreatment. The amounts of PrxI and PrxII in SK-N-BE2C and Rat2 were not increased either with the cisplatin-only treatment or the combination treatment with cisplatin and irradiation. SRs of irradiation group with or without NAC pretreatment and the combination group with or without NAC pretreatment were compared with each other in SK-N-BE2C and Rat2. SR was significantly high for the group with increased amount of PrxI, NAC pretreatment and lower the cisplatin concentration. SR of the group in SK-N-BE2C which had irradiation with NAC pretreatment tended to be slightly higher than the group who had irradiation without NAC pretreatment. SR of the group in Rat2 which had irradiation with NAC pretreatment was significantly higher than that the group which had irradiation without NAC pretreatment. Compared to the combination group, the irradiation-only group revealed statistically significant SR decrease with the maximal difference at 12 hours. However, at 48 hours the SR of the combination group was significantly lower than the irradiation-only group. CONCLUSION: PrxI is suggested to be an antioxidant enzyme because the amount of PrxI was increased by irradiation but decreased pretreatment NAC, a known antioxidants. Furthermore, cisplatin may inhibit PrxI production which may lead to increase cytotoxicity of irradiation. The expression of PrxI may play an important role in cytotoxicity mechanism caused by irradiation and cisplatin.
Acetylcysteine ; Animals ; Antioxidants ; Blotting, Western ; Cell Line ; Cisplatin* ; Fibroblasts* ; Humans* ; Neuroblastoma* ; Peroxiredoxins* ; Radiation, Ionizing* ; Rats* ; Survival Rate*

Despite recent economic prosperity, Korea still has high prevalence of tuberculosis. Molecular biologic characterization of Korean Mycobacterium tuberculosis strains might provide a deeper understanding of the forces contributing to the spread of tuberculosis in Korea. Therefore, we analyzed the cell lysate proteome of a representative Korean Mycobacterium tuberculosis isolate (K01) in comparison with laboratory reference strains H37Rv and H37Ra. Seven spots were strongly expressed only in K01 strain compared with M. tuberculosis H37Rv and H37Ra. Through continuous MALDI-MS analysis, these spots were identified as hypothetical protein Rv3849, secreted immunogenic protein Mpt64, Acetyl/propionyl-CoA Carbpxylase (AccD1), alkyl hydroperoxide reductase C (AhpC), N-acetylmuramyl-L-alanine amidase, a putative UDP glucose epimerase, and a transposase. A deeper study of these proteins may provide a clue in the development of effective new anti-tuberculosis vaccines against Korean M. tuberculosis isolates.
Korea ; Mycobacterium tuberculosis* ; Mycobacterium* ; Peroxiredoxins ; Prevalence ; Proteome* ; Spectrometry, Mass, Matrix-Assisted Laser Desorption-Ionization ; Transposases ; Tuberculosis ; UDPglucose 4-Epimerase ; Vaccines

Atherosclerotic vascular dysfunction is a chronic inflammatory process that spreads from the fatty streak and foam cells through lesion progression. Therefore, its early diagnosis and prevention is unfeasible. Reactive oxygen species (ROS) play important roles in the pathogenesis of atherosclerotic vascular disease. Intracellular redox status is tightly regulated by oxidant and antioxidant systems. Imbalance in these systems causes oxidative or reductive stress which triggers cellular damage or aberrant signaling, and leads to dysregulation. Paradoxically, large clinical trials have shown that non-specific ROS scavenging by antioxidant vitamins is ineffective or sometimes harmful. ROS production can be locally regulated by cellular antioxidant enzymes, such as superoxide dismutases, catalase, glutathione peroxidases and peroxiredoxins. Therapeutic approach targeting these antioxidant enzymes might prove beneficial for prevention of ROS-related atherosclerotic vascular disease. Conversely, the development of specific antioxidant enzyme-mimetics could contribute to the clinical effectiveness.
Atherosclerosis ; Catalase ; Early Diagnosis ; Foam Cells ; Glutathione ; Oxidation-Reduction ; Peroxidases ; Peroxiredoxins ; Reactive Oxygen Species ; Superoxides ; Vascular Diseases* ; Vitamins

Peroxiredoxin I (Prx I) is a member of the peroxiredoxins (Prxs) family, which are antioxidant enzymes that regulate various cellular process via intracellular oxidative signal pathways. In order to investigate the correlation between Prx I and the gamma-secretase complex, which causes Alzheimer's disease (AD), the expression level of Prx I was firstly evaluated in an animal model for AD. NSE/hPen-2 transgenic (Tg) mice, which were used as animal model in this study, showed a high level of Pen-2 expression and accumulation of Abeta-42 peptides in the hippocampus of brain. The expression level of Prx I was significantly higher on the mRNA and protein level in the brain of this model, while not change in Prx VI expression was observed. Furthermore, to verify the effect of Prx I on the gamma-secretase components in vitro, the expression level of these components was analyzed in the Prx I transfectants. Of the components of the gamma-secretase complex, the expression of PS-2 and Pen-2 was lower in the transfectants overexpressing Prx I compared to the vector transfectants. However, the expression of APP, NCT and APH-1 did not change in Prx I transfectants. Therefore, these results suggested that the expression of Prx I may be induced by the accumulation of Abeta-42 peptides and the overexpression of Prx I in neuroblastoma cells may regulate the expression of gamma-secretase components.
Alzheimer Disease ; Amyloid Precursor Protein Secretases ; Animals ; Brain ; Hippocampus ; Humans ; Mice ; Models, Animal ; Neuroblastoma ; Peptides ; Peroxiredoxins ; RNA, Messenger ; Signal Transduction