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1.
Article in English | WPRIM | ID: wpr-879951

ABSTRACT

:To investigate the effect of transient receptor potential melastatin 2 (TRPM2) inhibitor A10 on oxygen glucose deprivation/reperfusion (OGD/R) injury in SH-SY5Y cells.:Human neuroblastoma SH-SY5Y cells were subject to OGD/R injury,and then were divided into blank control group,model control group and A10 group randomly. The cell survival rate was detected by cell counting kit 8 (CCK-8); the level of cellular reactive oxygen species (ROS) was detected by reactive oxygen detection kit; the mitochondrial membrane potential was detected by tetramethylrhodamine (TMRM) method; the number of apoptotic cells was detected by TUNEL apoptosis assay kit; the protein expression level of cleaved caspase 3 was detected by Western blot.:Compared with 3,20,30,50, has lower cytotoxicity and better inhibition effect on channel activity. Compared with the model control group,ROS level was reduced,the mitochondrial membrane potential was improved,the number of apoptosis cells was reduced ,and the expression of cleaved caspase 3 was significantly reduced in the A10 group(all <0.05). : A10 can alleviate cell damage after OGD/R by inhibiting TRPM2 channel function,reducing extracellular calcium influx,reducing cell ROS levels,stabilizing mitochondrial membrane potential levels,and reducing apoptosis.


Subject(s)
Apoptosis , Benzeneacetamides , Cell Survival , Glucose , Humans , Oxygen/metabolism , Piperidones , Reactive Oxygen Species/metabolism , Reperfusion , TRPM Cation Channels
2.
Clinics ; 75: e1865, 2020. graf
Article in English | LILACS | ID: biblio-1133469

ABSTRACT

OBJECTIVES: Hypoxia leads to endothelial cell inflammation, apoptosis, and damage, which plays an important role in the complications associated with ischemic cardiovascular disease. As an oxidoreductase, p66Shc plays an important role in the regulation of reactive oxygen species (ROS) production and apoptosis. Ketamine is widely used in clinics. This study was designed to assess the potential protective effect of ketamine against hypoxia-induced injury in human umbilical vein endothelial cells (HUVECs). Moreover, we explored the potential mechanism by which ketamine protected against hypoxia-induced endothelial injury. METHODS: The protective effects of ketamine against hypoxia-induced injury was assessed using cell viability and adhesion assays, quantitative polymerase chain reaction, and western blotting. RESULTS: Our data showed that hypoxia reduced HUVEC viability, increased the adhesion between HUVECs and monocytes, and upregulated the expression of endothelial adhesion molecules at the protein and mRNA levels. Moreover, hypoxia increased ROS accumulation and upregulated p66Shc expression. Furthermore, hypoxia downregulated sirt1 expression in HUVECs. Alternatively, ketamine was shown to reverse the hypoxia-mediated reduction of cell viability and increase in the adhesion between HUVECs and monocytes, ameliorate hypoxia-induced ROS accumulation, and suppress p66Shc expression. Moreover, EX527, a sirt1 inhibitor, reversed the protective effects of ketamine against the hypoxia-mediated reduction of cell viability and increase in adhesion between HUVECs and monocytes. CONCLUSION: Ketamine reduces hypoxia-induced p66Shc expression and attenuates ROS accumulation via upregulating sirt1 in HUVECs, thus attenuating hypoxia-induced endothelial cell inflammation and apoptosis.


Subject(s)
Humans , Reactive Oxygen Species/metabolism , Apoptosis/drug effects , Human Umbilical Vein Endothelial Cells/drug effects , Ketamine/pharmacology , Hypoxia , Umbilical Veins , Cell Survival , Oxidative Stress , Human Umbilical Vein Endothelial Cells/metabolism , Src Homology 2 Domain-Containing, Transforming Protein 1
3.
Braz. arch. biol. technol ; 63: e20180659, 2020. tab, graf
Article in English | LILACS | ID: biblio-1132266

ABSTRACT

Abstract One of the main challenges in pepper production is to enhance seed germination energy and germination, and to grow healthy nursery plants with strong root system. Trichoderma species colonize roots as they grow and provide season-long benefits to plants, which is why Trichoderma species are widely used as plant growth promoter agents and promoters of plant defence mechanisms. This study evaluated the effectiveness of seed biopriming with Trichoderma isolates for growth promotion of pepper plants in early stage and their effects on seedling physiology. Nine out of ten Trichoderma isolates positively affected root weight of pepper seedlings, while three out of ten positively affected shoot weight. Root and shoot lengths were mainly unaffected. Germination energy was positively affected by five isolates with up to 40% increase compared to the control, while germination was significantly enhanced by two isolates with up to 22% increase. Considering seedling physiology, two different strain-dependent modes of actions were expressed. Promising Trichoderma isolates induced formation and accumulation of reactive oxygen species (ROS) which acted as signal molecules that increased germination energy and germination. Positive correlation was found between pyrogallol peroxidase, superoxide dismutase, catalase activity and germination in plants treated with these isolates.


Subject(s)
Soil Microbiology , Trichoderma/metabolism , Germination/physiology , Genus Pimenta/growth & development , Reactive Oxygen Species/metabolism
4.
J. appl. oral sci ; 28: e20190519, 2020. tab, graf
Article in English | LILACS, BBO | ID: biblio-1101254

ABSTRACT

Abstract Natural products have emerged as a rich source of bioactive compounds for adjunctive treatments of many infectious and inflammatory conditions, including periodontitis. Among the monoterpenes with significant biological properties, there is the perillyl alcohol (POH), which can be found in several essential oils and has shown immunomodulatory properties in recent studies, which may be interesting in the treatment of non-neoplastic inflammatory disorders. Objective To determine the antibacterial and immune modulatory activities of the POH. Methodology The minimum inhibitory concentration (MIC) and the minimum bactericidal concentration (MBC) of the POH for two significant Gram-negative periodontal pathogens were determined by macrodilution and subculture, respectively. Cell proliferation and cytotoxicity in RAW 264.7 macrophages were determined by Trypan Blue and mitochondrial enzymatic activity assay. The modulation of reactive oxygen species (ROS) was analyzed by flow cytometry and expression of TNF and arginase-1 by real-time PCR. Results The POH was effective against P. gingivalis (ATCC 33277) and F. nucleatum (ATCC 25586) with MIC= MBC=1600 μM. No cytotoxicity up to 100 µM was observed on macrophages. The cell proliferation was inhibited from 48 hours at 100 μM (p<0.05) and 250 μM (p<0.01). The POH increased ROS production at both 10 μM and 100 μM (p<0.05) in unstimulated cells. The PMA-induced ROS production was not affected by POH, whereas 100 μM significantly reduced lipopolysaccharide-induced (LPS-induced) ROS. The expression of TNF was not affected by POH in unstimulated cells or in cells polarized to M1 phenotype, whereas both concentrations of POH reduced (p<0.05) the expression of arginase-1 in M2-polarized macrophages. Conclusion The POH has antibacterial activity against periodontal pathogens and reduced proliferation of murine macrophages without significant cytotoxicity at concentrations up to 100 μM. In addition, the POH reduced the LPS-induced ROS and the expression of arginase-1 in M2-polarized macrophages.


Subject(s)
Animals , Mice , Fusobacterium nucleatum/drug effects , Reactive Oxygen Species/analysis , Porphyromonas/drug effects , Monoterpenes/pharmacology , Macrophages/drug effects , Anti-Bacterial Agents/pharmacology , Arginase/analysis , Time Factors , Biological Products/pharmacology , Microbial Sensitivity Tests , Gene Expression , Lipopolysaccharides/pharmacology , Reproducibility of Results , Tumor Necrosis Factor-alpha/analysis , Fusobacterium nucleatum/growth & development , Reactive Oxygen Species/metabolism , Porphyromonas/growth & development , Cell Proliferation/drug effects , Real-Time Polymerase Chain Reaction , Flow Cytometry , RAW 264.7 Cells , Macrophages/metabolism
5.
Rev. chil. enferm. respir ; 35(1): 49-57, mar. 2019. graf
Article in Spanish | LILACS | ID: biblio-1003646

ABSTRACT

Los incendios forestales representan un problema creciente de la salud pública a nivel mundial, especialmente para la población más vulnerable (niños, ancianos, embarazadas y portadores de enfermedades cardiovasculares o respiratorias crónicas) expuesta al humo y a otros contaminantes aéreos. A diferencia de la contaminación atmosférica habitual de grandes urbes, aquella derivada de los incendios forestales tiene una composición diferente y su ocurrencia es esporádica y difícil de prever. La exposición a contaminantes atmosféricos derivados de incendios forestales se asocia a aumento de la morbilidad respiratoria y cardiovascular, mediada por una respuesta inflamatoria pulmonar y sistémica, estrés oxidativo y disfunción endotelial. En sujetos expuestos a humo de incendios forestales se ha observado un aumento en la producción de citoquinas pro-inflamatorias, activación endotelial y disfunción del sistema nervioso autónomo, que produce daño tisular, aumento de los mecanismos protrombóticos, aumento de la presión arterial y cambios en el ritmo cardiaco. Esta revisión analiza los mecanismos que han sido involucrados en generar efectos nocivos para la salud de seres humanos expuestos a material particulado y gases emanados de incendios forestales.


Wildfires represent a growing global public health issue, especially to the most vulnerable segment of the population (children, old people, pregnant women, patients with cardiovascular or respiratory diseases) exposed to smoke and other air borne contaminants generated from these events. In contrast to great cities ' usual atmospheric pollution, that derives from forest fires differ in composition and its occurrence is sporadic and usually unpredictable. Exposure to atmospheric pollutants derived from forest fires has been associated to increased respiratory and cardiovascular morbidity, mediated by an inflammatory systemic response, oxidative stress and endothelial dysfunction. In people exposed to forest fire smoke an increased production of pro-inflammatory cytokines, endothelial activation and autonomic nervous system dysfunction has been observed, that leads to tissue injury, increased prothrombotic response, increased blood pressure and changes in heart rhythm. This review analyzes the mechanisms that have been involved in generating harmful health effects in humans exposed to inhaled particulate matter and gases steaming from wildfires.


Subject(s)
Humans , Cardiovascular Diseases/chemically induced , Wildfires , Air Pollution/adverse effects , Lung Diseases/chemically induced , Cardiovascular Diseases/physiopathology , Cerebrovascular Disorders/chemically induced , Cytokines/metabolism , Reactive Oxygen Species/metabolism , Oxidative Stress , Inhalation Exposure , Air Pollutants/adverse effects , Particulate Matter/adverse effects , Lung Diseases/physiopathology
6.
Braz. j. med. biol. res ; 52(4): e7626, 2019. graf
Article in English | LILACS | ID: biblio-1001516

ABSTRACT

Reactive oxygen species (ROS) are highly reactive chemical species that may cause irreversible tissue damage, and play a critical role in cardiovascular diseases. Hydrogen sulfide (H2S) is a gasotransmitter that acts as a ROS scavenger with cardio-protective effects. In this study, we investigated the cytoprotective effect of H2S against H2O2-induced apoptosis in cardiomyocytes. H9c2 rat cardiomyoblasts were treated with H2S (100 μM) 24 h before challenging with H2O2 (100 μM). Apoptosis was then assessed by annexin V and PI, and mitochondrial membrane potential was measured using a fluorescent probe, JC-1. Our results revealed that H2S improved cell viability, reduced the apoptotic rate, and preserved mitochondrial membrane potential. An increased Bcl-2 to Bax ratio was also seen in myocytes treated with H2S after H2O2-induced stress. Our findings indicated a therapeutic potential for H2S in preventing myocyte death following ischemia/reperfusion.


Subject(s)
Animals , Rats , Apoptosis/drug effects , Myoblasts, Cardiac/drug effects , Hydrogen Peroxide , Antioxidants/pharmacology , Reference Values , Sulfides/pharmacology , Cell Survival/drug effects , Cells, Cultured , Blotting, Western , Reproducibility of Results , Reactive Oxygen Species/metabolism , Apoptosis/physiology , Oxidative Stress/drug effects , Myocytes, Cardiac/drug effects , Myocytes, Cardiac/metabolism , Myoblasts, Cardiac/metabolism , Membrane Potential, Mitochondrial , Flow Cytometry/methods , Hydrogen Sulfide/pharmacology
7.
Biol. Res ; 52: 26, 2019. graf
Article in English | LILACS | ID: biblio-1011428

ABSTRACT

BACKGROUND: Acute myeloid leukemia (AML) is an aggressive and mostly incurable hematological malignancy with frequent relapses after an initial response to standard chemotherapy. Therefore, novel therapies are urgently required to improve AML clinical outcomes. 4-Amino-2-trifluoromethyl-phenyl retinate (ATPR), a novel all-trans retinoic acid (ATRA) derivative designed and synthesized by our team, has been proven to show biological anti-tumor characteristics in our previous studies. However, its potential effect on leukemia remains unknown. The present research aims to investigate the underlying mechanism of treating leukemia with ATPR in vitro. METHODS: In this study, the AML cell lines NB4 and THP-1 were treated with ATPR. Cell proliferation was analyzed by the CCK-8 assay. Flow cytometry was used to measure the cell cycle distribution and cell differentiation. The expression levels of cell cycle and differentiation-related proteins were detected by western blotting and immunofluorescence staining. The NBT reduction assay was used to detect cell differentiation. RESULTS: ATPR inhibited cell proliferation, induced cell differentiation and arrested the cell cycle at the G0/G1 phase. Moreover, ATPR treatment induced a time-dependent release of reactive oxygen species (ROS). Additionally, the PTEN/PI3K/Akt pathway was downregulated 24 h after ATPR treatment, which might account for the anti-AML effects of ATPR that result from the ROS-mediated regulation of the PTEN/PI3K/AKT signaling pathway. CONCLUSIONS: Our observations could help to develop new drugs targeting the ROS/PTEN/PI3K/Akt pathway for the treatment of AML.


Subject(s)
Humans , Retinoids/pharmacology , Reactive Oxygen Species/metabolism , Antineoplastic Agents/pharmacology , Fluoroimmunoassay , Leukemia, Myeloid, Acute , Signal Transduction , Down-Regulation , Cell Differentiation/drug effects , Cell Survival/drug effects , Phosphatidylinositol 3-Kinases/metabolism , Cell Line, Tumor , Cell Proliferation/drug effects , PTEN Phosphohydrolase/drug effects , PTEN Phosphohydrolase/metabolism , Proto-Oncogene Proteins c-akt/drug effects , Proto-Oncogene Proteins c-akt/metabolism
8.
Biol. Res ; 52: 15, 2019. graf
Article in English | LILACS | ID: biblio-1011417

ABSTRACT

BACKGROUND: Tumourigenic cells modify metabolic pathways In order to facilitate increased proliferation and cell survival resulting in glucose-and glutamine addiction. Previous research indicated that glutamine deprivation resulted in potential differential activity targeting tumourigenic cells more prominently. This is ascribed to tumourigenic cells utilising increased glutamine quantities for enhanced glycolysis-and glutaminolysis. In this study, the effects exerted by glutamine deprivation on reactive oxygen species (ROS) production, mitochondrial membrane potential, cell proliferation and cell death in breast tumourigenic cell lines (MCF-7, MDA-MB-231, BT-20) and a non-tumourigenic breast cell line (MCF-10A) were investigated. RESULTS: Spectrophotometry demonstrated that glutamine deprivation resulted in decreased cell growth in a time-dependent manner. MCF-7 cell growth was decreased to 61% after 96 h of glutamine deprivation; MDA-MB-231 cell growth was decreased to 78% cell growth after 96 h of glutamine deprivation, MCF-10A cell growth was decreased 89% after 96 h of glutamine deprivation and BT-20 cell growth decreased to 86% after 24 h of glutamine deprivation and remained unchanged until 96 h of glutamine deprivation. Glutamine deprivation resulted in oxidative stress where superoxide levels were significantly elevated after 96 h in the MCF-7-and MDA-MB-231 cell lines. Time-dependent production of hydrogen peroxide was accompanied by aberrant mitochondrial membrane potential. The effects of ROS and mitochondrial membrane potential were more prominently observed in the MCF-7 cell line when compared to the MDA-MB-231-, MCF-10A- and BT-20 cell lines. Cell cycle progression revealed that glutamine deprivation resulted in a significant increase in the S-phase after 72 h of glutamine deprivation in the MCF-7 cell line. Apoptosis induction resulted in a decrease in viable cells in all cell lines following glutamine deprivation. In the MCF-7 cells, 87.61% of viable cells were present after 24 h of glutamine deprivation. CONCLUSION: This study demonstrates that glutamine deprivation resulted in decreased cell proliferation, time-dependent- and cell line-dependent ROS generation, aberrant mitochondrial membrane potential and disrupted cell cycle progression. In addition, the estrogen receptor positive MCF-7 cell line was more prominently affected. This study contributes to knowledge regarding the sensitivity of breast cancer cells and non-tumorigenic cells to glutamine deprivation.


Subject(s)
Humans , Female , Breast Neoplasms/pathology , Cell Survival , Reactive Oxygen Species/metabolism , Oxidative Stress , Cell Proliferation , Glutamine/deficiency , Spectrophotometry , Breast Neoplasms/metabolism , Apoptosis , Cell Line, Tumor , Glutamine/metabolism
9.
Acta cir. bras ; 33(12): 1043-1051, Dec. 2018. graf
Article in English | LILACS | ID: biblio-973484

ABSTRACT

Abstract Purpose: To analyze the effect of methylene blue (MB) therapy during the liver ischemia-reperfusion injury (I/R) process. Methods: Thirty-five male Wistar rats were used, (70%) submitted to partial ischemia (IR) or not (NIR) (30%) were obtained from the same animal. These animals were divided into six groups: 1) Sham (SH), 2) Sham with MB (SH-MB); 3) I/R, submitted to 60 minutes of partial ischemia and 15 minutes of reperfusion; 4) NI/R, without I/R obtained from the same animal of group I/R; 5) I/R-MB submitted to I/R and MB and 6) NI/R-MB, without I/R. Mitochondrial function was evaluated. Osmotic swelling of mitochondria as well as the determination of malondialdehyde (MDA) was evaluated. Serum (ALT/AST) dosages were also performed. MB was used at the concentration of 15mg/kg, 15 minutes before hepatic reperfusion. Statistical analysis was done by the Mann Whitney test at 5%. Results: State 3 shows inhibition in all ischemic groups. State 4 was increased in all groups, except the I/R-MB and NI/R-MB groups. RCR showed a decrease in all I/R and NI/R groups. Mitochondrial osmotic swelling showed an increase in all I/R NI/R groups in the presence or absence of MB. About MDA, there was a decrease in SH values in the presence of MB and this decrease was maintained in the I/R group. AST levels were increased in all ischemic with or without MB. Conclusions: The methylene blue was not able to restore the mitochondrial parameters studied. Also, it was able to decrease lipid peroxidation, preventing the formation of reactive oxygen species.


Subject(s)
Humans , Animals , Male , Reperfusion Injury/prevention & control , Enzyme Inhibitors/therapeutic use , Liver/blood supply , Methylene Blue/therapeutic use , Oxygen Consumption , Aspartate Aminotransferases/blood , Reference Values , Time Factors , Mitochondria, Liver/drug effects , Mitochondria, Liver/metabolism , Lipid Peroxidation/drug effects , Reperfusion Injury/metabolism , Reproducibility of Results , Reactive Oxygen Species/analysis , Reactive Oxygen Species/metabolism , Rats, Wistar , Cell Respiration , Alanine Transaminase/blood , Enzyme Inhibitors/pharmacology , Mitochondrial Membranes/drug effects , Mitochondrial Membranes/metabolism , Liver/metabolism , Malondialdehyde/analysis , Methylene Blue/pharmacology , Mitochondrial Swelling/drug effects
10.
Rev. méd. Chile ; 146(6): 762-769, jun. 2018. graf
Article in Spanish | LILACS | ID: biblio-961457

ABSTRACT

One of the main features of cancer is the high rate of cell proliferation and growth. To do this, cancer cells need to redirect their metabolism mainly towards anaerobic glycolysis and an increased mitochondrial glutamine energy metabolism. Sirtuins are cellular proteins with regulatory functions on metabolic pathways, genomic stability, apoptosis, longevity, inflammation, energy metabolism and oxidative stress. Sirtuins have emerged recently as a potential therapeutic option to treat several chronic diseases including cancer. This review summarizes the tumor suppressor function of Sirtuin 3 (SIRT3), highlighting its repressor effect on glycolytic metabolism, promoting mitochondrial metabolism and oxidative stress reduction. SIRT3 activation by exercise is particularly described since it may represent a potent tool for several types of cancer treatment.


Subject(s)
Humans , Exercise/physiology , Sirtuin 3/physiology , Neoplasms/metabolism , Neoplasms/therapy , Reactive Oxygen Species/metabolism , Oxidative Stress/physiology , Tumor Suppressor Proteins/physiology , Exercise Therapy/methods , Mitochondria/metabolism
11.
Acta cir. bras ; 33(2): 134-143, Feb. 2018. tab, graf
Article in English | LILACS | ID: biblio-886257

ABSTRACT

Abstract Purpose: To investigate the effects of pycnogenol on peritoneal adhesions and additionally to investigate the immunohistochemical effects of free oxygen radicals and reactive lymph nodes detected in the adhesive tissue that was sampled surrounding the cecum on intra-abdominal adhesions. Methods: Twenty-seven Wistar Albino rats were divided into three groups. In group 1 (sham), laparotomy was performed and stitched up. In group 2 (control), after laparotomy was performed, punctate hemorrhage was induced by cecal abrasion in the cecum and each rat was intraperitoneally administered 2 cc of saline. In group 3 (experimental), after laparotomy was performed, punctate hemorrhage was induced by cecal abrasion in the cecum and each rat was intraperitoneally administered a sterile Pycnogenol derivative. The rats in all groups were re-laparotomized on postoperative day 7; samples were obtained from the peritoneal tissue surrounding the cecum, and the rats were sacrificed. Results: In group 3, there was a statistically significant difference in terms of inflammation, lymph node size, and free oxygen radicals; these parameters tended to increase. In terms of fibrosis evaluated using H&E and MT, there was no significant difference between groups 2 and 3. Conclusions: No positive outcomes indicating that pycnogenol reduces intra-abdominal adhesions were obtained. However, it caused severe inflammation in the tissue. Moreover, a significant increase in lymph node size was detected secondary to inflammation. Additionally, in immunohistochemical analyses conducted to detect oxidative stress, pycnogenol increased the production of free oxygen radicals in the tissue.


Subject(s)
Animals , Rats , Peritoneal Diseases/prevention & control , Peritoneum/surgery , Flavonoids/therapeutic use , Tissue Adhesions/prevention & control , Peritoneal Diseases/etiology , Peritoneum/pathology , Postoperative Complications , Flavonoids/adverse effects , Immunohistochemistry , Plant Extracts , Tissue Adhesions/etiology , Tissue Adhesions/pathology , Reactive Oxygen Species/metabolism , Rats, Wistar , Oxidative Stress/drug effects , Disease Models, Animal , Free Radicals/analysis , Inflammation/chemically induced , Inflammation/pathology , Laparotomy , Lymph Nodes/drug effects , Lymph Nodes/pathology , Anti-Inflammatory Agents/therapeutic use , Antioxidants/therapeutic use
12.
Clinics ; 73(supl.1): e548s, 2018. graf
Article in English | LILACS | ID: biblio-974955

ABSTRACT

OBJECTIVES: Oxidative stress results from an imbalance between the generation and elimination of oxidant species. This condition may result in DNA, RNA and protein damage, leading to the accumulation of genetic alterations that can favor malignant transformation. Persistent infection with high-risk human papillomavirus types is associated with inflammatory responses and reactive oxygen species production. In this context, oxidative stress, chronic inflammation and high-risk human papillomavirus can act in a synergistic manner. To counteract the harmful effects of oxidant species, protective molecules, known as antioxidant defenses, are produced by cells to maintain redox homeostasis. In recent years, the use of natural antioxidants as therapeutic strategies for cancer treatment has attracted the attention of the scientific community. This review discusses specific molecules and mechanisms that can act against or together with oxidative stress, presenting alternatives for cervical cancer prevention and treatment.


Subject(s)
Humans , Female , Uterine Cervical Neoplasms/metabolism , Uterine Cervical Neoplasms/drug therapy , Oxidative Stress/drug effects , Antioxidants/therapeutic use , Uterine Cervical Neoplasms/virology , Reactive Oxygen Species/metabolism , Apoptosis/drug effects , Papillomavirus Infections/metabolism , Papillomavirus Infections/drug therapy , Enzyme Inhibitors/therapeutic use
13.
Biol. Res ; 51: 22, 2018. graf
Article in English | LILACS | ID: biblio-950906

ABSTRACT

BACKGROUND: Our study aimed to investigate the roles of autophagy against high glucose induced response in retinal pigment epithelium (ARPE-19 cells). METHODS: The morphological changes and reactive oxygen species (ROS) generation in ARPE-19 cells under high glucose treatment were respectively detected using the transmission electron microscopy and flow cytometry. The expression levels of Parkin, PINK1, BNIP3L, LC3-I and LC3-II in ARPE-19 cells received high glucose treatment were measured by western blot after pretreatment of carbonyl cyanide m-chlorophenylhydrazone (CCCP), 3-methyladenine (3-MA), N-acetyl cysteine (NAC) or cyclosporin A (CsA) followed by high glucose treatment. RESULTS: ARPE-19 cells subjected to high glucose stress showed an obvious reduction in the LC3-I expression and significant increase in the number of autophagosomes, in the intracellular ROS level, and in the expression levels of Parkin, PINK1, BNIP3L and LC3-II (p < 0.05). Pretreatment with CCCP significantly reduced the LC3-I expression and increased the expression levels of Parkin, PINK1, BNIP3L and LC3-II (p < 0.05). ARPE-19 cells pretreated with CsA under high glucose stress showed markedly down-regulated expressions of Parkin, PINK1 and BNIP3L compared with the cells treated with high glucose (p < 0.05). Pretreatment of ARPE-19 cells with NAC or 3-MA under high glucose stress resulted in a marked reduction in the expression levels of PINK1, BNIP3L and LC3-II (p < 0.05). Meanwhile, the expression level of Parkin in the ARPE-19 cells pretreated with NAC under high glucose stress was comparable with that in the control cells. CONCLUSION: Autophagy might have protective roles against high glucose induced injury in ARPE19 cells via regulating PINK1/Parkin pathway and BNIP3L.


Subject(s)
Humans , Protein Kinases/drug effects , Autophagy/drug effects , Proto-Oncogene Proteins/drug effects , Tumor Suppressor Proteins/drug effects , Ubiquitin-Protein Ligases/drug effects , Retinal Pigment Epithelium/drug effects , Glucose/pharmacology , Membrane Proteins/drug effects , Protein Kinases/metabolism , Autophagy/physiology , Signal Transduction/physiology , Cell Line , Proto-Oncogene Proteins/metabolism , Reactive Oxygen Species/metabolism , Tumor Suppressor Proteins/metabolism , Ubiquitin-Protein Ligases/metabolism , Microscopy, Electron, Transmission , Retinal Pigment Epithelium/cytology , Flow Cytometry , Membrane Proteins/metabolism
14.
Biol. Res ; 51: 17, 2018. graf
Article in English | LILACS | ID: biblio-950903

ABSTRACT

BACKGROUND: Improper control on reactive oxygen species (ROS) elimination process and formation of free radicals causes tissue dysfunction. Pineal hormone melatonin is considered a potent regulator of such oxidative damage in different vertebrates. Aim of the current communication is to evaluate the levels of oxidative stress and ROS induced damage, and amelioration of oxidative status through melatonin induced activation of signaling pathways. Hepatocytes were isolated from adult Labeo rohita and exposed to H2O2 at three different doses (12.5, 25 and 50 µM) to observe peroxide induced damage in fish hepatocytes. Melatonin (25, 50 and 100 µg/ml) was administered against the highest dose of H2O2. Enzymatic and non-enzymatic antioxidants such as malondialdehyde (MDA), superoxide dismutase (SOD), catalase (CAT) and glutathione (GSH) was measured spectrophotometrically. Expression level of heat shock proteins (HSP70 and HSP90), HSPs-associated signaling molecules (Akt, ERK, cytosolic and nuclear NFkB), and melatonin receptor was also measured by western blotting analysis. RESULTS: H2O2 induced oxidative stress significantly altered (P < 0.05) MDA and GSH level, SOD and CAT activity, and up regulated HSP70 and HSP90 expression in carp hepatocytes. Signaling proteins exhibited differential modulation as revealed from their expression patterns in H2O2-exposed fish hepatocytes, in comparison with control hepatocytes. Melatonin treatment of H2O2-stressed fish hepatocytes restored basal cellular oxidative status in a dose dependent manner. Melatonin was observed to be inducer of signaling process by modulation of signaling molecules and melatonin receptor. CONCLUSIONS: The results suggest that exogenous melatonin at the concentration of 100 µg/ml is required to improve oxidative status of the H2O2-stressed fish hepatocytes. In H2O2 exposed hepatocytes, melatonin modulates expression of HSP70 and HSP90 that enable the hepatocytes to become stress tolerant and survive by altering the actions of ERK, Akt, cytosolic and nuclear NFkB in the signal transduction pathways. Study also confirms that melatonin could act through melatonin receptor coupled to ERK/Akt signaling pathways. This understanding of the mechanism by which melatonin regulates oxidative status in the stressed hepatocytes may initiate the development of novel strategies for hepatic disease therapy in future.


Subject(s)
Animals , Signal Transduction/drug effects , Oxidative Stress/drug effects , Hepatocytes/drug effects , Hydrogen Peroxide/pharmacology , Melatonin/pharmacology , Spectrophotometry , Superoxide Dismutase/drug effects , Catalase/drug effects , Catalase/metabolism , Blotting, Western , NF-kappa B/drug effects , NF-kappa B/metabolism , Reactive Oxygen Species/metabolism , MAP Kinase Signaling System/drug effects , Hepatocytes/metabolism , Proto-Oncogene Proteins c-akt/drug effects , Fishes , Glutathione/drug effects , Glutathione/metabolism , Malondialdehyde/metabolism
15.
Arq. gastroenterol ; 54(2): 123-129, Apr.-June 2017. tab, graf
Article in English | LILACS | ID: biblio-838843

ABSTRACT

ABSTRACT BACKGROUND Severe Acute Liver Failure (ALF) is a life-threatening clinical syndrome characterized by hepatocyte necrosis, loss of hepatic architecture, and impairment of liver functions. One of the main causes of ALF is hepatotoxicity from chemical agents, which damage hepatocytes and result in increase of reactive oxygen species. The vitamin E isoform is the one with the strongest biological antioxidant activity. OBJECTIVE To evaluate the antioxidant effect of vitamin E in this ALF model. METHODS We used 56 rats (mean weight of 300 g) divided into eight groups, four groups assessed at 24 hours and 4 assessed at 48 hours after induction: control group (CO); Vitamin E (Vit. E); Thioacetamide (TAA) and Thioacetamide + Vitamina E (TAA+Vit.E). Rats were submitted to injections of thioacetamide (400 mg/kg i.p.) at baseline and 8 hours later. Vitamin E (100 mg/kg ip) was administered 30 minutes after the second dose of thioacetamide. The 48-hour group rats received two additional doses of vitamin E (24h and 36h). At 24h or 48 hours after the administration of the first dose of TAA, rats were weighed and anesthetized and their blood sampled for evaluation of liver integrity through enzymes aspartate aminotransferase (AST) and alanine aminotransferase (ALT). Liver tissue was sampled for assessment of lipid peroxidation (LPO) by the technique TBARS, antioxidant enzymes SOD, CAT, GPx and GST activity, levels of the NO 2 /NO 3 and histology by H&E in two times. The results were expressed as mean ± standard deviation and statistically analyzed by ANOVA followed by Student-Newman-Keuls, with P <0.05 considered as significant. RESULTS After treatment with vitamin E, we observed a reduction in liver enzymes AST (U/L) (101.32±19.45 in 24 hours and 97.85±29.65 in 48 hours) related to the TAA group (469.56± 0.69 in 24 hours and 598.23±55.45 in 48 hours) and ALT (U/L) (76.59±8.56 in 24 hours and 68.47±6.49 in 48 hours) compared to the TAA group (312.21±10.23 in 24 hours and 359.15±17.58 in 48 hours). There was a reduction of LPO (nmol/mg Prot) in the TAA+Vit.E group (0.77±0.07 in 24 hours and 0.95±0.08 in 48 hours) compared to the TAA group (1.50±0.07 in 24 hours e 1.65±0.16 in 48 hours). SOD decreased in the TAA+Vit.E group (49.48±9.47 in 24 hours and 62.45±18, 47 in 48 hours), related to the TAA group (98.46±15.48 in 24 hours and 154.13±21.46 in 48 hours), as well as GST (nmol/min/mg Prot) in the TAA+Vit.E group (350.57±36.93 in 24 hours and 453.29±13.84 in 48 hours) compared to the TAA group (561.57±64.56 in 24 hours and 673.43±38.13 in 48 hours). There was an increase in CAT (pmol/min/mg Prot) in the TAA+Vit.E group (3.40±0.44 in 24 hours and 3.0±0.35 in 48 hours) compared to the TAA group (1.65±0.21 in 24 hours and 1.86±0.42 in 48 hours). The GPx (nmol/min/mg Prot) increased in 24 hours in the TAA+Vit.E group (1.01±0.16) compared to the TAA group (0.41±0.04) and decreased in 48 hours (1.19±0.17) compared to the TAA group (1.76±0.21). There was a reduction in NO2/NO3 (mmol/L) levels in the TAA+Vit.E group (31.47±4.26 in 24 hours and 38.93±5.20 in 48 hours) compared to the TAA group (49.37±5.12 in 24 hours and 53.53±5.97 in 48 hours). The histopathological evaluation showed a decrease in liver injury (necrosis and inflammation) in both studied times. CONCLUSION These results suggest that vitamin E was able to protect the liver from lesions caused by thioacetamide.


RESUMO CONTEXTO A Insuficiência Hepática Aguda Grave (IHAG) é uma síndrome clínica potencialmente fatal, na qual ocorre necrose dos hepatócitos, perda da arquitetura hepática e deterioração de suas funções. Dentre as principais causas da IHAG está a hepatotoxicidade decorrente de agentes químicos, que lesam os hepatócitos e acarretam aumento das espécies reativas de oxigênio. A vitamina E tem alta atividade antioxidante biológica e é amplamente distribuída nos tecidos. OBJETIVO Avaliar o efeito antioxidante da Vitamina E no modelo de IHAG. MÉTODOS Foram utilizados 56 ratos, com peso médio de 300 g, divididos em oito grupos, quatro grupos avaliados em 24 horas e quatro em 48 horas após a indução: grupo controle (CO); Vitamina E (Vit.E); Tioacetamida (TAA) e Tioacetamida + Vitamina E (TAA+Vit.E). Os ratos foram submetidos a injeções de tioacetamida, na dose de 400 mg/Kg de peso i.p., no início do experimento e, posteriormente, após 8 horas. A vit E (100 mg//Kg i.p.) foi administrada 30 minutos após a segunda dose de tioacetamida. Os animais do tempo 48 horas receberam mais duas doses de vit. E (24h e 36h). Transcorridas 24 ou 48 horas após a administração da primeira dose de TAA, os animais foram pesados, anestesiados e o sangue retirado para a avaliação da integridade hepática através das enzimas Aspartatoaminotransferase (AST) e Alanina aminotransferase (ALT). O tecido hepático foi retirado para avaliação da lipoperoxidação através da técnica de TBARS, atividade das enzimas antioxidantes SOD, CAT, GPx, e GST, avaliação de NO 2 /NO 3 e avaliação histológica pela coloração de hematoxilina e eosina nos dois tempos. Os resultados foram expressos como média ± erro padrão e a análise estatística utilizada foi ANOVA, seguido de teste de Student-Newman-Keuls, considerado significativo P <0,05. RESULTADOS Após o tratamento com a vit. E, observamos uma redução nas enzimas de integridade hepática AST (U/L) (101,32±19,45 em 24h e 97,85±29,65 em 48h) relacionado ao grupo TAA (469,56±20,69 em 24h e 598,23±55,45 em 48h) e ALT (U/L) (76,59±8,56 em 24h e 68,47±6,49 em 48h) comparado ao grupo TAA (312,21±10,23 em 24h e 359,15±17,58 em 48h). Houve uma redução da LPO (nmol/mg Prot), no grupo TAA+Vit.E (0,77±0,07 em 24h e 0,95±0,08 em 48h) comparado ao grupo TAA (1,50±0,07 em 24h e 1,65±0,16 em 48h). A SOD (USOD/min/mg Prot) diminuiu no grupo TAA+Vit.E (49,48±9,47 em 24h e 62,45±18,47 em 48h) relacionado ao grupo TAA (98,46±15,48 em 24h e 154,13±21,46 em 48h), assim como a GST (nmol/min/mg Prot) no grupo TAA+Vit.E (350,57±36,93 em 24h e 453,29±13,84 em 48h) comparado ao grupo TAA (561,57±64,56 em 24h e 673,43±38,13 em 48h). Houve aumento da CAT (pmol/min/mg Prot) no grupo TAA+Vit.E (3,40±0,44 em 24h e 3,01±0,35 em 48h) em relação ao grupo TAA (1,65±0,21 em 24h e 1,86±0,42 em 48h). A GPx (nmol/min/mg Prot) aumentou em 24h no grupo TAA+Vit.E (1,01±0,16) comparado ao grupo TAA (0,41±0,04) e diminuiu em 48h (1,19±0,17) em relação ao grupo TAA (1,76±0,21). Verificou-se redução nos níveis de NO 2 /NO 3 (mmol/L) no grupo TAA+Vit.E (31,47±4,26 em 24h e 38,93±5,20 em 48h) em relação ao grupo TAA (49,37±5,12 em 24h e 53,53±5,97 em 48h). A avaliação histopatológica mostrou diminuição da lesão hepática (necrose e inflamação) em ambas os tempos estudados. CONCLUSÃO Estes resultados sugerem que a vitamina E foi capaz de proteger o fígado de lesões causadas por tioacetamida.


Subject(s)
Animals , Male , Rats , Vitamin E/therapeutic use , Liver Failure, Acute/prevention & control , Antioxidants/therapeutic use , Aspartate Aminotransferases/blood , Severity of Illness Index , Reactive Oxygen Species/metabolism , Rats, Wistar , Liver Failure, Acute/enzymology , Liver Failure, Acute/pathology , Reactive Nitrogen Species/metabolism , Alanine Transaminase/blood , Disease Models, Animal , Alkaline Phosphatase/blood
16.
Braz. j. microbiol ; 48(2): 326-332, April.-June 2017. tab, graf
Article in English | LILACS | ID: biblio-839372

ABSTRACT

Abstract Stress tolerance is a key attribute that must be considered when using yeast cells for industrial applications. High temperature is one factor that can cause stress in yeast. High environmental temperature in particular may exert a natural selection pressure to evolve yeasts into thermotolerant strains. In the present study, three yeasts (Saccharomyces cerevisiae, MC4, and Kluyveromyces marxianus, OFF1 and SLP1) isolated from hot environments were exposed to increased temperatures and were then compared with a laboratory yeast strain. Their resistance to high temperature, oxidative stress, and antioxidant response were evaluated, along with the fatty acid composition of their cell membranes. The SLP1 strain showed a higher specific growth rate, biomass yield, and biomass volumetric productivity while also showing lower duplication time, reactive oxygen species (ROS) production, and lipid peroxidation. In addition, the SLP1 strain demonstrated more catalase activity after temperature was increased, and this strain also showed membranes enriched in saturated fatty acids. It is concluded that the SLP1 yeast strain is a thermotolerant yeast with less oxidative stress and a greater antioxidant response. Therefore, this strain could be used for fermentation at high temperatures.


Subject(s)
Saccharomyces cerevisiae/physiology , Stress, Physiological , Kluyveromyces/physiology , Oxidative Stress , Antioxidants/metabolism , Saccharomyces cerevisiae/growth & development , Saccharomyces cerevisiae/radiation effects , Saccharomyces cerevisiae/chemistry , Kluyveromyces/growth & development , Kluyveromyces/radiation effects , Kluyveromyces/chemistry , Lipid Peroxidation , Catalase/analysis , Cell Membrane/chemistry , Reactive Oxygen Species/metabolism , Biomass , Fatty Acids/analysis , Hot Temperature
17.
Arch. endocrinol. metab. (Online) ; 61(2): 152-159, Mar.-Apr. 2017. tab
Article in English | LILACS | ID: biblio-838433

ABSTRACT

ABSTRACT Background Obesity is characterized by a deposition of abnormal or excessive fat in adipose tissue, and is linked with a risk of damage to several metabolic and pathological processes associated with oxidative stress. To date, salivary oxidative biomarkers have been minimally explored in obese individuals. Thus, the aim of this study was to assess the concentrations of salivary oxidative biomarkers (ferric-reducing antioxidant power, uric acid, sulfhydryl groups) and lipid peroxidation in obese and overweight young subjects. Materials and methods Levels of lipid peroxidation, ferric-reducing antioxidant power, uric acid, and SH groups were determined in the saliva and serum of 149 young adults, including 54 normal weight, 27 overweight, and 68 obese individuals. Anthropometric measurements were also evaluated. Results Salivary levels of ferric-reducing antioxidant power, sulfhydryl groups, and lipid peroxidation, as well as serum levels of ferric-reducing antioxidant power, uric acid, and lipid peroxidation were higher in obese patients when compared with individuals with normal weight. There were correlations between salivary and serum ferric-reducing antioxidant power and salivary and serum uric acid in the obese and normal-weight groups. Conclusions Our results indicate that the increase in salivary levels of ferric-reducing antioxidant power, sulfhydryl groups, and lipid peroxidation, and serum levels of ferric-reducing antioxidant power, uric acid, and lipid peroxidation could be related to the regulation of various processes in the adipose tissue. These findings may hold promise in identifying new oxidative markers to assist in diagnosing and monitoring overweight and obese patients.


Subject(s)
Humans , Male , Female , Adult , Young Adult , Saliva/metabolism , Saliva/chemistry , Uric Acid/analysis , Lipid Peroxidation/physiology , Overweight/blood , Antioxidants/analysis , Obesity/blood , Oxidation-Reduction , Reference Values , Sulfhydryl Compounds/analysis , Biomarkers/analysis , Case-Control Studies , Anthropometry , Reactive Oxygen Species/metabolism , Statistics, Nonparametric , Oxidative Stress/physiology
18.
Braz. j. med. biol. res ; 50(12): e6533, 2017. graf
Article in English | LILACS | ID: biblio-888965

ABSTRACT

N-acetylcysteine (NAC) inhibits nociceptive transmission. This effect has been associated partly with its antioxidant properties. However, the effect of NAC on the levels of lipid hydroperoxides (a pro-oxidant marker), content of ascorbic acid (a key antioxidant molecule of nervous tissue) and total antioxidant capacity (TAC) is unknown. Thus, our study assessed these parameters in the lumbosacral spinal cord of rats with chronic constriction injury (CCI) of the sciatic nerve, one of the most commonly employed animal models of neuropathic pain. Thirty-six male Wistar rats weighing 200-300 g were equally divided into the following groups: Naive (rats did not undergo surgical manipulation); Sham (rats in which all surgical procedures involved in CCI were used except the ligature), and CCI (rats in which four ligatures were tied loosely around the right common sciatic nerve). All rats received intraperitoneal injections of NAC (150 mg·kg−1·day−1) or saline for 1, 3, or 7 days. Rats were killed 1, 3, and 7 days after surgery. NAC treatment prevented the CCI-induced increase in lipid hydroperoxide levels only at day 1, although the amount was higher than that found in naive rats. NAC treatment also prevented the CCI-induced increase in ascorbic acid content, which occurred at days 1, 3, and 7. No significant change was found in TAC with NAC treatment. The changes observed here may be related to the antinociceptive effect of NAC because modulation of oxidative-stress parameters seemed to help normalize the spinal cord oxidative status altered by pain.


Subject(s)
Animals , Male , Acetylcysteine/pharmacology , Free Radical Scavengers/pharmacology , Neuralgia/drug therapy , Neuralgia/metabolism , Oxidative Stress/drug effects , Spinal Cord/drug effects , Spinal Cord/metabolism , Antioxidants , Ascorbic Acid/analysis , Biomarkers/analysis , Constriction , Lipid Peroxides/analysis , Rats, Wistar , Reactive Oxygen Species/metabolism , Reproducibility of Results , Sciatic Neuropathy , Time Factors , Treatment Outcome
19.
Int. j. morphol ; 34(2): 431-435, June 2016. ilus
Article in Spanish | LILACS | ID: lil-787016

ABSTRACT

El estrés oxidativo es definido como un desbalance entre la producción de oxidantes y antioxidantes. La inducción de tolerancia a estrés en los ovocitos conllevaría a un mejor desarrollo embrionario. En bovinos, la incubación de ovocitos maduros con diferentes estresores (térmicos, alta presión hidrostática, oxidativos) incrementaría la tasa de generación de blastocitos. Este estudio evalúa el efecto de la modulación del estado redox incrementando el estrés oxidativo con H2O2 en ovocitos maduros bajo condiciones de cultivo in vitro y su efecto sobre el potencial de desarrollo embrionario. Para ello, ovocitos procedentes de ovarios de matadero fueron madurados en medio TCM-199 suplementado durante 22­23 h, a 38,5 °C, 5 % CO2 y humedad a saturación. Al final de las 22­23 h se incubaron los ovocitos maduros con 0, 50, 100 y 200 µM H2O2. La fecundación in vitro se realizó co-incubando los ovocitos durante 18 h con una concentración final de 1x106 espermatozoides/mL. Los presuntos cigotos fueron denudados y cultivados en medio KSOM-0,4 % BSA a 38,5 °C en atmósfera de baja tensión de O2 (5 % O2, 5 % CO2 y 90 % N2) y humedad a saturación. El estrés oxidativo inducido con H2O2 a una concentración de 50 y 100 µM produce una tasa de división de los embriones similar al control (88,7 %, 83,2 % y 86,4 % respectivamente, p>0,05), disminuyendo significativamente al utilizar una concentración de 200 µM (58,8 %, p<0,05). Asimismo, H2O2 causó un efecto similar en la tasa de blastocitos con 50 µM (20,4 % vs. 25,8 % control, p>0.05) pero disminuyó significativamente con 100 y 200 µM (10,7 % y 3,3 % respectivamente, p<0,05). Es posible, que estos embriones resistentes al estrés oxidativo puedan tener una mayor sobrevida durante los procesos de criopreservación que generan altos niveles de especies reactivas de oxígeno en los embriones.


Oxidative stress is defined as an imbalance between the production of oxidants and antioxidants. The induction of stress tolerance in oocytes leads to a better embryonic development. In cattle incubating mature oocytes with different stressors (thermal, high hydrostatic pressure, oxidative) increase the generation rate of blastocysts. The purpose of this study was to evaluate the effect of modulating the redox state increasing the oxidative stress through H2O2 in mature oocyte under in vitro culture conditions and its effect on the potential of embryonic development. To do this, oocytes from slaughterhouse ovaries were matured in TCM-199 medium supplemented for 22­23 h at 38.5 °C, 5 % CO2 and humidified atmosphere. At the end of 22­23 h, the treatments with 0, 50, 100 and 200 µM H2O2 were applied for 1 h. IVF was performed co-incubating the eggs for 18 h with a final concentration of 1x106 sperm/mL. The presumptive zygotes were denuded and cultured in medium KSOM-0.4 % BSA to 38.5 °C in an atmosphere of low concentration of O2 (5 % O2, 5 % CO2 and 90 % N2) and humidified atmosphere. The results show that the induction of oxidative stress by H2O2 produces a similar effect using a concentration of 50 and 100 mM in the cleavage rate of embryos compared to control (88.7 %, 83.2 % and 86,4 % respectively, p>0.05) and decreasing significantly by using a concentration of 200 mM (58.8 %, p<0.05). Also, H2O2 caused a similar effect on the rate of blastocysts with 50 µM (20.4 % vs. 25.8 control, p>0.05) but decreased significantly with 100 and 200 µM (10.7 % and 3.3 % respectively, p<0.05). It is possible that these embryos resistant to oxidative stress may have a higher survival in the cryopreservation processes that generating high levels of reactive oxygen species.


Subject(s)
Animals , Cattle , Adaptation, Physiological , Embryo, Mammalian/physiology , Hydrogen Peroxide/metabolism , Oxidative Stress , Reactive Oxygen Species/metabolism , Blastocyst/metabolism , Fertilization in Vitro
20.
Acta cir. bras ; 31(2): 126-132, Feb. 2016. tab, graf
Article in English | LILACS | ID: lil-775566

ABSTRACT

PURPOSE: To investigate the potential protective effect of allopurinol on reperfusion injury by determining the inflammatory response through the measurement of tumor necrosis factor-alpha (TNF-alpha). METHODS: Sixty rats were distributed into two groups: control and allopurinol and each group was divided into three subgroups, ischemia for two hours, ischemia for three hours and ischemia simulation. Allopurinol group rats received 100mg/kg dose of allopurinol, whereas control group rats received an equivalent dose of saline. Clamping of the infrarenal aorta was performed for two or three hours depending on the subgroup. Ischemia simulation subgroups did not suffer ischemia, just aortic dissection, and maintenance for three hours. After 72 hours of reperfusion, blood was collected by cardiac puncture for TNF-alpha measurement. RESULTS: Allopurinol reduced TNF-alpha significantly (p <0.001) when compared to the matching control subgroups (control X allopurinol in ischemia for two hours and for three hours). CONCLUSION: Allopurinol reduced the concentrations of serum TNF-alpha when used at different times of ischemia followed by reperfusion, which might indicate reduction of the inflammation provoked by the reperfusion injury.


Subject(s)
Animals , Reperfusion Injury/metabolism , Allopurinol/pharmacology , Abdominal Cavity/blood supply , Ischemia/surgery , Antimetabolites/pharmacology , Time Factors , Reperfusion Injury/prevention & control , Random Allocation , Tumor Necrosis Factor-alpha/analysis , Tumor Necrosis Factor-alpha/drug effects , Reactive Oxygen Species/metabolism , Rats, Wistar , Models, Animal , Inflammation/metabolism
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