• Food Science of Animal Resources
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• v.40 no.1
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• pp.1-10
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• 2020

Various processing methods have a great impact on the physiochemical and nutritional properties of meat that are of health concern. Hence, the postmortem processing of meat by different methods is likely to intensify the potential effects on protein oxidation. The influence of meat protein oxidation on the modulation of the systemic redox status and underlying mechanism is well known. However, the effects of processed meat proteins isolated from different sources on gut microbiota, oxidative stress biomarkers, and metabolomic markers associated with metabolic syndromes are of growing interest. The application of advanced methodological approaches based on OMICS, and mass spectrometric technologies has enabled to better understand the molecular basis of the effect of processed meat oxidation on human health and the aging process. Animal studies indicate the involvement of dietary proteins isolated from different sources on health disorders, which emphasizes the impact of processed meat protein on the richness of bacterial taxa such as (Mucispirillum, Oscillibacter), accompanied by increased expression of lipogenic genes. This review explores the most recent evidences on meat processing techniques, meat protein oxidation, underlying mechanisms, and their potential effects on nutritional value, gut microbiota composition and possible implications on human health.

• BMB Reports
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• v.36 no.1
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• pp.95-109
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• 2003

Inflammatory lung diseases are characterized by chronic inflammation and oxidant/antioxidant imbalance. The sources of the increased oxidative stress in patients with chronic inflammatory lung diseases such as asthma and chronic obstructive pulmonary disease (COPD) derive from the increased burden of inhaled oxidants, and from the increased amounts of reactive oxygen species (ROS) generated by several inflammatory, immune and various structural cells of the airways. Increased levels of ROS produced in the airways is reflected by increased markers of oxidative stress in the airspaces, sputum, breath, lungs and blood in patients with lung diseases. ROS, either directly or via the formation of lipid peroxidation products such as 4-hydroxy-2-nonenal may play a role in enhancing the inflammation through the activation of stress kinases (JNK, MAPK, p38) and redox sensitive transcription factors such as NF-${\kappa}B$ and AP-1. Recent evidences have indicated that oxidative stress and pro-inflammatory mediators can alter nuclear histone acetylation/deacetylation allowing access for transcription factor DNA binding leading to enhanced pro-inflammatory gene expression in various lung cells. Understanding of the mechanisms of redox signaling, NF-${\kappa}B$/AP-1 regulation, the balance between histone acetylation and deacetylation and the release and expression of pro- and anti-inflammatory mediators may lead to the development of novel therapies based on the pharmacological manipulation of antioxidants in lung inflammation and injury. Antioxidants that have effective wide spectrum activity and good bioavailability, thiols or molecules which have dual antioxidant and anti-inflammatory activity, may be potential therapeutic agents which not only protect against the direct injurious effects of oxidants, but may fundamentally alter the underlying inflammatory processes which play an important role in the pathogenesis of chronic inflammatory lung diseases.

• Tuberculosis and Respiratory Diseases
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• v.69 no.5
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• pp.323-330
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• 2010

A key mechanism in the pathogenesis of chronic obstructive pulmonary disease is thought to be an abnormal inflammatory response in the lungs to the inhalation of toxic particles and gases, derived from tobacco smoke, air pollution, and/or occupational exposures. This review highlights the potential participation of several alternative pathogenetic processes, particularly involving the potential participation of biological and pathobiological processes related to aging, including oxidative stress and enhanced expression of markers of senescence/aging in emphysematous lungs, and the potential for enhanced tissue destruction involving alveolar cell apoptosis.

• Proceedings of the Korean Society of Toxicology Conference
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• 2001.10a
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• pp.24-25
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• 2001

Persistent cellular oxidative stress and enhanced lipid peroxidation (LPO) of PUFAs, leading to macromolecular damage and disruption of signaling pathways, are implicated in the development of human malignancies and other chronic degenerative diseases. LPO generates by oxidation of linoleic acid (LA) or arachidonic acid ($\omega$ -6 PUPAs) reactive aldehydes, such as trans-4-hydroxy-2-nonenal, which form etheno $\varepsilon$ -DNA adducts in a variety of human tissues and thus can contribute to diet-related cancers.(omitted)

• Asian-Australasian Journal of Animal Sciences
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• v.24 no.6
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• pp.818-824
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• 2011

Eight LW${\times}$D crossbred, castrated weanling piglets were used to examine the effect of hyperglycemia by streptozotocin (STZ)-injection on oxidative and anti-oxidative status in circulating fluid. Every two of the eight piglets were intravenously administrated STZ at a dose of 0 (control), 100, 125 or 150 mg/kg BW, respectively, and on 15th day after the STZ-injection, some markers of the oxidative stress in circulating fluid were measured to evaluate oxidative and anti-oxidative status in the piglets. First, piglets with hyperglycemia were selected from the STZ-injected piglets as measured by the levels of fasting plasma glucose (FPG) during 2 weeks after the STZ-injection. Additionally, data obtained from the intravenous glucose tolerance test (IVGTT) on 14th day were analyzed. Secondly, the data obtained in this experiment were divided into the control group and the hyperglycemic (STZ) group, and compared. The FPG level or area under curve (AUC) for plasma glucose during the IVGTT in the STZ-induced diabetic piglets was slightly significantly (FPG, p = 0.070; AUC, p = 0.072) higher compared with the control. On the other hand, the plasma level of lipid peroxidation in the STZ-induced diabetic piglets was significantly (p<0.05) higher compared with the control. These results raise the possibility that STZ-induced diabetic piglets produced in this study can be used as a diabetic animal model to research the pathogenic mechanisms or therapy of complications in diabetic mellitus.

• Biomolecules & Therapeutics
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• v.30 no.6
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• pp.570-575
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• 2022

Stress breaks body balance, which can cause diverse physiological disorders and worsen preexisting diseases. However, recent studies have reported that controllable stress and overcoming from stress reinforce resilience to resist against more intense stress afterwards. In this study, we investigated the protective effect of corticosterone (CORT), a representative stress hormone against hydrogen peroxide (H₂O₂)-induced neuronal cell death and its underlying molecular mechanism in SH-SY5Y cells, a human neuroblastoma cell line. The decreased cell viability by H₂O₂ was effectively restored by the pretreatment with low concentration of CORT (0.03 μM for 72 h) in the cells. H₂O₂-increased expression of apoptotic markers such as PUMA and Bim was decreased by CORT pretreatment. Furthermore, pretreatment of CORT attenuated H₂O₂-mediated oxidative damages by upregulation of antioxidant enzymes via activation of nuclear factor erythroid 2-related factor 2 (Nrf2). These findings suggest that low concentration of CORT with eustressed condition enhances intracellular self-defense against H₂O₂-mediated oxidative cell death, suggesting a role of low concentration of CORT as one of key molecules for resilience and neuronal cell survival.

• BMB Reports
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• v.48 no.12
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• pp.702-707
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• 2015

To overcome the disadvantages of stem cell-based cell therapy like low cell survival at the disease site, we used stanniocalcin 2 (STC2), a family of secreted glycoprotein hormones that function to inhibit apoptosis and oxidative damage and to induce proliferation. STC2 gene was transfected into two kinds of stem cells to prolong cell survival and protect the cells from the damage by oxidative stress. The stem cells expressing STC2 exhibited increased cell viability and improved cell survival as well as elevated expression of the pluripotency and self-renewal markers (Oct4 and Nanog) under sub-lethal oxidative conditions. Up-regulation of CDK2 and CDK4 and down-regulation of cell cycle inhibitors p16 and p21 were observed after the delivery of STC2. Furthermore, STC2 transduction activated pAKT and pERK 1/2 signal pathways. Taken together, the STC2 can be used to enhance cell survival and maintain long-term stemness in therapeutic use of stem cells.

• Asian Pacific Journal of Cancer Prevention
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• v.13 no.9
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• pp.4393-4402
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• 2012

Colon cancer is the third most common malignant neoplasm in the world and it remains an important cause of death, especially in western countries. The toxic environmental pollutant, 1, 2-dimethylhydrazine (DMH), is also a colon-specific carcinogen. Tannic acid (TA) is reported to be effective against various types of chemically induced toxicity and also carcinogenesis. In the present study, we evaluated the chemopreventive efficacy of TA against DMH induced colon toxicity in a rat model. Efficacy of TA against the colon toxicity was evaluated in terms of biochemical estimation of antioxidant enzyme activities, lipid peroxidation, histopathological changes and expression of early molecular markers of inflammation and tumor promotion. DMH treatment induced oxidative stress enzymes (p<0.001) and an early inflammatory and tumor promotion response in the colons of Wistar rats. TA treatment prevented deteriorative effects induced by DMH through a protective mechanism that involved reduction of oxidative stress as well as COX-2, i-NOS, PCNA protein expression levels and TNF-${\alpha}$ (p<0.001) release. It could be concluded from our results that TA markedly protects against chemically induced colon toxicity and acts plausibly by virtue of its antioxidant, anti-inflammatory and antiproliferative activities.

• Advances in environmental research
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• v.5 no.3
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• pp.179-187
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• 2016

This study evaluated some markers of oxidative stress in the organs of African Catfish, Clarias gariepinus from Eleyele River in Oyo State, Nigeria. Clarias gariepinus (250 g-400 g) were collected from Eleyele River (a suspected polluted River) and Clarias gariepinus from a clean fish farm (Durantee fisheries) were used as the control. Levels of Malondialdehyde (index of lipid peroxidation), Glutathione (GSH) and activities of antioxidant enzymes- Superoxide dismutase (SOD), Catalase and Glutathione-S-Transferase (GST) were evaluated in the liver, kidney and gills of the fish. From the results, there were significant (p<0.001) increases in malondialdehyde and GSH levels in the liver, kidney and gills of Clarias gariepinus from Eleyele River compared with control. The activity of GST increased significantly (p<0.05; p<0.001) in the liver and kidney of fish from Eleyele River compared with control. There was a significant decrease (p<0.05; p<0.001) in SOD activity in all the organs of Clarias gariepinus from Eleyele River compared with conrol and also a significant (p<0.001) decrease in catalase activity in the gills and kidney of the fish but catalase activity increased in the liver. Increase in lipid peroxidation and alterations in antioxidant status in Clarias gariepinus from Eleyele River show that the fish were under oxidative stress. These suggest that the River is polluted probably as a result of various wastes frequently discharged into the River. This could pose serious health risks to consumers of water and aquatic organisms from the River.

• The World Journal of Men's Health
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• v.34 no.2
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• pp.137-144
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• 2016

Purpose: We compared a transperineal ligation model and a transperitoneal ligation model in male rats to determine which animal model of overactive bladder (OAB) was more useful based on cystometrography, estimations of oxidative stress, and measurements of pro-inflammatory cytokine levels. Materials and Methods: Male rats were randomly divided into three groups (n=15 in each): the control group, the transperineal ligation group, and the transperitoneal ligation group. Four weeks after the ligation procedure, cystometrography was performed and oxidative stress, pro-inflammatory cytokine levels, and histologic changes were evaluated. Oxidative stress was assessed by measuring 8-hydroxy-20-deoxyguanosine and superoxide dismutase, and pro-inflammatory cytokine activity was investigated by measuring levels of interleukin (IL)-6, IL-8, and tumor necrosis $factor-{\alpha}$. Results: The transperineal model led to results similar to those observed for the transperitoneal model, namely (1) increased voiding frequency and reductions in the non-voiding contraction interval and the maximal vesical pressure, (2) increased levels of oxidative stress markers, (3) increased pro-inflammatory cytokine levels, and (4) fibrotic changes in the bladder tissue. Conclusions: We suggest that the transperineal procedure can be used as an alternative OAB model in male rats.