Through the history of modern medicine, bioactive components in natural products have been either employed directly as medicines or used as prototypes for synthetic drug development. This brief Research Highlights paper considers 3H-1,2-dithiole-3-thione (D3T), a member of the 1,2-dithiole-3-thiones-compounds which may naturally occur in cruciferous vegetables. Among 1,2-dithiole-3-thiones, D3T is the most potent member with regard to the capacity of inducing tissue defenses against oxidative and inflammatory stress. Oxidative and inflammatory stress is a major pathophysiological process involved in numerous human disorders, including cancer, cardiovascular diseases, neurodegeneration, and sepsis, to name just a few. This article surveys recent major research findings on D3T as an inducer of tissue antioxidative and antiinflammatory defenses and as a potential therapeutic modality for sepsis intervention.
{"title":"3H-1,2-Dithiole-3-Thione as a Potentially Novel Therapeutic Compound for Sepsis Intervention.","authors":"Y. Li, Z. Jia, Hong Zhu","doi":"10.20455/ROS.2019.847","DOIUrl":"https://doi.org/10.20455/ROS.2019.847","url":null,"abstract":"Through the history of modern medicine, bioactive components in natural products have been either employed directly as medicines or used as prototypes for synthetic drug development. This brief Research Highlights paper considers 3H-1,2-dithiole-3-thione (D3T), a member of the 1,2-dithiole-3-thiones-compounds which may naturally occur in cruciferous vegetables. Among 1,2-dithiole-3-thiones, D3T is the most potent member with regard to the capacity of inducing tissue defenses against oxidative and inflammatory stress. Oxidative and inflammatory stress is a major pathophysiological process involved in numerous human disorders, including cancer, cardiovascular diseases, neurodegeneration, and sepsis, to name just a few. This article surveys recent major research findings on D3T as an inducer of tissue antioxidative and antiinflammatory defenses and as a potential therapeutic modality for sepsis intervention.","PeriodicalId":91793,"journal":{"name":"Reactive oxygen species (Apex, N.C.)","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2019-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"46066489","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
O. Abdel-Salam, A. Sleem, E. Youness, N. Mohammed, E. Omara, Marwa E. Shabana
In this study, the neuroprotective potential of the glutathione precursor N-acetylcysteine in the rotenone-induced Parkinson’s disease (PD) was investigated. Rats were administered rotenone (1.5 mg/kg/day) once every other day for 2 weeks by subcutaneous injection. Starting from the first day of rotenone treatment, rats received the vehicle control or N-acetylcysteine (NAC) at doses of 10 and 30 mg/kg orally given at time of rotenone injection. Rats were evaluated for brain malondialdehyde (MDA), reduced glutathione (GSH), nitric oxide content, and paraoxonase-1 (PON-1) activity in the striatum, cerebral cortex, and the rest of the brain tissue. The level of the anti-apoptotic Bcl-2 was also determined in the striatum. In addition, histopathological examination and the expression of cycloxygenase-2 (COX-2) in the striatum and cerebral cortex were performed. Rotenone treatment caused a significant increase in MDA and nitric acid content in the striatum, cerebral cortex, and the rest of the brain tissue. It also significantly decreased brain GSH content and PON-1 activity in these regions and decreased striatal Bcl-2 level compared to control values. Rotenone treatment caused neuronal necrosis, apoptosis, and vacuolization, and increased the expression of COX-2 in both the striatum and cerebral cortex. NAC given at doses of 10 and 30 mg/kg to rotenone-treated rats caused a dose-dependent significant decrease in MDA levels in the cortex and the rest of the brain tissue and at the dose of 30 mg/kg significantly decreased the striatal MDA level. It also significantly decreased the nitric oxide level, increased GSH content and PON-1 activity in the striatum, cerebral cortex, and the rest of the brain when given at doses of 10 and 30 mg/kg. Additionally, there was a significant increase in the striatal Bcl-2 level by NAC at 30 mg/kg. NAC decreased neuronal necrosis and apoptosis as well as COX-2 immunostaining in both the striatum and cerebral cortex in a dose-dependent manner. These findings suggest a potential benefit for NAC in alleviating brain oxidative stress, neuroinflammation, and neurodegeneration in the rotenone model of PD in rats. NAC could thus be a useful adjunct in the treatment of patients with PD.
{"title":"Neuroprotective Effects of the Glutathione Precursor N-Acetylcysteine against Rotenone-Induced Neurodegeneration","authors":"O. Abdel-Salam, A. Sleem, E. Youness, N. Mohammed, E. Omara, Marwa E. Shabana","doi":"10.20455/ROS.2019.845","DOIUrl":"https://doi.org/10.20455/ROS.2019.845","url":null,"abstract":"In this study, the neuroprotective potential of the glutathione precursor N-acetylcysteine in the rotenone-induced Parkinson’s disease (PD) was investigated. Rats were administered rotenone (1.5 mg/kg/day) once every other day for 2 weeks by subcutaneous injection. Starting from the first day of rotenone treatment, rats received the vehicle control or N-acetylcysteine (NAC) at doses of 10 and 30 mg/kg orally given at time of rotenone injection. Rats were evaluated for brain malondialdehyde (MDA), reduced glutathione (GSH), nitric oxide content, and paraoxonase-1 (PON-1) activity in the striatum, cerebral cortex, and the rest of the brain tissue. The level of the anti-apoptotic Bcl-2 was also determined in the striatum. In addition, histopathological examination and the expression of cycloxygenase-2 (COX-2) in the striatum and cerebral cortex were performed. Rotenone treatment caused a significant increase in MDA and nitric acid content in the striatum, cerebral cortex, and the rest of the brain tissue. It also significantly decreased brain GSH content and PON-1 activity in these regions and decreased striatal Bcl-2 level compared to control values. Rotenone treatment caused neuronal necrosis, apoptosis, and vacuolization, and increased the expression of COX-2 in both the striatum and cerebral cortex. NAC given at doses of 10 and 30 mg/kg to rotenone-treated rats caused a dose-dependent significant decrease in MDA levels in the cortex and the rest of the brain tissue and at the dose of 30 mg/kg significantly decreased the striatal MDA level. It also significantly decreased the nitric oxide level, increased GSH content and PON-1 activity in the striatum, cerebral cortex, and the rest of the brain when given at doses of 10 and 30 mg/kg. Additionally, there was a significant increase in the striatal Bcl-2 level by NAC at 30 mg/kg. NAC decreased neuronal necrosis and apoptosis as well as COX-2 immunostaining in both the striatum and cerebral cortex in a dose-dependent manner. These findings suggest a potential benefit for NAC in alleviating brain oxidative stress, neuroinflammation, and neurodegeneration in the rotenone model of PD in rats. NAC could thus be a useful adjunct in the treatment of patients with PD.","PeriodicalId":91793,"journal":{"name":"Reactive oxygen species (Apex, N.C.)","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2019-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"46332006","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
While until recently reactive oxygen species (ROS) were thought to mainly act as agents of cell damage, there is growing information on the role of ROS as mediators of signaling to regulate cellular homeostasis. In an article published in Cell Metabolism (2018 November 28; 6:764–775. doi: 10.1016/j.cmet.2018.07.012), Dogan and colleagues reported a notable decline of the clinical and biochemical phenotype in a double mutant model of cytochromec oxidase-defective mitochondrial myopathy and alternative oxidase (AOX). AOX directly oxidizes ubiquinone, preserving electron flow from carriers NADH and FADH2, and abolishes the contribution of complexes III and IV to membrane potential in the mitochondrial respiratory chain. Although AOX can limit the generation of ROS and preserve redox homeostasis, thereby maintaining tricarboxylic acid cycle activity, the authors highlight that antioxidants can inhibit the homeostatic response to bioenergetic failure by modulating mitochondrial biogenesis. The result supports that interruption of ROS signaling might negatively impact the induction of mitochondrial biogenesis and antioxidant gene expression. This prevents cellular processes that are subject to redox regulation for oxidative damage chain, thereby leading to mitochondrial dysfunction.
{"title":"Blocking Reactive Oxygen Species Generation Inhibits Biogenesis in Mitochondrial Dysfunction","authors":"Waleska Dornas, V. Lagente","doi":"10.20455/ROS.2019.839","DOIUrl":"https://doi.org/10.20455/ROS.2019.839","url":null,"abstract":"While until recently reactive oxygen species (ROS) were thought to mainly act as agents of cell damage, there is growing information on the role of ROS as mediators of signaling to regulate cellular homeostasis. In an article published in Cell Metabolism (2018 November 28; 6:764–775. doi: 10.1016/j.cmet.2018.07.012), Dogan and colleagues reported a notable decline of the clinical and biochemical phenotype in a double mutant model of cytochromec oxidase-defective mitochondrial myopathy and alternative oxidase (AOX). AOX directly oxidizes ubiquinone, preserving electron flow from carriers NADH and FADH2, and abolishes the contribution of complexes III and IV to membrane potential in the mitochondrial respiratory chain. Although AOX can limit the generation of ROS and preserve redox homeostasis, thereby maintaining tricarboxylic acid cycle activity, the authors highlight that antioxidants can inhibit the homeostatic response to bioenergetic failure by modulating mitochondrial biogenesis. The result supports that interruption of ROS signaling might negatively impact the induction of mitochondrial biogenesis and antioxidant gene expression. This prevents cellular processes that are subject to redox regulation for oxidative damage chain, thereby leading to mitochondrial dysfunction.","PeriodicalId":91793,"journal":{"name":"Reactive oxygen species (Apex, N.C.)","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2019-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"43557228","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
The exact cause of brain tumor is still unknown, and it is a multi-factorial disease. Brain tumor can originate from brain cells or secondary from other organs via metastasis. Generally, tumor cells show aberrant metabolism of free radicals. The current study aims at evaluating creatine kinase BB (CK-BB) and total oxidative stress (TOS) levels among brain tumor patients for diagnosis, prognosis, and treatment strategy. Hospital-based comparative cross-sectional study was conducted on a total of 90 participants (50 brain tumor patients and 40 healthy controls) from April 2018 to October 2018. Venous blood samples were collected for TOSand CK-BB activity measurement. Purposive sampling technique was implemented to select study participants in the hospital. Catalytic activity of CK-BB and TOS were significantly increased in the serum of brain tumor patients as compared to controls. TOS levels in patients with malignant brain tumor were significantly higher than those with benign tumor, but CK-BB levels were not significantly different between benign and malignant types of brain tumor. Both serum levels of TOS and CK-BB were significantly associated with brain tumor. The CK-BB activity was significantly associated with brain tumor and can be used as markers for diagnosis. Participants with increased TOS had significantly higher risk of brain tumor development compared to healthy controls. In conclusion, oxidative stress status and CK-BB level may be used as possible brain tumor markers.
{"title":"Oxidative Stress and Serum Creatine Kinase BB Levels can Help Mark Severity and Stage of Brain Tumor","authors":"Fitalew Tadele, S. Genet, M. Menon, Abat Sahlu","doi":"10.20455/ROS.2019.837","DOIUrl":"https://doi.org/10.20455/ROS.2019.837","url":null,"abstract":"The exact cause of brain tumor is still unknown, and it is a multi-factorial disease. Brain tumor can originate from brain cells or secondary from other organs via metastasis. Generally, tumor cells show aberrant metabolism of free radicals. The current study aims at evaluating creatine kinase BB (CK-BB) and total oxidative stress (TOS) levels among brain tumor patients for diagnosis, prognosis, and treatment strategy. Hospital-based comparative cross-sectional study was conducted on a total of 90 participants (50 brain tumor patients and 40 healthy controls) from April 2018 to October 2018. Venous blood samples were collected for TOSand CK-BB activity measurement. Purposive sampling technique was implemented to select study participants in the hospital. Catalytic activity of CK-BB and TOS were significantly increased in the serum of brain tumor patients as compared to controls. TOS levels in patients with malignant brain tumor were significantly higher than those with benign tumor, but CK-BB levels were not significantly different between benign and malignant types of brain tumor. Both serum levels of TOS and CK-BB were significantly associated with brain tumor. The CK-BB activity was significantly associated with brain tumor and can be used as markers for diagnosis. Participants with increased TOS had significantly higher risk of brain tumor development compared to healthy controls. In conclusion, oxidative stress status and CK-BB level may be used as possible brain tumor markers.","PeriodicalId":91793,"journal":{"name":"Reactive oxygen species (Apex, N.C.)","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2019-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"47705337","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Acne vulgaris (acne for simplicity) is the most common skin disorder with dysregulated inflammation as a prominent underling pathophysiology. While the exact etiologies of acne remain elusive, it has long been suggested that the development of acne is heavily influenced by dietary factors, which in turn provides a basis for dietary intervention of this disease. In this article, we survey recent randomized controlled trials demonstrating an efficacy for multiple dietary modalities in the intervention of acne. These include adoption of low glycemic index/load diets and dietary supplementation with omega-3 fatty acids/fish oil and lactoferrin, as well as a prescription dietary supplement, namely, NicAzel forte tablets. We discuss the potential biological mechanisms underlying the anti-acne efficacy of the above dietary modalities and propose antiinflammation as the final common pathway of dietary intervention of this most common skin disease.
{"title":"Dietary Intervention of Acne Vulgaris: Antiinflammation as the Final Common Pathway","authors":"Jing Zhang, Harper Z. Bird, R. Hopkins","doi":"10.20455/ROS.2019.843","DOIUrl":"https://doi.org/10.20455/ROS.2019.843","url":null,"abstract":"Acne vulgaris (acne for simplicity) is the most common skin disorder with dysregulated inflammation as a prominent underling pathophysiology. While the exact etiologies of acne remain elusive, it has long been suggested that the development of acne is heavily influenced by dietary factors, which in turn provides a basis for dietary intervention of this disease. In this article, we survey recent randomized controlled trials demonstrating an efficacy for multiple dietary modalities in the intervention of acne. These include adoption of low glycemic index/load diets and dietary supplementation with omega-3 fatty acids/fish oil and lactoferrin, as well as a prescription dietary supplement, namely, NicAzel forte tablets. We discuss the potential biological mechanisms underlying the anti-acne efficacy of the above dietary modalities and propose antiinflammation as the final common pathway of dietary intervention of this most common skin disease.","PeriodicalId":91793,"journal":{"name":"Reactive oxygen species (Apex, N.C.)","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2019-05-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"47875561","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Gram-negative bacteria mediate multiple organ damage through eliciting systemic inflammatory response and extensive oxidative stress in affected humans and animals. This study was done to evaluatethe effect of grape seed extract (GSE) given alone or in combination with vitamin C (Vit C) on organ toxicity in mice treated with lipopolysaccharide (LPS). Mice received intraperitoneal injections of LPS on day 1 (4 mg/kg) and day 8 (2 mg/kg) of the study and starting from the first day were orally treated with GSE (50 and 100 mg/kg), GSE (50 mg/kg) plus Vit C (50 mg/kg) or saline (plus vehicle control) for 15 successive days. The no vehicle control group was treated with saline only. Results indicated that compared to the saline-treated group, LPS injection significantly increased alanine aminotransferase (ALT), aspartate aminotransferase (AST), creatinine, uric acid, and decreased paraoxonase-1(PON-1) in the serum. Moreover, LPS treatment significantly increased oxidative stress status and decreased the reduced glutathione (GSH) in the liver, kidney, and brain tissues. GSE given at doses of 50 and 100 mg/kg significantly decreased serum markers of liver and kidney tissue injury and decreased oxidative stress in the liver, kidney, and brain of LPS-treated mice. The resultant effect of combined treatment with GSE and Vit C was greater than that of GSE alone. Moreover, immunohistochemical studies of liver, kidney, and brain tissue sections were conducted. The LPS-induced intense immunohistochemical staining of tumor necrosis factor-alpha (TNF-α) and caspase-3 expression was decreased by treatment with GSE or GSE + Vit C in the following manner: Vit C + GSE > GSE 100 mg/kg > GSE 50 mg/kg. Our data indicate that the combination of GSE and Vit C can mitigate multiple organ toxicity in LPS-treated mice.
革兰氏阴性菌通过引发人体和动物的全身炎症反应和广泛的氧化应激介导多器官损伤。本研究旨在评价葡萄籽提取物(GSE)单独或与维生素C (Vit C)联合给药对脂多糖(LPS)处理小鼠器官毒性的影响。小鼠在研究的第1天(4 mg/kg)和第8天(2 mg/kg)腹腔注射LPS，从第一天开始，连续15天口服GSE(50和100 mg/kg)、GSE (50 mg/kg)加Vit C (50 mg/kg)或生理盐水(加对照物)。无载体对照组仅给予生理盐水处理。结果显示，与盐水处理组相比，LPS显著升高了血清中丙氨酸转氨酶(ALT)、天冬氨酸转氨酶(AST)、肌酐、尿酸，降低了对氧磷酶-1(PON-1)。此外，LPS处理显著增加了肝脏、肾脏和脑组织中的氧化应激状态，降低了还原性谷胱甘肽(GSH)。50和100 mg/kg剂量的GSE显著降低lps处理小鼠的肝脏和肾脏组织损伤的血清标志物，降低肝、肾和脑的氧化应激。GSE与Vit C联合治疗的综合效果大于GSE单独治疗。此外，还对肝脏、肾脏和脑组织切片进行了免疫组化研究。GSE或GSE + Vit C以以下方式降低lps诱导的肿瘤坏死因子-α (TNF-α)和caspase-3表达的强烈免疫组化染色:Vit C + GSE > GSE 100 mg/kg > GSE 50 mg/kg。我们的数据表明，GSE和Vit C联合使用可以减轻lps处理小鼠的多器官毒性。
{"title":"Grape Seed Extract and Vitamin C Combination Blocked LPS-Induced Multiple Organ Toxicity in Mice","authors":"S. Nada, M. El-Shamarka, E. Omara, O. Abdel-Salam","doi":"10.20455/ROS.2019.827","DOIUrl":"https://doi.org/10.20455/ROS.2019.827","url":null,"abstract":"Gram-negative bacteria mediate multiple organ damage through eliciting systemic inflammatory response and extensive oxidative stress in affected humans and animals. This study was done to evaluatethe effect of grape seed extract (GSE) given alone or in combination with vitamin C (Vit C) on organ toxicity in mice treated with lipopolysaccharide (LPS). Mice received intraperitoneal injections of LPS on day 1 (4 mg/kg) and day 8 (2 mg/kg) of the study and starting from the first day were orally treated with GSE (50 and 100 mg/kg), GSE (50 mg/kg) plus Vit C (50 mg/kg) or saline (plus vehicle control) for 15 successive days. The no vehicle control group was treated with saline only. Results indicated that compared to the saline-treated group, LPS injection significantly increased alanine aminotransferase (ALT), aspartate aminotransferase (AST), creatinine, uric acid, and decreased paraoxonase-1(PON-1) in the serum. Moreover, LPS treatment significantly increased oxidative stress status and decreased the reduced glutathione (GSH) in the liver, kidney, and brain tissues. GSE given at doses of 50 and 100 mg/kg significantly decreased serum markers of liver and kidney tissue injury and decreased oxidative stress in the liver, kidney, and brain of LPS-treated mice. The resultant effect of combined treatment with GSE and Vit C was greater than that of GSE alone. Moreover, immunohistochemical studies of liver, kidney, and brain tissue sections were conducted. The LPS-induced intense immunohistochemical staining of tumor necrosis factor-alpha (TNF-α) and caspase-3 expression was decreased by treatment with GSE or GSE + Vit C in the following manner: Vit C + GSE > GSE 100 mg/kg > GSE 50 mg/kg. Our data indicate that the combination of GSE and Vit C can mitigate multiple organ toxicity in LPS-treated mice.","PeriodicalId":91793,"journal":{"name":"Reactive oxygen species (Apex, N.C.)","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2019-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"46072718","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
S. Sunemi, F. Silva, E. Antonio, P. Tucci, A. Serra
Many of the studies, that have evaluated the role of photobiomodulation (PBM) in alleviating excessive oxidative stress induced by exercise, were carried out in the setting of aerobic activities. In line with this notion, the aim of this Research Highlights article was to summarize the new role of PBM in the oxidative stress resulting from anaerobic exercise. Thus, this Research Highlights article briefly summarizes the findings reported in a recent article published in Oxidative Medicine and Cellular Longevity (February 18, 2018; doi: 10.1155/2018/5763256) by de Oliveira et al., which reported that low-level laser therapy (LLLT) can protect skeletal muscles from oxidative stress induced by acute resistance exercise (RE). In fact, rats that underwent laser irradiation in the gastrocnemius muscle prior to RE bout showed a similar lipoperoxidation level to that of non-exercised rats. Animals in the LLLT group were also protected from attack by reactive oxygen species on their amino acids, as was revealed by the changes in the oxidized proteincontent. This study by de Oliveira et al. provides novel insights into the PBM process, which acts as a suppressor of the excessive oxidative stress evoked by RE.
{"title":"Photobiomodulation: Newly Discovered Actions in Resistance Exercise","authors":"S. Sunemi, F. Silva, E. Antonio, P. Tucci, A. Serra","doi":"10.20455/ROS.2019.829","DOIUrl":"https://doi.org/10.20455/ROS.2019.829","url":null,"abstract":"Many of the studies, that have evaluated the role of photobiomodulation (PBM) in alleviating excessive oxidative stress induced by exercise, were carried out in the setting of aerobic activities. In line with this notion, the aim of this Research Highlights article was to summarize the new role of PBM in the oxidative stress resulting from anaerobic exercise. Thus, this Research Highlights article briefly summarizes the findings reported in a recent article published in Oxidative Medicine and Cellular Longevity (February 18, 2018; doi: 10.1155/2018/5763256) by de Oliveira et al., which reported that low-level laser therapy (LLLT) can protect skeletal muscles from oxidative stress induced by acute resistance exercise (RE). In fact, rats that underwent laser irradiation in the gastrocnemius muscle prior to RE bout showed a similar lipoperoxidation level to that of non-exercised rats. Animals in the LLLT group were also protected from attack by reactive oxygen species on their amino acids, as was revealed by the changes in the oxidized proteincontent. This study by de Oliveira et al. provides novel insights into the PBM process, which acts as a suppressor of the excessive oxidative stress evoked by RE.","PeriodicalId":91793,"journal":{"name":"Reactive oxygen species (Apex, N.C.)","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2019-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"44049968","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Oxidative stress has been implicated in obesity-associated dyslipidemia and microvascular complications. In this study, the lipid profile and oxidative stress indices were evaluated in obese women. Ninety women (22–55 years) comprising 40 obese, 20 overweight and 30 controls were studied. Total cholesterol (TC), triglycerides (TG), high-density lipoprotein (HDL), malondialdehyde (MDA), lipid hydroperoxides, total antioxidant capacity (TAC), reduced form of glutathione (GSH), and nitric oxide (NO) were estimated colorimetrically, and low-density lipoprotein (LDL), very low-density lipoprotein (VLDL), oxidative stress index (OSI), and atherogenic index of plasma (AIP) were determined by calculation. Anthropometric indices and blood pressure (BP) were also obtained. Our results showed that obese women had lower antioxidants and higher BP, lipid peroxidation, and OSI with unfavorable lipid profile (higher TC, TG, LDL, VLDL, and AIP; lower HDL) compared to overweight and controls (p < 0.05). Overweight women had higher BP, lipid peroxidation, and decreased antioxidants compared to controls (p < 0.05). Positive correlations were observed between MDA and TC (r = 0.336, p = 0.034) and LDL (r = 0.322, p = 0.043), and negative correlation between HDL and AIP (r = –0.636, p < 0.001) in obese women. In conclusion, obesity is associated with increased LDL-C, lipid peroxidation, and reduced antioxidants which may lead to oxidative stress and increased risk for atherosclerosis in obese women studied.
氧化应激与肥胖相关的血脂异常和微血管并发症有关。本研究对肥胖女性的血脂和氧化应激指标进行了评价。研究对象为90名女性(22-55岁)，其中肥胖女性40名，超重女性20名，对照组30名。比色法测定总胆固醇(TC)、甘油三酯(TG)、高密度脂蛋白(HDL)、丙二醛(MDA)、脂质氢过氧化物、总抗氧化能力(TAC)、还原型谷胱甘肽(GSH)和一氧化氮(NO)，计算测定血浆低密度脂蛋白(LDL)、极低密度脂蛋白(VLDL)、氧化应激指数(OSI)和动脉粥样硬化指数(AIP)。测量人体测量指标和血压(BP)。我们的研究结果显示，肥胖女性抗氧化剂水平较低，血压、脂质过氧化和OSI水平较高，脂质特征不利(TC、TG、LDL、VLDL和AIP较高;HDL降低)，与超重和对照组相比(p < 0.05)。与对照组相比，超重妇女血压升高、脂质过氧化和抗氧化剂降低(p < 0.05)。肥胖女性MDA与TC (r = 0.336, p = 0.034)、LDL (r = 0.322, p = 0.043)呈正相关，HDL与AIP (r = -0.636, p < 0.001)呈负相关。总之，肥胖与LDL-C升高、脂质过氧化和抗氧化剂减少有关，这可能导致肥胖女性氧化应激和动脉粥样硬化风险增加。
{"title":"Cardiovascular Risk Factors and Oxidative Stress Indices in Obese Women in Southern Nigeria","authors":"A. Nsonwu-Anyanwu, C. Agu","doi":"10.20455/ROS.2019.831","DOIUrl":"https://doi.org/10.20455/ROS.2019.831","url":null,"abstract":"Oxidative stress has been implicated in obesity-associated dyslipidemia and microvascular complications. In this study, the lipid profile and oxidative stress indices were evaluated in obese women. Ninety women (22–55 years) comprising 40 obese, 20 overweight and 30 controls were studied. Total cholesterol (TC), triglycerides (TG), high-density lipoprotein (HDL), malondialdehyde (MDA), lipid hydroperoxides, total antioxidant capacity (TAC), reduced form of glutathione (GSH), and nitric oxide (NO) were estimated colorimetrically, and low-density lipoprotein (LDL), very low-density lipoprotein (VLDL), oxidative stress index (OSI), and atherogenic index of plasma (AIP) were determined by calculation. Anthropometric indices and blood pressure (BP) were also obtained. Our results showed that obese women had lower antioxidants and higher BP, lipid peroxidation, and OSI with unfavorable lipid profile (higher TC, TG, LDL, VLDL, and AIP; lower HDL) compared to overweight and controls (p < 0.05). Overweight women had higher BP, lipid peroxidation, and decreased antioxidants compared to controls (p < 0.05). Positive correlations were observed between MDA and TC (r = 0.336, p = 0.034) and LDL (r = 0.322, p = 0.043), and negative correlation between HDL and AIP (r = –0.636, p < 0.001) in obese women. In conclusion, obesity is associated with increased LDL-C, lipid peroxidation, and reduced antioxidants which may lead to oxidative stress and increased risk for atherosclerosis in obese women studied.","PeriodicalId":91793,"journal":{"name":"Reactive oxygen species (Apex, N.C.)","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2019-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"47673887","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
While it is well known that bacterial infection is the predominant cause of sepsis, the molecular pathophysiology of this clinical syndrome remains ill-defined. In this Research Highlights article, we discuss the recent research findings regarding a protective role for glutathione peroxidase-4 (GPx4) in bacterial infection and polymicrobial sepsis via modulating ferroptosis and pyroptosis, two novel modes of regulated cell death. It is suggested that GPx4, being a requisite gateway to both ferroptosis and pyroptosis, may serve as a critical molecular target for developing effective drugs for controlling infection and sepsis.
{"title":"GPx4 in Bacterial Infection and Polymicrobial Sepsis: Involvement of Ferroptosis and Pyroptosis.","authors":"Hong Zhu, Arben Santo, Zhenquan Jia, Y Robert Li","doi":"10.20455/ros.2019.835","DOIUrl":"https://doi.org/10.20455/ros.2019.835","url":null,"abstract":"<p><p>While it is well known that bacterial infection is the predominant cause of sepsis, the molecular pathophysiology of this clinical syndrome remains ill-defined. In this Research Highlights article, we discuss the recent research findings regarding a protective role for glutathione peroxidase-4 (GPx4) in bacterial infection and polymicrobial sepsis via modulating ferroptosis and pyroptosis, two novel modes of regulated cell death. It is suggested that GPx4, being a requisite gateway to both ferroptosis and pyroptosis, may serve as a critical molecular target for developing effective drugs for controlling infection and sepsis.</p>","PeriodicalId":91793,"journal":{"name":"Reactive oxygen species (Apex, N.C.)","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2019-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.20455/ros.2019.835","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"37418424","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Luteolin is a natural flavonoid compound mainly present as glycosides in vegetables, fruits, and herbs including carrot, cabbage, artichoke, tea, celery, and apple. Evidence has revealed that luteolin possesses profound biological properties such as antimutagenic, antitumorigenic, antioxidative, immunomodulatory, anticarcinogenic, antibacterial, antiapoptotic, and anti-inflammatory capacities. In particular, luteolin helps preserve the oxidation and antioxidation balance, the disruption of which plays a crucial role in the pathophysiologic processes of various diseases including cardiovascular disorders, cancers, and neurodegenerative diseases. This mini-review briefly summarizes the established beneficial effect of luteolin with regard to the maintenance of balance between pro- and anti-oxidation. We will provide an overview of luteolin and its therapeutic application in cardiovascular diseases, cancers, and neurodegenerative diseases.
{"title":"A Review on the Antioxidative and Prooxidative Properties of Luteolin","authors":"Haixia Xu, B. S. Linn, Yingmei Zhang, Jun Ren","doi":"10.20455/ROS.2019.833","DOIUrl":"https://doi.org/10.20455/ROS.2019.833","url":null,"abstract":"Luteolin is a natural flavonoid compound mainly present as glycosides in vegetables, fruits, and herbs including carrot, cabbage, artichoke, tea, celery, and apple. Evidence has revealed that luteolin possesses profound biological properties such as antimutagenic, antitumorigenic, antioxidative, immunomodulatory, anticarcinogenic, antibacterial, antiapoptotic, and anti-inflammatory capacities. In particular, luteolin helps preserve the oxidation and antioxidation balance, the disruption of which plays a crucial role in the pathophysiologic processes of various diseases including cardiovascular disorders, cancers, and neurodegenerative diseases. This mini-review briefly summarizes the established beneficial effect of luteolin with regard to the maintenance of balance between pro- and anti-oxidation. We will provide an overview of luteolin and its therapeutic application in cardiovascular diseases, cancers, and neurodegenerative diseases.","PeriodicalId":91793,"journal":{"name":"Reactive oxygen species (Apex, N.C.)","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2019-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"48610438","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
京公网安备 11010802042870号
京ICP备2023020795号-1
扫码关注我们
求助内容：
应助结果提醒方式：