scholarly journals Tryptophan-kynurenine pathway as a novel link between gut microbiota and schizophrenia: A review

2021 ◽  
Vol 18 (4) ◽  
pp. 897-905
Author(s):  
Yaping Wang ◽  
Xiuxia Yuan ◽  
Yulin Kang ◽  
Xueqin Song
Keyword(s):  
Oxidative Stress ◽  
Gut Microbiota ◽  
Neuronal Excitability ◽  
Kynurenine Pathway ◽  
Inflammatory Factors ◽  
Biological Processes ◽  
Oxygen Species ◽  
Tryptophan Catabolism ◽  
And Oxidative Stress

Gut microbiota and its metabolite tryptophan play an important role in regulating neurotransmission, immune homeostasis and oxidative stress which are critical for brain development. The kynurenine pathway is the main route of tryptophan catabolism. Kynurenine metabolites regulate many biological processes including host-microbiome communication, immunity and oxidative stress, as well as neuronal excitability. The accumulation of metabolites produced by kynurenine pathway in brain results in the activation of the immune system (increase in the levels of inflammatory factors) and oxidative stress (production of reactive oxygen species, ROS), which are associated with mental disorders, for example schizophrenia. Thus, it was hypothesized that perturbations in kynurenine pathway could cause activation of immunity, and that oxidative stress may be involved in the etiology of schizophrenia. The present work is a review of the latest studies on the possible role of kynurenine pathway in schizophrenia, and mechanism(s) involved.

scholarly journals Gut microbiota accelerates cisplatin-induced acute liver injury associated with robust inflammation and oxidative stress in mice

2021 ◽  
Vol 19 (1) ◽  
Author(s):  
Shenhai Gong ◽  
Yinglin Feng ◽  
Yunong Zeng ◽  
Huanrui Zhang ◽  
Meiping Pan ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
16S Rrna ◽  
Gut Microbiota ◽  
Gene Sequencing ◽  
16S Rrna Gene Sequencing ◽  
Rrna Gene ◽  
Metabolomic Analysis ◽  
Rrna Gene Sequencing ◽  
And Oxidative Stress

Abstract Background Gut microbiota has been reported to be disrupted by cisplatin, as well as to modulate chemotherapy toxicity. However, the precise role of intestinal microbiota in the pathogenesis of cisplatin hepatotoxicity remains unknown. Methods We compared the composition and function of gut microbiota between mice treated with and without cisplatin using 16S rRNA gene sequencing and via metabolomic analysis. For understanding the causative relationship between gut dysbiosis and cisplatin hepatotoxicity, antibiotics were administered to deplete gut microbiota and faecal microbiota transplantation (FMT) was performed before cisplatin treatment. Results 16S rRNA gene sequencing and metabolomic analysis showed that cisplatin administration caused gut microbiota dysbiosis in mice. Gut microbiota ablation by antibiotic exposure protected against the hepatotoxicity induced by cisplatin. Interestingly, mice treated with antibiotics dampened the mitogen-activated protein kinase pathway activation and promoted nuclear factor erythroid 2-related factor 2 nuclear translocation, resulting in decreased levels of both inflammation and oxidative stress in the liver. FMT also confirmed the role of microbiota in individual susceptibility to cisplatin-induced hepatotoxicity. Conclusions This study elucidated the mechanism by which gut microbiota mediates cisplatin hepatotoxicity through enhanced inflammatory response and oxidative stress. This knowledge may help develop novel therapeutic approaches that involve targeting the composition and metabolites of microbiota.

scholarly journals The Role of MicroRNAs in Diabetes-Related Oxidative Stress

2019 ◽  
Vol 20 (21) ◽  
pp. 5423 ◽  
Author(s):  
Mirza Muhammad Fahd Qadir ◽  
Dagmar Klein ◽  
Silvia Álvarez-Cubela ◽  
Juan Domínguez-Bendala ◽  
Ricardo Luis Pastori
Keyword(s):  
Oxidative Stress ◽  
Target Gene ◽  
Cellular Stress ◽  
Cellular Damage ◽  
Oxygen Species ◽  
Non Coding Rnas ◽  
And Oxidative Stress

Cellular stress, combined with dysfunctional, inadequate mitochondrial phosphorylation, produces an excessive amount of reactive oxygen species (ROS) and an increased level of ROS in cells, which leads to oxidation and subsequent cellular damage. Because of its cell damaging action, an association between anomalous ROS production and disease such as Type 1 (T1D) and Type 2 (T2D) diabetes, as well as their complications, has been well established. However, there is a lack of understanding about genome-driven responses to ROS-mediated cellular stress. Over the last decade, multiple studies have suggested a link between oxidative stress and microRNAs (miRNAs). The miRNAs are small non-coding RNAs that mostly suppress expression of the target gene by interaction with its 3’untranslated region (3′UTR). In this paper, we review the recent progress in the field, focusing on the association between miRNAs and oxidative stress during the progression of diabetes.

scholarly journals Role of Forkhead Transcription Factors in Diabetes-Induced Oxidative Stress

2012 ◽  
Vol 2012 ◽  
pp. 1-7 ◽  
Author(s):  
Bhaskar Ponugoti ◽  
Guangyu Dong ◽  
Dana T. Graves
Keyword(s):  
Oxidative Stress ◽  
Transcription Factors ◽  
Cellular Response ◽  
Cell Damage ◽  
Cell Types ◽  
Biological Processes ◽  
Oxygen Species ◽  
Forkhead Transcription Factors ◽  
Foxo Transcription Factors

Diabetes is a chronic metabolic disorder, characterized by hyperglycemia resulting from insulin deficiency and/or insulin resistance. Recent evidence suggests that high levels of reactive oxygen species (ROS) and subsequent oxidative stress are key contributors in the development of diabetic complications. The FOXO family of forkhead transcription factors including FOXO1, FOXO3, FOXO4, and FOXO6 play important roles in the regulation of many cellular and biological processes and are critical regulators of cellular oxidative stress response pathways. FOXO1 transcription factors can affect a number of different tissues including liver, retina, bone, and cell types ranging from hepatocytes to microvascular endothelial cells and pericytes to osteoblasts. They are induced by oxidative stress and contribute to ROS-induced cell damage and apoptosis. In this paper, we discuss the role of FOXO transcription factors in mediating oxidative stress-induced cellular response.

scholarly journals Role of Polyphenols as Antioxidant Supplementation in Ischemic Stroke

2021 ◽  
Vol 2021 ◽  
pp. 1-19
Author(s):  
Yuan Zhou ◽  
Shanshan Zhang ◽  
Xiang Fan
Keyword(s):  
Oxidative Stress ◽  
Ischemic Stroke ◽  
Cause Of Death ◽  
Experimental Studies ◽  
Reactive Oxygen Species Generation ◽  
Oxygen Species ◽  
Potential Therapeutic Target ◽  
Antioxidant Effects ◽  
And Oxidative Stress

Stroke is the second most common cause of death globally and the leading cause of death in China. The pathogenesis of cerebral ischemia injury is complex, and oxidative stress plays an important role in the fundamental pathologic progression of cerebral damage in ischemic stroke. Previous studies have preliminarily confirmed that oxidative stress should be a potential therapeutic target and antioxidant as a treatment strategy for ischemic stroke. Emerging experimental studies have demonstrated that polyphenols exert the antioxidant potential to play the neuroprotection role after ischemic stroke. This comprehensive review summarizes antioxidant effects of some polyphenols, which have the most inhibition effects on reactive oxygen species generation and oxidative stress after ischemic stroke.

scholarly journals The role of reactive oxygen species and oxidative stress in carbon monoxide toxicity: An in-depth analysis

Redox Report ◽  
2014 ◽  
Vol 19 (5) ◽  
pp. 180-189 ◽  
Author(s):  
Sumeyya Akyol ◽  
Serpil Erdogan ◽  
Nuri Idiz ◽  
Safa Celik ◽  
Mehmet Kaya ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Carbon Monoxide ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Depth Analysis ◽  
And Oxidative Stress

The role of reactive oxygen species and oxidative stress in environmental carcinogenesis and biomarker development

2010 ◽  
Vol 188 (2) ◽  
pp. 334-339 ◽  
Author(s):  
Dominique Ziech ◽  
Rodrigo Franco ◽  
Alexandros G. Georgakilas ◽  
Stavroula Georgakila ◽  
Vasiliki Malamou-Mitsi ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Environmental Carcinogenesis ◽  
And Oxidative Stress

scholarly journals Immunválasz és oxidatív stressz hepatitis C-vírus-infekcióban

2015 ◽  
Vol 156 (47) ◽  
pp. 1898-1903
Author(s):  
Alajos Pár ◽  
Gabriella Pár
Keyword(s):  
Oxidative Stress ◽  
Hepatitis C Virus ◽  
Hepatitis C ◽  
Immune Responses ◽  
Current Knowledge ◽  
Oxygen Species ◽  
Adaptive Immune Responses ◽  
Adaptive Immune ◽  
And Oxidative Stress

This review summarizes our current knowledge on the innate and adaptive immune responses induced by hepatitis C virus, and on the genetic polymorphisms that may determine the outcome of the disease. In addition, the authors discuss the role of reactive oxygen species and oxidative stress in hepatitis C virus-related pathogenic processess, such as hepatitis, fibrosis, hepatocellular carcinoma, steatosis and insulin resistance. Orv. Hetil., 2015, 156(47), 1898–1903.

scholarly journals The Role of Metal Regulatory Proteins in Brain Oxidative Stress: A Tutorial

2012 ◽  
Vol 2012 ◽  
pp. 1-9 ◽  
Author(s):  
Wayne Briner
Keyword(s):  
Oxidative Stress ◽  
Redox Activity ◽  
Biological Processes ◽  
Physiological Processes ◽  
Pharmacological Targets ◽  
Wide Range ◽  
Brain Oxidative Stress ◽  
The Brain ◽  
And Oxidative Stress

The proteins that regulate the metabolism of a metal must also play a role in regulating the redox activity of the metal. Metals are intrinsic to a substantial number of biological processes and the proteins that regulate those activities are also considerable in number. The role these proteins play in a wide range of physiological processes involves them directly and indirectly in a variety of disease processes. Similarly, it may be therapeutically advantageous to pharmacologically alter the activity of these metal containing proteins to influence disease processes. This paper will introduce the reader to a number of important proteins in both metal metabolism and oxidative stress, with an emphasis on the brain. Potential pharmacological targets will be considered.

scholarly journals Mitophagy and Oxidative Stress: The Role of Aging

Antioxidants ◽  
2021 ◽  
Vol 10 (5) ◽  
pp. 794
Author(s):  
Anna De Gaetano ◽  
Lara Gibellini ◽  
Giada Zanini ◽  
Milena Nasi ◽  
Andrea Cossarizza ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Mitochondrial Damage ◽  
Ros Production ◽  
Oxygen Species ◽  
Prime Mover ◽  
Age Related ◽  
Chronic Oxidative Stress ◽  
Parkinson’S Diseases ◽  
And Oxidative Stress

Mitochondrial dysfunction is a hallmark of aging. Dysfunctional mitochondria are recognized and degraded by a selective type of macroautophagy, named mitophagy. One of the main factors contributing to aging is oxidative stress, and one of the early responses to excessive reactive oxygen species (ROS) production is the induction of mitophagy to remove damaged mitochondria. However, mitochondrial damage caused at least in part by chronic oxidative stress can accumulate, and autophagic and mitophagic pathways can become overwhelmed. The imbalance of the delicate equilibrium among mitophagy, ROS production and mitochondrial damage can start, drive, or accelerate the aging process, either in physiological aging, or in pathological age-related conditions, such as Alzheimer’s and Parkinson’s diseases. It remains to be determined which is the prime mover of this imbalance, i.e., whether it is the mitochondrial damage caused by ROS that initiates the dysregulation of mitophagy, thus activating a vicious circle that leads to the reduced ability to remove damaged mitochondria, or an alteration in the regulation of mitophagy leading to the excessive production of ROS by damaged mitochondria.

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