Reactive Oxygen Species {90000432}

Shared Reference Notes

• [1.1] [#Natural Skin Microbiome] 
  - The generation of reactive oxygen species secondary to normal aerobic metabolism, and exogenous factors, such as #UV radiation, is the main cause of skin #Aging
• [1.2] [#Short Chain Fatty Acid] [#Sport] 
  - the gut microbiota and its metabolites, such as short chain fatty acids and #Secondary bile acids, also contribute to host energy production, ROS modulation and inflammation in the gut by attenuating TNFα- mediated immune responses and inflammasomes such as NLRP3.
• [1.3] 
  - #Sphingomonas and #Erythrobacteraceae, may have the ability to protect against #UV radiation as they produce potentially protective compounds. Indeed, further analysis showed that a #Sphingomonas spp. was able to reduce reactive oxygen species levels in human keratinocytes.
• [1.4] [#Parkinson’s Disease] 
  - #Hydrogen sulfide produced by several #Enterobacteriaceae and #Desulfovibrionaceae can enter host cells, cause the release of cytochrome c protein from mitochondria into the cytoplasm, mediate the accumulation of cytosolic iron and reactive oxygen species, thus boosting α-synuclein synthesis
• [1.5] [#Multiple Sclerosis] 
  - #Lactate, produced by activated Dendritic cells (DCs) and other immune cells, boosts the expression of NDUFA4L2 through a mechanism mediated by hypoxia-inducible factor 1α (HIF-1α). - NDUFA4L2 limits the production of mitochondrial reactive oxygen species that activate XBP1-driven transcriptional modules in DCs that are involved in the control of pathogenic autoimmune T cells. - a #Probiotic that produces #Lactate and suppresses T cell autoimmunity through the activation of HIF-1α–NDUFA4L2 signalling in DCs.
• [1.6] [#Prostate cancer] 
  - Increased reactive oxygen and nitrogen species and increased free estrogens result in apurinic DNA sites that trigger mutations and the beginning of oncogenesis in prostate cells
• [1.7] [#Keto diet] 
  -The KD has also been associated with antioxidant effects, generating a reduced amount of ROS (reactive oxygen species) and reshaping gut microbiota
• [1.8] [#TNF-alfa] 
  - TNF-α strongly induces the production of reactive oxygen compounds, leukotrienes, prostaglandins, and metalloproteinases. - TNF leads to a reduction in the number of osteogenic cells and fibroblasts. - In contrast to high doses of TNF-α, which are related to tumor destruction, exposure to low doses of this molecule are related to tumor promotion. - Activation of oncogenic signaling pathways in epithelial cells, including Wnt and NF-κB, is critical for TNF-α-induced tumor growth. - TNF-α possesses the ability to induce DNA damage by production of reactive oxygen species. - TNF-α has been shown to influence processes of motility and invasion by induction of MMPs expression and simulation of the production of various angiogenic factors, such as interleukin-8, VEGF, and basic fibroblast growth factor
• [1.9] [#UV radiation] 
  - Chronic UV exposure induces reactive oxygen species (ROS) production, activating three major #Skin aging cascades. - Resveratrol > prevent photo-#Aging through anti-inflammatory, antioxidant, and antitumour pathways. - The viability of cultured human keratinocytes (HaCaT cell line) pretreated with different doses of resveratrol significantly increased up to 94%.
• - #Propionibacteriaceae are Gram-positive, anaerobic rods associated with human infections, including corneal infections, and are often found in #Acne vulgaris patients. - Intradermal infections of #Propionibacteriaceae generate ROS and #Nitric Oxide and induce the synthesis of pro-inflammatory cytokines. Since an imbalance of these ROS and antioxidative tear proteins favors the development of tear film instability
• [1.11] [#Autoimmune disease] [#Parabacteroides distasonis] 
  - P. distasonis , along with #Prevotella copri, increased IFN-gamma-producing cells, possibly a trigger for auto-immunity, and mouse models suggest that P. distasonis may be proinflammatory, activating pathogenic toxins and contributing to reactive oxygen species via catalase production.
• [1.12] [#Rheumatoid Arthritis] 
  - The content of mitochondrial ROS in monocytes of RA patients increases fivefold. - #Oxidative stress caused by ROS may be associated with the pathogenesis of RA.
• [1.13] [#Cervical cancer] 
  - #Chlamydia spp. have been described in cervical and #Ovarian cancer > decrease p53 signaling and DNA damage response, in facilitating the pathogen’s intracellular replication, induction of ROS production and DNA damage
• [1.14] 
  - mitochondrial ROS on gut microbiota is direct killing at higher concentrations
• [1.15] [#Antimicrobial peptides] 
  - #Lysozyme, the major AMP, can directly reduce the propagation of reactive oxygen species in #Colitis by releasing bacterial #Superoxide dismutase from #Lactobacillus lactis
• [1.16] [#Drug-resistant Epilepsy] [#Keto diet] 
  - reactive oxygen species is elevated during #Seizure activity due to #Oxidative stress-associated neuronal death, which can further contribute to epileptogenesis. - The KD reportedly reduces #Oxidative stress by promoting antioxidant enzymatic activity.
• [1.17] [#Aspergillus fumigatus] 
  - The ability of A. fumigatus to generate reactive oxygen species linked to #Oral cancer
• [1.18] [#Pancreatic Cancer] [#Porphyromonas gingivalis] 
  - P. gingivalis migrated from the oral cavity to the pancreas in mice and can be detected in human PanIN lesions. - Repetitive P. gingivalis administration to wild-type mice induced pancreatic acinar-to-ductal metaplasia (ADM), and altered the composition of the intrapancreatic microbiome. - In iKC mice, P. gingivalis accelerated PanIN to PDAC progression. In vitro, P. gingivalis infection induced acinar cell ADM markers SOX9 and CK19, and intracellular bacteria protected PDAC cells from reactive oxygen species-mediated cell death resulting from nutrient stress.
• [1.19] [#Alzheimer’s disease] [#Ursodeoxycholic acid] 
  - UDCA reduces the levels of ROS, tumor necrosis factor alpha (TNFα), and interleukin-1 beta (IL-1β), exerting anti-apoptotic, #Oxidative stress and inflammatory effects in AD

References Notes