scholarly journals Chronic intermittent hypoxia induces oxidative stress and inflammation in brain regions associated with early-stage neurodegeneration

2017 ◽  
Vol 5 (9) ◽  
pp. e13258 ◽  
Author(s):  
Brina Snyder ◽  
Brent Shell ◽  
J. Thomas Cunningham ◽  
Rebecca L. Cunningham
Keyword(s):  
Oxidative Stress ◽  
Intermittent Hypoxia ◽  
Early Stage ◽  
Brain Regions ◽  
Chronic Intermittent Hypoxia

scholarly journals Chronic intermittent hypoxia increases sympathetic control of blood pressure: role of neuronal activity in the hypothalamic paraventricular nucleus

2013 ◽  
Vol 305 (12) ◽  
pp. H1772-H1780 ◽  
Author(s):  
Amanda L. Sharpe ◽  
Alfredo S. Calderon ◽  
Mary Ann Andrade ◽  
J. Thomas Cunningham ◽  
Steven W. Mifflin ◽  
...  
Keyword(s):  
Sleep Apnea ◽  
Neuronal Activity ◽  
Paraventricular Nucleus ◽  
Intermittent Hypoxia ◽  
Body Fluid ◽  
Early Stage ◽  
Brain Regions ◽  
Hypothalamic Paraventricular Nucleus ◽  
Chronic Intermittent Hypoxia ◽  
Increased Sensitivity

Like humans with sleep apnea, rats exposed to chronic intermittent hypoxia (CIH) experience arterial hypoxemias and develop hypertension characterized by exaggerated sympathetic nerve activity (SNA). To gain insights into the poorly understood mechanisms that initiate sleep apnea/CIH-associated hypertension, experiments were performed in rats exposed to CIH for only 7 days. Compared with sham-treated normoxic control rats, CIH-exposed rats ( n = 8 rats/group) had significantly increased hematocrit ( P < 0.001) and mean arterial pressure (MAP; P < 0.05). Blockade of ganglionic transmission caused a significantly ( P < 0.05) greater reduction of MAP in rats exposed to CIH than control rats ( n = 8 rats/group), indicating a greater contribution of SNA in the support of MAP even at this early stage of CIH hypertension. Chemical inhibition of neuronal discharge in the hypothalamic paraventricular nucleus (PVN) (100 pmol muscimol) had no effect on renal SNA but reduced lumbar SNA ( P < 0.005) and MAP ( P < 0.05) more in CIH-exposed rats ( n = 8) than control rats ( n = 7), indicating that CIH increased the contribution of PVN neuronal activity in the support of lumbar SNA and MAP. Because CIH activates brain regions controlling body fluid homeostasis, the effects of internal carotid artery injection of hypertonic saline were tested and determined to increase lumbar SNA more ( P < 0.05) in CIH-exposed rats than in control rats ( n = 9 rats/group). We conclude that neurogenic mechanisms are activated early in the development of CIH hypertension such that elevated MAP relies on increased sympathetic tonus and ongoing PVN neuronal activity. The increased sensitivity of Na+/osmosensitive circuitry in CIH-exposed rats suggests that early neuroadaptive responses among body fluid regulatory neurons could contribute to the initiation of CIH hypertension.

scholarly journals Chronic Intermittent Hypoxia Induces Early-Stage Metabolic Dysfunction Independently of Adipose Tissue Deregulation

Antioxidants ◽  
2021 ◽  
Vol 10 (8) ◽  
pp. 1233
Author(s):  
Fátima O. Martins ◽  
Joana F. Sacramento ◽  
Elena Olea ◽  
Bernardete F. Melo ◽  
Jesus Prieto-Lloret ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Insulin Resistance ◽  
Adipose Tissue ◽  
Intermittent Hypoxia ◽  
Early Stage ◽  
Tissue Hypoxia ◽  
Whole Body ◽  
Chronic Intermittent Hypoxia ◽  
Adipose Tissue Dysfunction ◽  
Obstructive Sleep

Several studies demonstrated a link between obstructive sleep apnea (OSA) and the development of insulin resistance. However, the main event triggering insulin resistance in OSA remains to be clarified. Herein, we investigated the effect of mild and severe chronic intermittent hypoxia (CIH) on whole-body metabolic deregulation and visceral adipose tissue dysfunction. Moreover, we studied the contribution of obesity to CIH-induced dysmetabolic states. Experiments were performed in male Wistar rats submitted to a control and high-fat (HF) diet. Two CIH protocols were tested: A mild CIH paradigm (5/6 hypoxic (5% O2) cycles/h, 10.5 h/day) during 35 days and a severe CIH paradigm (30 hypoxic (5% O2) cycles, 8 h/day) during 15 days. Fasting glycemia, insulinemia, insulin sensitivity, weight, and fat mass were assessed. Adipose tissue hypoxia, inflammation, angiogenesis, oxidative stress, and metabolism were investigated. Mild and severe CIH increased insulin levels and induced whole-body insulin resistance in control animals, effects not associated with weight gain. In control animals, CIH did not modify adipocytes perimeter as well as adipose tissue hypoxia, angiogenesis, inflammation or oxidative stress. In HF animals, severe CIH attenuated the increase in adipocytes perimeter, adipose tissue hypoxia, angiogenesis, and dysmetabolism. In conclusion, adipose tissue dysfunction is not the main trigger for initial dysmetabolism in CIH. CIH in an early stage might have a protective role against the deleterious effects of HF diet on adipose tissue metabolism.

scholarly journals Chronic intermittent hypoxia induces hypoxic sensitivity in adult rat adrenal medulla via oxidative stress

2006 ◽  
Vol 20 (4) ◽  
Author(s):  
Ganesh K Kumar ◽  
Vandana Rai ◽  
Suresh Sharma ◽  
DeviPrasadh Ramakrishnan ◽  
Ying‐Jie Peng ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Adrenal Medulla ◽  
Intermittent Hypoxia ◽  
Chronic Intermittent Hypoxia ◽  
Adult Rat

Hydrogen ameliorates chronic intermittent hypoxia-induced neurocognitive impairment via inhibiting oxidative stress

2018 ◽  
Vol 143 ◽  
pp. 225-233 ◽  
Author(s):  
Wenya Li ◽  
Shengchang Yang ◽  
Fu-Yang Yu ◽  
Yashuo Zhao ◽  
Zhi-Min Sun ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Intermittent Hypoxia ◽  
Neurocognitive Impairment ◽  
Chronic Intermittent Hypoxia

scholarly journals RNA and Oxidative Stress in Alzheimer’s Disease: Focus on microRNAs

2020 ◽  
Vol 2020 ◽  
pp. 1-16
Author(s):  
Akihiko Nunomura ◽  
George Perry
Keyword(s):  
Oxidative Stress ◽  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Protein Misfolding ◽  
Early Stage ◽  
Brain Regions ◽  
Prodromal Stage ◽  
Adaptive Mechanisms ◽  
Therapeutic Tools ◽  
Key Events

Oxidative stress (OS) is one of the major pathomechanisms of Alzheimer’s disease (AD), which is closely associated with other key events in neurodegeneration such as mitochondrial dysfunction, inflammation, metal dysregulation, and protein misfolding. Oxidized RNAs are identified in brains of AD patients at the prodromal stage. Indeed, oxidized mRNA, rRNA, and tRNA lead to retarded or aberrant protein synthesis. OS interferes with not only these translational machineries but also regulatory mechanisms of noncoding RNAs, especially microRNAs (miRNAs). MiRNAs can be oxidized, which causes misrecognizing target mRNAs. Moreover, OS affects the expression of multiple miRNAs, and conversely, miRNAs regulate many genes involved in the OS response. Intriguingly, several miRNAs embedded in upstream regulators or downstream targets of OS are involved also in neurodegenerative pathways in AD. Specifically, seven upregulated miRNAs (miR-125b, miR-146a, miR-200c, miR-26b, miR-30e, miR-34a, miR-34c) and three downregulated miRNAs (miR-107, miR-210, miR-485), all of which are associated with OS, are found in vulnerable brain regions of AD at the prodromal stage. Growing evidence suggests that altered miRNAs may serve as targets for developing diagnostic or therapeutic tools for early-stage AD. Focusing on a neuroprotective transcriptional repressor, REST, and the concept of hormesis that are relevant to the OS response may provide clues to help us understand the role of the miRNA system in cellular and organismal adaptive mechanisms to OS.

scholarly journals Hydrogen Gas Alleviates Chronic Intermittent Hypoxia-Induced Renal Injury through Reducing Iron Overload

Molecules ◽  
2019 ◽  
Vol 24 (6) ◽  
pp. 1184 ◽  
Author(s):  
Peng Guan ◽  
Zhi-Min Sun ◽  
Li-Fei Luo ◽  
Ya-Shuo Zhao ◽  
Sheng-Chang Yang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Iron Overload ◽  
Renal Injury ◽  
Intermittent Hypoxia ◽  
Hydrogen Gas ◽  
Chronic Intermittent Hypoxia ◽  
Protective Effects ◽  
Divalent Metal Transporter 1 ◽  
Divalent Metal Transporter ◽  
And Oxidative Stress

Iron-induced oxidative stress has been found to be a central player in the pathogenesis of kidney injury. Recent studies have indicated H2 can be used as a novel antioxidant to protect cells. The present study was designed to investigate the protective effects of H2 against chronic intermittent hypoxia (CIH)-induced renal injury and its correlation mechanism involved in iron metabolism. We found that CIH-induced renal iron overloaded along with increased apoptosis and oxidative stress. Iron accumulates mainly occurred in the proximal tubule epithelial cells of rats as showed by Perl’s stain. Moreover, we found that CIH could promote renal transferrin receptor and divalent metal transporter-1 expression, inhibit ceruloplasmin expression. Renal injury, apoptosis and oxidative stress induced by CIH were strikingly attenuated in H2 treated rats. In conclusion, hydrogen may attenuate CIH-induced renal injury at least partially via inhibiting renal iron overload.

scholarly journals Chronic intermittent hypoxia induces hypoxia-evoked catecholamine efflux in adult rat adrenal medulla via oxidative stress

2006 ◽  
Vol 575 (1) ◽  
pp. 229-239 ◽  
Author(s):  
Ganesh K. Kumar ◽  
Vandana Rai ◽  
Suresh D. Sharma ◽  
Devi Prasadh Ramakrishnan ◽  
Ying-Jie Peng ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Adrenal Medulla ◽  
Intermittent Hypoxia ◽  
Chronic Intermittent Hypoxia ◽  
Adult Rat
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