Long term effects of fetal undernutrition on rat heart. Role of hypertension and oxidative stress

The wide range of factors associated with the induction of autism is invariably linked with either inflammation or oxidative stress, and sometimes both. The use of acetaminophen in babies and young children may be much more strongly associated with autism than its use during pregnancy, perhaps because of well-known deficiencies in the metabolic breakdown of pharmaceuticals during early development. Thus, one explanation for the increased prevalence of autism is that increased exposure to acetaminophen, exacerbated by inflammation and oxidative stress, is neurotoxic in babies and small children. This view mandates extreme urgency in probing the long-term effects of acetaminophen use in babies and the possibility that many cases of infantile autism may actually be induced by acetaminophen exposure shortly after birth.

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The role of vanin-1 and oxidative stress–related pathways in distinguishing acute and chronic pediatric ITP

Blood ◽

10.1182/blood-2010-09-304931 ◽

2011 ◽

Vol 117 (17) ◽

pp. 4569-4579 ◽

Cited By ~ 60

Author(s):

Bing Zhang ◽

Clara Lo ◽

Lei Shen ◽

Ruchira Sood ◽

Carol Jones ◽

...

Keyword(s):

Oxidative Stress ◽

Gene Expression ◽

Gene Expression Analysis ◽

Mononuclear Cells ◽

Stress Sensor ◽

Chronic Itp ◽

Acute Itp ◽

And Oxidative Stress

Abstract Pediatric immune thrombocytopenia (ITP) is usually self-limited. However, approximately 20% of children develop chronic ITP, which can be associated with significant morbidity because of long-term immunosuppression and splenectomy in refractory cases. To explore the molecular mechanism of chronic ITP compared with acute ITP, we studied 63 pediatric patients with ITP. Gene expression analysis of whole blood revealed distinct signatures for acute and chronic ITP. Oxidative stress–related pathways were among the most significant chronic ITP-associated pathways. Overexpression of VNN1, an oxidative stress sensor in epithelial cells, was most strongly associated with progression to chronic ITP. Studies of normal persons demonstrated VNN1 expression in a variety of blood cells. Exposure of blood mononuclear cells to oxidative stress inducers elicited dramatic up-regulation of VNN1 and down-regulation of PPARγ, indicating a role for VNN1 as a peripheral blood oxidative stress sensor. Assessment of redox state by tandem mass spectrometry demonstrated statistically significant lower glutathione ratios in patients with ITP versus healthy controls; lower glutathione ratios were also seen in untreated patients with ITP compared with recently treated patients. Our work demonstrates distinct patterns of gene expression in acute and chronic ITP and implicates oxidative stress pathways in the pathogenesis of chronic pediatric ITP.

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Elevated exposure to prenatal thyroid hormones affects embryonic mortality but has no clear effects into adulthood

10.1101/757260 ◽

2019 ◽

Author(s):

Tom Sarraude ◽

Bin-Yan Hsu ◽

Ton G.G. Groothuis ◽

Suvi Ruuskanen

Keyword(s):

Oxidative Stress ◽

Thyroid Hormones ◽

Hatching Success ◽

Long Term Effects ◽

Short Term ◽

Short And Long Term ◽

Long Term Consequences ◽

Maternal Thyroid ◽

And Oxidative Stress

AbstractMaternal thyroid hormones (THs) are known to be crucial in embryonic development in humans, but their influence on other, especially wild, animals remains poorly understood. So far, the studies that experimentally investigated the consequences of maternal THs focused on short-term effects, while early organisational effects with long-term consequences, as shown for other prenatal hormones, could also be expected. In this study, we aimed at investigating both the short- and long-term effects of prenatal THs in a bird species, the Japanese quail Coturnix japonica. We experimentally elevated yolk TH content (the prohormone T4, and its active metabolite T3, as well as a combination of both hormones). We analysed hatching success, embryonic development, offspring growth and oxidative stress as well as their potential organisational effects on reproduction, moult, and oxidative stress in adulthood. We found that eggs injected with both hormones had a higher hatching success compared with control eggs, suggesting conversion of T4 into T3 by the embryo. We detected no other clear short-term or long-term effects of yolk THs. These results suggest that yolk thyroid hormones are important in the embryonic stage of precocial birds, but other short- and long-term consequences remain unclear. Research on maternal thyroid hormones will greatly benefit from studies investigating how embryos use and respond to this maternal signalling. Long-term studies on prenatal THs in other taxa in the wild are needed for a better understanding of this hormone-mediated maternal pathway.

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Long Term Effects of Low Dose Radiation Exposure During Late Gestation on Cardiac Metabolism and Oxidative Stress

The FASEB Journal ◽

10.1096/fasebj.2020.34.s1.04824 ◽

2020 ◽

Vol 34 (S1) ◽

pp. 1-1

Author(s):

Ashley Nemec-Bakk ◽

Sarah Niccoli ◽

Caitlund Davidson ◽

Douglas Boreham ◽

Simon Lees ◽

...

Keyword(s):

Oxidative Stress ◽

Radiation Exposure ◽

Low Dose ◽

Cardiac Metabolism ◽

Late Gestation ◽

Long Term Effects ◽

Low Dose Radiation ◽

And Oxidative Stress ◽

Dose Radiation

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Neuronal degeneration and oxidative stress in the SNc of 6-OHDA intoxicated rats; improving role of silymarin long-term treatment

Naunyn-Schmiedeberg s Archives of Pharmacology ◽

10.1007/s00210-020-01954-7 ◽

2020 ◽

Vol 393 (12) ◽

pp. 2427-2437 ◽

Cited By ~ 1

Author(s):

Rasool Haddadi ◽

Shahla Eyvari-Brooshghalan ◽

Alireza Mohajjel Nayebi ◽

Mohammadmahdi Sabahi ◽

Sara Ami Ahmadi

Keyword(s):

Oxidative Stress ◽

Neuronal Degeneration ◽

Term Treatment ◽

Long Term Treatment ◽

And Oxidative Stress

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Nebivolol and metoprolol: long-term effects on inflammation and oxidative stress in essential hypertension

Scandinavian Journal of Clinical and Laboratory Investigation ◽

10.3109/00365513.2012.691991 ◽

2012 ◽

Vol 72 (5) ◽

pp. 427-432 ◽

Cited By ~ 19

Author(s):

Martin Serg ◽

Priit Kampus ◽

Jaak Kals ◽

Maksim Zagura ◽

Mihkel Zilmer ◽

...

Keyword(s):

Oxidative Stress ◽

Essential Hypertension ◽

Long Term Effects ◽

And Oxidative Stress

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Testing the short-and long-term effects of elevated prenatal exposure to different forms of thyroid hormones

PeerJ ◽

10.7717/peerj.10175 ◽

2020 ◽

Vol 8 ◽

pp. e10175

Author(s):

Tom Sarraude ◽

Bin-Yan Hsu ◽

Ton Groothuis ◽

Suvi Ruuskanen

Keyword(s):

Oxidative Stress ◽

Embryonic Development ◽

Thyroid Hormones ◽

Hatching Success ◽

Long Term Effects ◽

Short Term ◽

Short And Long Term ◽

Long Term Consequences ◽

And Oxidative Stress

Maternal thyroid hormones (THs) are known to be crucial in embryonic development in humans, but their influence on other, especially wild, animals remains poorly understood. So far, the studies that experimentally investigated the consequences of maternal THs focused on short-term effects, while early organisational effects with long-term consequences, as shown for other prenatal hormones, could also be expected. In this study, we aimed at investigating both the short- and long-term effects of prenatal THs in a bird species, the Japanese quail Coturnix japonica. We experimentally elevated yolk TH content (the prohormone T4, and its active metabolite T3, as well as a combination of both hormones). We analysed hatching success, embryonic development, offspring growth and oxidative stress as well as their potential organisational effects on reproduction, moult and oxidative stress in adulthood. We found that eggs injected with T4 had a higher hatching success compared with control eggs, suggesting conversion of T4 into T3 by the embryo. We detected no evidence for other short-term or long-term effects of yolk THs. These results suggest that yolk THs are important in the embryonic stage of precocial birds, but other short- and long-term consequences remain unclear. Research on maternal THs will greatly benefit from studies investigating how embryos use and respond to this maternal signalling. Long-term studies on prenatal THs in other taxa in the wild are needed for a better understanding of this hormone-mediated maternal pathway.

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Inflammation and Oxidative Stress: Potential Targets for Improving Prognosis After Subarachnoid Hemorrhage

Frontiers in Cellular Neuroscience ◽

10.3389/fncel.2021.739506 ◽

2021 ◽

Vol 15 ◽

Author(s):

Fan Wu ◽

Zongchi Liu ◽

Ganglei Li ◽

Lihui Zhou ◽

Kaiyuan Huang ◽

...

Keyword(s):

Oxidative Stress ◽

Subarachnoid Hemorrhage ◽

Immune Cells ◽

Brain Dysfunction ◽

New Ideas ◽

Negative Role ◽

The Central Nervous System ◽

And Oxidative Stress

Subarachnoid hemorrhage (SAH) has a high mortality rate and causes long-term disability in many patients, often associated with cognitive impairment. However, the pathogenesis of delayed brain dysfunction after SAH is not fully understood. A growing body of evidence suggests that neuroinflammation and oxidative stress play a negative role in neurofunctional deficits. Red blood cells and hemoglobin, immune cells, proinflammatory cytokines, and peroxidases are directly or indirectly involved in the regulation of neuroinflammation and oxidative stress in the central nervous system after SAH. This review explores the role of various cellular and acellular components in secondary inflammation and oxidative stress after SAH, and aims to provide new ideas for clinical treatment to improve the prognosis of SAH.

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Resveratrol restored Nrf2 function, reduced renal inflammation, and mitigated hypertension in spontaneously hypertensive rats

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.00308.2014 ◽

2015 ◽

Vol 308 (10) ◽

pp. R840-R846 ◽

Cited By ~ 41

Author(s):

Apurva A. Javkhedkar ◽

Yasmir Quiroz ◽

Bernardo Rodriguez-Iturbe ◽

Nosratola D. Vaziri ◽

Mustafa F. Lokhandwala ◽

...

Keyword(s):

Oxidative Stress ◽

Spontaneously Hypertensive Rats ◽

Hypertensive Rats ◽

Renal Inflammation ◽

Spontaneously Hypertensive ◽

Term Administration ◽

And Oxidative Stress ◽

Gst Activity

Compelling evidence supports the role of oxidative stress and renal interstitial inflammation in the pathogenesis of hypertension. Resveratrol is a polyphenolic stilbene, which can lower oxidative stress by activating the transcription factor nuclear factor-E2-related factor-2 (Nrf2), the master regulator of numerous genes encoding antioxidant and phase II-detoxifying enzymes and molecules. Given the role of oxidative stress and inflammation in the pathogenesis of hypertension, we conducted this study to test the hypothesis that long-term administration of resveratrol will attenuate renal inflammation and oxidative stress and, hence, progression of hypertension in the young spontaneously hypertensive rats (SHR). SHR and control [Wistar-Kyoto (WKY)] rats were treated for 9 wk with resveratrol or vehicle in their drinking water. Vehicle-treated SHR exhibited renal inflammatory injury and oxidative stress, as evidenced by glomerulosclerosis, tubulointerstitial injury, infiltration of inflammatory cells, and increased levels of renal 8-isoprostane and protein carbonylation. This was associated with reduced antioxidant capacity and downregulations of Nrf2 and phase II antioxidant enzyme glutathione-S-transferase (GST). Resveratrol treatment mitigated renal inflammation and injury, reduced oxidative stress, normalized antioxidant capacity, restored Nrf2 and GST activity, and attenuated the progression of hypertension in SHR. However, resveratrol had no effect on these parameters in WKY rats. In conclusion, development and progression of hypertension in the SHR are associated with inflammation, oxidative stress, and impaired Nrf2-GST activity in the kidney. Long-term administration of resveratrol restores Nrf2 expression, ameliorates inflammation, and attenuates development of hypertension in SHR. Clinical studies are needed to explore efficacy of resveratrol in human hypertension.

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Inhibition of microRNA-155 Alleviates Neurological Dysfunction Following Transient Global Ischemia and Contribution of Neuroinflammation and Oxidative Stress in the Hippocampus

Current Pharmaceutical Design ◽

10.2174/1381612825666190926162229 ◽

2020 ◽

Vol 25 (40) ◽

pp. 4310-4317 ◽

Cited By ~ 4

Author(s):

Lichao Sun ◽

Shouqin Ji ◽

Jihong Xing

Keyword(s):

Oxidative Stress ◽

Brain Edema ◽

Severity Score ◽

Global Ischemia ◽

Signal Pathways ◽

Neurological Severity Score ◽

Tnf Α ◽

Transient Global Ischemia ◽

And Oxidative Stress

Background/Aims: Central pro-inflammatory cytokine (PIC) signal is involved in neurological deficits after transient global ischemia induced by cardiac arrest (CA). The present study was to examine the role of microRNA- 155 (miR-155) in regulating IL-1β, IL-6 and TNF-α in the hippocampus of rats with induction of CA. We further examined the levels of products of oxidative stress 8-isoprostaglandin F2α (8-iso PGF2α, indication of oxidative stress); and 8-hydroxy-2’-deoxyguanosine (8-OHdG, indication of protein oxidation) after cerebral inhibition of miR-155. Methods: CA was induced by asphyxia and followed by cardiopulmonary resuscitation in rats. ELISA and western blot analysis were used to determine the levels of PICs and products of oxidative stress; and the protein expression of NADPH oxidase (NOXs) in the hippocampus. In addition, neurological severity score and brain edema were examined to assess neurological functions. Results: We observed amplification of IL-1β, IL-6 and TNF-α along with 8-iso PGF2α and 8-OHdG in the hippocampus of CA rats. Cerebral administration of miR-155 inhibitor diminished upregulation of PICs in the hippocampus. This also attenuated products of oxidative stress and upregulation of NOX4. Notably, inhibition of miR-155 improved neurological severity score and brain edema and this was linked to signal pathways of PIC and oxidative stress. Conclusion: We showed the significant role of blocking miR-155 signal in improving the neurological function in CA rats likely via inhibition of signal pathways of neuroinflammation and oxidative stress, suggesting that miR-155 may be a target in preventing and/or alleviating development of the impaired neurological functions during CA-evoked global cerebral ischemia.

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