Substance abuse and neuroprogression

2019 ◽  
pp. 191-206
Author(s):  
Anne Orgler Sordi ◽  
Silvia Bassani Schuch-Goi ◽  
Lisia von Diemen
Keyword(s):  
Oxidative Stress ◽  
Substance Abuse ◽  
Inflammatory Markers ◽  
Chronic Exposure ◽  
Allostatic Load ◽  
Brain Morphology ◽  
Accelerated Ageing ◽  
Growing Body ◽  
Staging Model ◽  
And Function

There is a growing body of evidence suggesting that neuroprogression occurs in addiction in the same way as in other psychiatric disorders. Biological markers of neuroprogression will be reviewed in the light of the staging model of addiction proposed by Volkow and Koob (intoxication, withdrawal and negative affect, and preoccupation and anticipation) and of allostatic load theory. Chronic exposure to drugs leads to allostatic load or overload through these stages. Neuroadaptation in this process disrupts brain morphology and function. Evidence regarding neuroprogression in drug addiction will focus on neuroimaging findings as well as neurotrophins, inflammatory markers, oxidative stress, and accelerated ageing.

Effects of Chronic Exposure to Electromagnetic Waves at 930 MHz Frequency on Oxidative Stress in Plasma and Some Organs of Wistar Rats

2012 ◽  
Vol 3 (7) ◽  
pp. 1-7
Author(s):  
L. TAZROUT L. TAZROUT ◽  
◽  
K. TALEA K. TALEA ◽  
S. EL AMRANI S. EL AMRANI ◽  
I. M’TOUGUY I. M’TOUGUY ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Chronic Exposure ◽  
Electromagnetic Waves ◽  
Wistar Rats

scholarly journals 145 President Oral Presentation Pick: Prenatal stress increases skeletal muscle mitochondrial volume density and function in yearling Brahman calves

2020 ◽  
Vol 98 (Supplement_4) ◽  
pp. 120-121
Author(s):  
Chloey P Guy ◽  
Catherine L Wellman ◽  
David G Riley ◽  
Charles R Long ◽  
Ron D Randel ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Creatine Kinase ◽  
Muscle Damage ◽  
Prenatal Stress ◽  
Citrate Synthase ◽  
Volume Density ◽  
Assembly Factor ◽  
Mitochondrial Volume ◽  
Mitochondrial Volume Density ◽  
And Function

Abstract We previously determined that prenatal stress (PNS) differentially affected methylation of DNA from leukocytes of 28-d-old calves. Specifically, COX14 (cytochrome c oxidase (COX) assembly factor) and CKMT1B (mitochondrial creatine kinase U-type) were hypomethylated and COA5 (COX assembly factor 5), COX5A (COX subunit 5A), NRF1 (nuclear respiratory factor 1), and GSST1 (glutathione S-transferase theta-1) were hypermethylated in PNS compared to non-PNS calves (P ≤ 0.05). Our current objective was to test the hypothesis that PNS exhibit impaired mitochondrial function and greater oxidative stress than non-PNS calves. Blood and longissimus dorsi muscle samples were collected from yearling Brahman calves whose mothers were stressed by 2 h transportation at 60, 80, 100, 120, and 140 days of gestation (PNS; 8 bulls, 6 heifers) and non-PNS calves (4 bulls, 6 heifers). Serum was evaluated for the stress hormone, cortisol, and muscle damage marker, creatine kinase; muscle was analyzed for mitochondrial volume density and function by citrate synthase (CS) and COX activities, respectively, concentration of malondialdehyde, a lipid peroxidation marker, and activity of the antioxidant, superoxide dismutase (SOD). Data were analyzed using mixed linear models with treatment and sex as fixed effects. Serum cortisol was numerically higher in PNS than non-PNS calves but was not statistically different. Muscle CS and COX activities relative to protein were greater in PNS than non-PNS calves (P ≤ 0.03), but COX relative to CS activity was similar between groups. Activity of COX was greater in bulls than heifers (P = 0.03), but no other measure was affected by sex. All other measures were unaffected by PNS. Prenatal stress did not affect markers of muscle damage and oxidative stress in yearling Brahman calves at rest but mitochondrial volume density and function were greater in PNS calves. Acute stressors induce oxidative stress, so implications of differences in mitochondria in PNS calves following a stressor should be investigated.

scholarly journals N-acetyl Cysteine Alleviates Cytotoxicity of Bone Substitute

2010 ◽  
Vol 89 (4) ◽  
pp. 411-416 ◽  
Author(s):  
M. Yamada ◽  
T. Ueno ◽  
H. Minamikawa ◽  
N. Sato ◽  
F. Iwasa ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Bone Substitute ◽  
Bone Substitutes ◽  
Amino Acid Derivative ◽  
Bovine Bone ◽  
Intracellular Ros ◽  
Cytokine Levels ◽  
Acetyl Cysteine ◽  
And Function ◽  
Bone Particles

Lack of cytocompatibility in bone substitutes impairs healing in surrounding bone. Adverse biological events around biomaterials may be associated with oxidative stress. We hypothesized that a clinically used inorganic bone substitute is cytotoxic to osteoblasts due to oxidative stress and that N-acetyl cysteine (NAC), an antioxidant amino acid derivative, would detoxify such material. Only 20% of rat calvaria osteoblasts were viable when cultured on commercial deproteinized bovine bone particles for 24 hr, whereas this percentage doubled on bone substitute containing NAC. Intracellular ROS levels markedly increased on and under bone substitutes, which were reduced by prior addition of NAC to materials. NAC restored suppressed alkaline phosphatase activity in the bone substitute. Proinflammatory cytokine levels from human osteoblasts on the bone substitute decreased by one-third or more with addition of NAC. NAC alleviated cytotoxicity of the bone substitute to osteoblastic viability and function, implying enhanced bone regeneration around NAC-treated inorganic biomaterials.

scholarly journals Telomere Length and Oxidative Stress and Its Relation with Metabolic Syndrome Components in the Aging

Biology ◽  
2021 ◽  
Vol 10 (4) ◽  
pp. 253
Author(s):  
Graciela Gavia-García ◽  
Juana Rosado-Pérez ◽  
Taide Laurita Arista-Ugalde ◽  
Itzen Aguiñiga-Sánchez ◽  
Edelmiro Santiago-Osorio ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Metabolic Syndrome ◽  
Telomere Length ◽  
Scientific Evidence ◽  
Telomeric Dna ◽  
Biochemical Alterations ◽  
The Metabolic Syndrome ◽  
Age Related ◽  
And Function

A great amount of scientific evidence supports that Oxidative Stress (OxS) can contribute to telomeric attrition and also plays an important role in the development of certain age-related diseases, among them the metabolic syndrome (MetS), which is characterised by clinical and biochemical alterations such as obesity, dyslipidaemia, arterial hypertension, hyperglycaemia, and insulin resistance, all of which are considered as risk factors for type 2 diabetes mellitus (T2DM) and cardiovascular diseases, which are associated in turn with an increase of OxS. In this sense, we review scientific evidence that supports the association between OxS with telomere length (TL) dynamics and the relationship with MetS components in aging. It was analysed whether each MetS component affects the telomere length separately or if they all affect it together. Likewise, this review provides a summary of the structure and function of telomeres and telomerase, the mechanisms of telomeric DNA repair, how telomere length may influence the fate of cells or be linked to inflammation and the development of age-related diseases, and finally, how the lifestyles can affect telomere length.

scholarly journals Alcohol-and-HIV-Induced Lysosomal Dysfunction Regulates Extracellular Vesicles Secretion in Vitro and in Liver-Humanized Mice

Biology ◽  
2021 ◽  
Vol 10 (1) ◽  
pp. 29
Author(s):  
Raghubendra Singh Dagur ◽  
Moses New-Aaron ◽  
Murali Ganesan ◽  
Weimin Wang ◽  
Svetlana Romanova ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Extracellular Vesicles ◽  
Treated Group ◽  
Human Hepatocytes ◽  
In Vivo Studies ◽  
People Living With Hiv ◽  
Humanized Mouse Model ◽  
And Function

Background: Alcohol abuse is common in people living with HIV-1 and dramaticallyenhances the severity of HIV-induced liver damage by inducing oxidative stress and lysosomaldysfunction in the liver cells. We hypothesize that the increased release of extracellular vesicles(EVs) in hepatocytes and liver humanized mouse model is linked to lysosome dysfunction. Methods:The study was performed on primary human hepatocytes and human hepatoma RLWXP-GFP (Huh7.5 cells stably transfected with CYP2E1 and XPack-GFP) cells and validated on ethanol-fed liverhumanizedfumarylacetoacetate hydrolase (Fah)-/-, Rag2-/-, common cytokine receptor gamma chainknockout (FRG-KO) mice. Cells and mice were infected with HIV-1ADA virus. Results: We observedan increase in the secretion of EVs associated with a decrease in lysosomal activity and expressionof lysosomal-associated membrane protein 1. Next-generation RNA sequencing of primary humanhepatocytes revealed 63 differentially expressed genes, with 13 downregulated and 50 upregulatedgenes in the alcohol–HIV-treated group. Upstream regulator analysis of differentially expressedgenes through Ingenuity Pathway Analysis identified transcriptional regulators affecting downstreamgenes associated with increased oxidative stress, lysosomal associated disease, and function andEVs biogenesis. Our in vitro findings were corroborated by in vivo studies on human hepatocytetransplantedhumanized mice, indicating that intensive EVs’ generation by human hepatocytes andtheir secretion to serum was associated with increased oxidative stress and reduction in lysosomalactivities triggered by HIV infection and ethanol diet. Conclusion: HIV-and-ethanol-metabolisminducedEVs release is tightly controlled by lysosome status in hepatocytes and participates in thedevelopment of double-insult-induced liver injury.

scholarly journals Nitric oxide synthase 3 deficiency limits adverse ventricular remodeling after pressure overload in insulin resistance

2011 ◽  
Vol 301 (5) ◽  
pp. H2093-H2101 ◽  
Author(s):  
Baptiste Kurtz ◽  
Helene B. Thibault ◽  
Michael J. Raher ◽  
John R. Popovich ◽  
Sharon Cawley ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Nitric Oxide ◽  
Insulin Resistance ◽  
Mitochondrial Respiration ◽  
Pressure Overload ◽  
Lv Remodeling ◽  
Stress Levels ◽  
Nitric Oxide Synthase 3 ◽  
And Function ◽  
Oxide Synthase

Insulin resistance (IR) and systemic hypertension are independently associated with heart failure. We reported previously that nitric oxide synthase 3 (NOS3) has a beneficial effect on left ventricular (LV) remodeling and function after pressure-overload in mice. The aim of our study was to investigate the interaction of IR and NOS3 in pressure-overload-induced LV remodeling and dysfunction. Wild-type (WT) and NOS3-deficient (NOS3−/−) mice were fed either a standard diet (SD) or a high-fat diet (HFD) to induce IR. After 9 days of diet, mice underwent transverse aortic constriction (TAC). LV structure and function were assessed serially using echocardiography. Cardiomyocytes were isolated, and levels of oxidative stress were evaluated using 2′,7′-dichlorodihydrofluorescein diacetate. Cardiac mitochondria were isolated, and mitochondrial respiration and ATP production were measured. TAC induced LV remodeling and dysfunction in all mice. The TAC-induced decrease in LV function was greater in SD-fed NOS3−/− mice than in SD-fed WT mice. In contrast, HFD-fed NOS3−/− developed less LV remodeling and dysfunction and had better survival than did HFD-fed WT mice. Seven days after TAC, oxidative stress levels were lower in cardiomyocytes from HFD-fed NOS3−/− than in those from HFD-fed WT. Nω-nitro-l-arginine methyl ester and mitochondrial inhibitors (rotenone and 2-thenoyltrifluoroacetone) decreased oxidative stress levels in cardiomyocytes from HFD-fed WT mice. Mitochondrial respiration was altered in NOS3−/− mice but did not worsen after HFD and TAC. In contrast with its protective role in SD, NOS3 increases LV adverse remodeling after pressure overload in HFD-fed, insulin resistant mice. Interactions between NOS3 and mitochondria may be responsible for increased oxidative stress levels in HFD-fed WT mice hearts.

scholarly journals Chronic exposure to U18666A is associated with oxidative stress in cultured murine cortical neurons

2006 ◽  
Vol 98 (4) ◽  
pp. 1278-1289 ◽  
Author(s):  
Chor Hui Vivien Koh ◽  
Matthew Whiteman ◽  
Qiao-Xin Li ◽  
Barry Halliwell ◽  
Andrew M. Jenner ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cortical Neurons ◽  
Chronic Exposure

scholarly journals Chronic exposure to emissions from photocopiers in copy shops causes oxidative stress and systematic inflammation among photocopier operators in India

2013 ◽  
Vol 12 (1) ◽  
Author(s):  
Nithya Elango ◽  
Vallikkannu Kasi ◽  
Bhuvaneswari Vembhu ◽  
Jeyanthi Govindasamy Poornima
Keyword(s):  
Oxidative Stress ◽  
Chronic Exposure

Mercury Exposure and Endothelial Dysfunction

2015 ◽  
Vol 34 (4) ◽  
pp. 300-307 ◽  
Author(s):  
Swati Omanwar ◽  
M. Fahim
Keyword(s):  
Oxidative Stress ◽  
Nitric Oxide ◽  
Endothelial Dysfunction ◽  
Vascular Endothelium ◽  
Circulatory System ◽  
Vital Role ◽  
Mercury Exposure ◽  
And Function ◽  
The Impact ◽  
And Oxidative Stress

Vascular endothelium plays a vital role in the organization and function of the blood vessel and maintains homeostasis of the circulatory system and normal arterial function. Functional disruption of the endothelium is recognized as the beginning event that triggers the development of consequent cardiovascular disease (CVD) including atherosclerosis and coronary heart disease. There is a growing data associating mercury exposure with endothelial dysfunction and higher risk of CVD. This review explores and evaluates the impact of mercury exposure on CVD and endothelial function, highlighting the interplay of nitric oxide and oxidative stress.

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