Gold nanoparticles alter parameters of oxidative stress and energy metabolism in organs of adult rats

2015 ◽  
Vol 93 (6) ◽  
pp. 548-557 ◽  
Author(s):  
Gabriela Kozuchovski Ferreira ◽  
Eria Cardoso ◽  
Francieli Silva Vuolo ◽  
Monique Michels ◽  
Elton Torres Zanoni ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Gold Nanoparticles ◽  
Energy Metabolism ◽  
Acute Administration ◽  
Sod Activity ◽  
Adult Rats ◽  
Protein Levels ◽  
Carbonyl Protein ◽  
Term Administration

This study evaluated the parameters of oxidative stress and energy metabolism after the acute and long-term administration of gold nanoparticles (GNPs, 10 and 30 nm in diameter) in different organs of rats. Adult male Wistar rats received a single intraperitoneal injection or repeated injections (once daily for 28 days) of saline solution, GNPs-10 or GNPs-30. Twenty-four hours after the last administration, the animals were killed, and the liver, kidney, and heart were isolated for biochemical analysis. We demonstrated that acute administration of GNPs-30 increased the TBARS levels, and that GNPs-10 increased the carbonyl protein levels. The long-term administration of GNPs-10 increased the TBARS levels, and the carbonyl protein levels were increased by GNPs-30. Acute administration of GNPs-10 and GNPs-30 increased SOD activity. Long-term administration of GNPs-30 increased SOD activity. Acute administration of GNPs-10 decreased the activity of CAT, whereas long-term administration of GNP-10 and GNP-30 altered CAT activity randomly. Our results also demonstrated that acute GNPs-30 administration decreased energy metabolism, especially in the liver and heart. Long-term GNPs-10 administration increased energy metabolism in the liver and decreased energy metabolism in the kidney and heart, whereas long-term GNPs-30 administration increased energy metabolism in the heart. The results of our study are consistent with other studies conducted in our research group and reinforce the fact that GNPs can lead to oxidative damage, which is responsible for DNA damage and alterations in energy metabolism.

Long-term administration of high-dose methylphenidate-induced cerebellar morphology and function damage in adult rats

2020 ◽  
Vol 103 ◽  
pp. 101712 ◽  
Author(s):  
Amir Raoofi ◽  
Abass Aliaghaei ◽  
Mohammad-Amin Abdollahifar ◽  
Mahdi Eskandarian Boroujeni ◽  
Sara Sadat Javadinia ◽  
...  
Keyword(s):  
High Dose ◽  
Adult Rats ◽  
Term Administration ◽  
And Function

Long-Term Exposure to Inorganic Mercury Leads to Oxidative Stress in Peripheral Blood of Adult Rats

2020 ◽  
Author(s):  
Victória dos Santos Chemelo ◽  
Leonardo Oliveira Bittencourt ◽  
Walessa Alana Bragança Aragão ◽  
Sávio Monteiro dos Santos ◽  
Renata Duarte Souza-Rodrigues ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Peripheral Blood ◽  
Inorganic Mercury ◽  
Adult Rats

Antioxidant Responses and Lipid Peroxidation of Penaeus Indicus Postlarvae Subjected to Sublethal Copper Exposure

Crustaceana ◽  
2011 ◽  
Vol 84 (10) ◽  
pp. 1197-1210 ◽  
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Antioxidant Enzymes ◽  
Copper Toxicity ◽  
Sod Activity ◽  
Lipid Peroxidation Products ◽  
Coastal Marine ◽  
Potential Biomarker ◽  
Penaeus Indicus

AbstractThe objective of this study was to determine the effect of sublethal copper concentrations on certain antioxidant enzymes and lipid peroxidation products in the postlarvae (PL) of Penaeus indicus when subjected to short- and long-term exposure in the laboratory. The PL of P. indicus were exposed to 0.1641 ppm (sublethal) copper for a period of 30 days along with a parallel control. Sampling was carried out at six different time intervals, i.e., 24, 48, and 96 hrs (shortterm), and 10, 20, and 30 days (long-term). Variations in the activity of the antioxidant enzymes, namely, catalase (CAT) and superoxide dismutase (SOD), as well as lipid peroxidation products (LPP) were measured as biomarkers of metal toxicity. Our results showed a significant (P < 0.05) increase in LPP (indicating oxidative stress) and CAT activity (indicating an adaptive response of the PL for protection against oxidative stress) in the exposed PL for all periods of exposure. However, SOD activity significantly (P < 0.05) decreased on 20 and 30 days exposure, indicating susceptibility of the PL to oxidative stress upon long-term exposure. Therefore, CAT can serve as a better biomarker of oxidative stress than SOD to long-term copper toxicity. Our results indicate that copper contamination causes oxidative stress even at sublethal doses in Penaeus indicus PL, which can thus be used as a potential biomarker of copper toxicity for long-term monitoring of coastal marine ecosystems.

Alteration of Energy Metabolism and Antioxidative Processing in the Hippocampus of Rats Reared in Long-Term Environmental Enrichment

2016 ◽  
Vol 38 (3) ◽  
pp. 186-194 ◽  
Author(s):  
Hee Kang ◽  
Dong-Hee Choi ◽  
Su-Kang Kim ◽  
Jongmin Lee ◽  
Youn-Jung Kim
Keyword(s):  
Oxidative Stress ◽  
Energy Metabolism ◽  
Protein Expression ◽  
Environmental Enrichment ◽  
Synaptic Activity ◽  
Antioxidant Defenses ◽  
Laboratory Animals ◽  
Oxidative Stress Marker ◽  
Altered Expression

Environmental enrichment (EE) is a typical experimental method that promotes levels of novelty and complexity that enhance experience-dependent neuroplasticity and cognitive behavior function in laboratory animals. Early EE is associated with resilience in the face of later-life challenges. Since increased synaptic activity enhances endogenous neuronal antioxidant defenses, we hypothesized that long-term EE beginning at an early stage may alter the levels of oxidative stress. We investigated global protein expression and oxidative stress in hippocampal proteins from rats nurtured for a 6-month EE beginning in the prenatal period. The analysis of protein expression was carried out using 2-dimensional gel electrophoresis with matrix-associated laser desorption ionization time-of-flight mass spectrometry. Proteins with altered expression were involved in energy metabolism (phosphoglycerate mutase 1, α-enolase isoform 1, adenylate kinase 1, and triose phosphate isomerase) and antioxidant enzymes (superoxide dismutase 1, glutathione S-transferase ω type 1, peroxiredoxin 5, DJ-1, and glial maturation factor β). Using Western blot assays, some of the proteins with altered expression and NADPH oxidase 2 were confirmed to be decreased. Further confirmation was demonstrated with attenuated expression of 7,8-dihydro-8-oxo-deoxyguanine, a DNA oxidative stress marker, in the hippocampus of EE group rats. Our data demonstrate that a long-term EE program beginning in the prenatal and early postnatal phase of development modulates energy metabolism and reduced oxidant stress possibly through enhanced synaptic activity. We provide evidence that EE can be developed as a tool to protect the brain from oxidative stress-induced injury.

scholarly journals Effect of Short- and Long-Term Administration of Baclofen on Spatial Learning and Memory in Rats

2018 ◽  
pp. 133-141 ◽  
Author(s):  
M. HOLAJOVA ◽  
M. FRANEK
Keyword(s):  
Learning And Memory ◽  
Spatial Learning ◽  
Receptor Agonist ◽  
Gabab Receptor ◽  
Spatial Learning And Memory ◽  
Adult Rats ◽  
Treatment Groups ◽  
Term Administration ◽  
Short And Long Term

Baclofen is the only clinically available metabotropic GABAB receptor agonist. In our experiment, we tested the hypothesis that long-term baclofen administration can impair learning and memory in rats. The experiment consisted of three parts. In the first part of the study the drug was administered simultaneously with the beginning of the behavioral tests. In the second and third part of the experiment baclofen was administered daily for 14 days and for one month before the tests. In each part of the experiment, adult rats were randomly divided into four treatment groups. Three groups were given an injection of baclofen at doses of 1 mg/kg, 5 mg/kg, 10 mg/kg, while the fourth group was injected with saline. The injections were given after each session. Spatial learning and memory were tested using the Morris water maze, involving three types of tests: Acquisition, Probe, and Re-acquisition. This work reveals that baclofen did not affect spatial learning at any of the tested doses and regardless of the length of administration. Memory was observed to be affected, but only at the highest dose of baclofen and only temporarily. This conclusion is in line with previously published clinical cases.

scholarly journals Oxidized tissue proteins after intestinal reperfusion injury in rats

2005 ◽  
Vol 20 (6) ◽  
pp. 434-436 ◽  
Author(s):  
Alberto Schanaider ◽  
Vinícius José Martinho Toledo Menezes ◽  
Aline Cury Borchardt ◽  
Pedro Lagerblad de Oliveira ◽  
Kalil Madi
Keyword(s):  
Oxidative Stress ◽  
Reperfusion Injury ◽  
Intestinal Ischemia ◽  
Ischemia And Reperfusion ◽  
Ischemia And Reperfusion Injury ◽  
Group Iii ◽  
Protein Levels ◽  
Group I ◽  
Carbonyl Protein ◽  
Male Wistar Rats

PURPOSE: To analyse if the carbonyl proteins measurement could be validated as a method that allows the identification of an intestinal oxidative stress after ischemia and reperfusion injury. METHODS: Twenty-five male Wistar rats (n =21) weighting 200 to 250g were divided into three groups. Group I - control (n = 10). Group II - sham (n = 5) and Group III (n = 10) subjected to 60 minutes of intestinal ischemia and equal period of reperfusion. For this purpose it was clamped the superior mesenteric artery in its distal third. Histological changes and carbonyl protein levels were determined in the samples of all groups. In group III, samples of both normal and reperfused ileal segment were studied. RESULTS: All the reperfused segments showed mucosal and submucosal swelling and inflammatory infiltrate of the lamina propria. Levels of carbonyl protein rose in group III, including in the non-ischemic segments. The sensitivity and specificity of the carbonyl protein tissue levels were respectively 94% and 88%. CONCLUSION: The carbonyl protein method is a useful biologic marker of oxidative stress after the phenomenon of intestinal ischemia and reperfusion in rats. It was also noteworthy that the effects of oxidative stress could be seen far from the locus of the primary injury.

Cholesterol-enriched diet inhibits cardioprotection by ATP-sensitive K+ channel activators cromakalim and diazoxide

2014 ◽  
Vol 306 (3) ◽  
pp. H405-H413 ◽  
Author(s):  
Csaba Csonka ◽  
Krisztina Kupai ◽  
Péter Bencsik ◽  
Anikó Görbe ◽  
János Pálóczi ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Energy Metabolism ◽  
Normal Diet ◽  
Cardioprotective Effect ◽  
K Channel ◽  
Cholesterol Diet ◽  
Subunit Gene ◽  
Protein Levels ◽  
Myocardial Oxidative Stress ◽  
Vehicle Treated Control

It has been previously shown that hyperlipidemia interferes with cardioprotective mechanisms. Here, we investigated the interaction of hyperlipidemia with cardioprotection induced by pharmacological activators of ATP-sensitive K+ (KATP) channels. Hearts isolated from rats fed a 2% cholesterol-enriched diet or normal diet for 8 wk were subjected to 30 min of global ischemia and 120 min of reperfusion in the presence or absence of KATP modulators. In normal diet-fed rats, either the nonselective KATP activator cromakalim at 10−5 M or the selective mitochondrial (mito)KATP opener diazoxide at 3 × 10−5 M significantly decreased infarct size compared with vehicle-treated control rats. Their cardioprotective effect was abolished by coadministration of the nonselective KATP blocker glibenclamide or the selective mitoKATP blocker 5-hydroxydecanoate, respectively. However, in cholesterol-fed rats, the cardioprotective effect of cromakalim or diazoxide was not observed. Therefore, we further investigated how cholesterol-enriched diet influences cardiac KATP channels. Cardiac expression of a KATP subunit gene (Kir6.1) was significantly downregulated in cholesterol-fed rats; however, protein levels of Kir6.1 and Kir6.2 were not changed. The cholesterol diet significantly decreased cardiac ATP, increased lactate content, and enhanced myocardial oxidative stress, as shown by increased cardiac superoxide and dityrosine formation. This is the first demonstration that cardioprotection by KATP channel activators is impaired in cholesterol-enriched diet-induced hyperlipidemia. The background mechanism may include hyperlipidemia-induced attenuation of mitoKATP function by altered energy metabolism and increased oxidative stress in the heart.

scholarly journals Exercise training regulates SOD-1 and oxidative stress in porcine aortic endothelium

2003 ◽  
Vol 284 (4) ◽  
pp. H1378-H1387 ◽  
Author(s):  
James W. E. Rush ◽  
James R. Turk ◽  
M. Harold Laughlin
Keyword(s):  
Oxidative Stress ◽  
Exercise Training ◽  
Aerobic Exercise ◽  
Vascular Function ◽  
Aerobic Exercise Training ◽  
Heme Oxygenase 1 ◽  
Sod Activity ◽  
Aortic Endothelial Cells ◽  
Protein Levels ◽  
Markers Of Oxidative Stress

Vascular oxidative stress contributes to endothelial dysfunction. Aerobic exercise training improves vascular function. The purpose of this study was to test the hypothesis that exercise training would improve the balance of antioxidant to prooxidant enzymes and reduce markers of oxidative stress in aortic endothelial cells (AEC). Female Yucatan miniature pigs either remained sedentary (SED) or were exercise trained (EX) for 16–19 wk. EX pigs had increased AEC SOD-1 protein levels and Cu/Zn SOD activity of the whole aorta compared with SED pigs. Protein levels of other antioxidant enzymes (SOD-2, catalase) were not affected by exercise training. Protein levels of p67phox, a subunit of the prooxidant enzyme NAD(P)H oxidase, were reduced in EX vs. SED AEC. These EX adaptations were associated with lower AEC malondialdehyde levels and decreased phosphorylation of ERK-1/2. Endothelial nitric oxide synthase protein, protein nitrotyrosine content, and heme oxygenase-1 protein were not different in EX vs. SED pigs. We conclude that chronic aerobic exercise training influenced both antioxidant and prooxidant enzymes and decreased indexes of oxidative stress in AEC. These adaptations may contribute to improved endothelial function with exercise training.

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