Exposure to silver nanoparticles induces oxidative stress and memory deficits in laboratory rats

2011 ◽  
Vol 6 (4) ◽  
pp. 497-509 ◽  
Author(s):  
Lucian Hritcu ◽  
Marius Stefan ◽  
Laura Ursu ◽  
Anca Neagu ◽  
Marius Mihasan ◽  
...  

AbstractCurrently most of the applications of silver nanoparticles are in antibacterial/antifungal agents in medicine and biotechnology, textile engineering, water treatment and silver-based consumer products. However, the effects of silver nanoparticles on human body, especially on the central nervous system, are still unclear. To study the mechanisms underlying the effects of silverpoly(amidehydroxyurethane) coated silver nanoparticles on brain functions, we subjected male Wistar rats to chronic treatments with silver-29 nm (5 µg/kg and 10 µg/kg) and silver-23 nm (5 µg/kg and 10 µg/kg) nanoparticles for 7 days. We evaluated the effects of nanoparticles size and structure on rat memory function. Memory processes were studied by means of two cognitive tasks (Y-maze and radial arm-maze). Exposure to silver nanoparticles significantly decreased spontaneous alternation in the Y-maze task and working memory functions in the radial arm-maze task, suggesting that nanoparticles have effects on short-term memory. We found no effects on long-term memory, which we assessed by reference memory trials in the radial arm-maze task. We found that memory deficits were significantly correlated with oxidative stress generation only in the Y-maze task. Our findings suggest that silver nanoparticles may induce an impairment of memory functions by increasing oxidative stress in the brain. The use of silver nanoparticles for medical purposes therefore requires careful consideration, particularlyif it involves exposure of the human brain.

Hypertension ◽  
2016 ◽  
Vol 68 (suppl_1) ◽  
Author(s):  
Akash George ◽  
Kennedy Richardson ◽  
Yuankun Zhai ◽  
Suresh C Tyagi ◽  
Neetu Tyagi

Alcohol consumption is a potent inducer of oxidative stress (OS). Oxidative stress cause disturbance of endoplasmic reticulum (ER) homeostasis, that triggers ER stress (ERS), cause neuronal damage in the brain. Our Previous data indicate that Alcohol consumption induces mitochondrial dysfunction and free radical production in mouse cerebral cortex. Exercise has been recommended by clinicians as a secondary protective therapy; however, its effect on brain functions through ER stress has not been fully explored. Therefore, we hypothesized that exercise improves Alcohol-induced neurodegeneration and decline in cognitive function through ER stress mitigation. To test this hypothesis, we selected 10-12 weeks old male wild-type mice (C57BL/6, WT), grouped as follows: 1) WT, 2) WT+ Alcohol, 3) WT+ Exercise, 4) WT+ Alcohol + Exercise. Mice were given an intraperitoneal injection of Alcohol (1.5g/kg BW) or saline solution every day for 8 weeks. The mice were exercised for 8 weeks on a treadmill with a controlled speed of 7 meters/min for the first week, the speed of 10 meters/min for the second week and 11 meters/min in the following weeks and a total of 330 meters every day. After each 110 meters mice were given rest of 10 minutes. Cognitive and behavior alterations were assessed by novel object recognition, Passive avoidance, and Y-maze tests. Our result showed there is a significantly impaired cognitive and behavior functions (600.00 ± 0.00 vs 480 ± 20.00, P<0.05) in Alcohol-treated group compared to WT control mice. However exercised significantly improved (0.37 ± 0.05 vs 0.63 ± 0.04 P<0.01) these functions as compared to Alcohol-treated group. Also, we observed an elevated blood pressure in the Alcohol-treated group (123.50 ± 1.17) and exercise brought that to the normal level (108.98 ± 4.47, P<0.01). In addition, the effect of exercise on neuronal survival in the Alcohol-treated mouse brain was confirmed by a decrease in by fluoro-jade C reactivity. Taken together, our results indicate a myriad of beneficiary effects of exercise over ER mitigation in Alcohol-treated mice. Furthermore, our findings suggest exercise alleviates neurodegeneration and cognitive dysfunction and thereby improving total brain function. This work was supported by NIH grant HL107640-NT


2009 ◽  
Vol 24 (S1) ◽  
pp. 1-1 ◽  
Author(s):  
L. Hritcu ◽  
W. Bild ◽  
A. Ciobica ◽  
V. Artenie ◽  
I. Haulica

Aims:The brain renin-angiotensin system is involved in learning and memory, but the actual role of angiotensin II and its metabolites in this process has been difficult to comprehend. In the present study we assessed the role of the angiotensin AT1 receptors in certain behavioral effects of angiotensin II using their selective antagonist losartan and PD123319, intracerebroventricularly (icv) administrated.Methods:Male Wistar rats were divided into three groups: 1. sham-operated; 2. Losartan; 3. PD123319. All drugs were stereotaxically icv injected. Learning and memory tests began 2 weeks after the operation, and the ability of the rats to acquire the operant task was studied by means of Y-maze task and passive avoidance task, respectively. The anxiety state was measured in elevated plus maze.Results:Losartan and PD123319 significantly impaired spatial memory in Y-maze task, suggesting significant effects on short-term memory. In passive avoidance task, both angiotensin II antagonist, significantly decreased step-through-latency, suggesting significant effects on long-term memory. In elevated plus maze measuring anxiety, both drugs diminished anxiety state.Conclusions:Our results suggest the considerable involvement of the brain ATi angiotensin receptors in the cognition improving effects of angiotensin.


2009 ◽  
Vol 4 (2) ◽  
pp. 179-185 ◽  
Author(s):  
Lucian Hritcu ◽  
Toshitaka Nabeshima

AbstractThe effects of lesioning the ventral tegmental area (VTA) or substantia nigra (SN) neurons by means of bilateral stereotaxic microinjections of kainic acid (KA) (0.4 mM) were investigated to clarify the role of the VTA and the SN neurons in learning and memory processes. The present study demonstrates that KA in the SN and the VTA lesioned rats significantly decreased spontaneous alternation in Y-maze task, working memory and reference memory in radial 8 arm-maze task, suggesting effects on spatial memory performance. Our findings provide further support for the role of the VTA and the SN neurons in processing and storage of information.


2019 ◽  
Vol 2019 ◽  
pp. 1-11 ◽  
Author(s):  
Elena Todirascu-Ciornea ◽  
Heba A.S. El-Nashar ◽  
Nada M. Mostafa ◽  
Omayma A. Eldahshan ◽  
Razvan Stefan Boiangiu ◽  
...  

Schinus terebinthifolius is a plant well recognized for its therapeutic profile such as anti-inflammatory and antitumor activities, promoting antibacterial activity and antioxidant and antidiabetic properties. This study aimed at examining whether Schinus terebinthifolius memory-enhancing activities are mediated by cholinergic and brain antioxidant systems in a scopolamine zebrafish model. Schinus terebinthifolius essential oil (10, 25, and 50 μL/L) was delivered to zebrafish by immersion in water for 8 days. Memory deficits were induced by scopolamine (100 μM) administration. Zebrafish were divided into seven groups (n = 15/group): vehicle group, scopolamine (100 μM) group, Schinus terebinthifolius essential oil groups (STF; 10, 25, and 50 μL/L), the imipramine group (IMP; 20 mg/L, as the positive control in the NTT test), and the donepezil group (DP; 10 mg/L, as the positive control in the Y-maze test). Memory status was estimated by the novel tank diving test (NTT) and the Y-maze test and finally was validated by comparison with imipramine (20 mg/L) and donepezil (10 mg/L). Gas chromatography-mass spectrometry (GC-MS) was used to detect oil compounds. Brain levels of acetylcholinesterase (AChE) and antioxidant enzymes were measured. After being exposed to Schinus terebinthifolius essential oil, the scopolamine zebrafish exhibited an improvement of memory processes in the NTT and Y-maze tests. The essential oil attenuated the elevated level of AChE and brain oxidative stress. Schinus terebinthifolius essential oil was found to support memory formation through the inhibition of the AChE activity and decreasing oxidative stress in the scopolamine-treated zebrafish brains.


2009 ◽  
Vol 4 (3) ◽  
pp. 335-342 ◽  
Author(s):  
Lucian Hritcu ◽  
Alin Ciobica ◽  
Lucian Gorgan

AbstractMale Wistar rats were subjected to chronic nicotine treatment (0.3 mg/kg; 7 continuous days) and their memory performance was studied by means of Y-maze and multi-trial passive avoidance tasks. Nicotine significantly decreased spontaneous alternation in Y-maze task and step-through-latency in the multi-trial passive avoidance task, suggesting effects on both short-term memory and long-term memory, respectively. In addition, nicotine induced neuronal apoptosis, DNA fragmentation, reduced antioxidant enzymes activity, and increased production of lipid peroxidation and reactive oxygen species, suggesting pro-oxidant activity. Our results provide further support that nicotine-induced memory impairment is due to an increase in brain oxidative stress in rats.


2008 ◽  
Vol 3 (3) ◽  
pp. 250-257 ◽  
Author(s):  
Lucian Hritcu ◽  
Alin Ciobica ◽  
Vlad Artenie

AbstractMale Wistar rats were subjected to right-unilateral 6-hydroxydopamine (6-OHDA) (2 μg/μl) lesions of the ventral tegmental area (VTA) or the substantia nigra (SN), or were sham-operated, and their ability to acquire the operant task was studied by means of Y-maze and shuttle-box tasks. Lesions of both the VTA and the SN resulted in an impairment of conditioned avoidance response and increase of crossing latency tested by means of shuttle-box task, suggesting significant effects of long-term memory. 6-OHDA significantly decreased spontaneous alternation in Y-maze task, suggesting effects on spatial memory, especially on short-term memory. In addition, 6-OHDA lesions of the VTA and the SN induced reductions in superoxide dismutase (SOD), glutathione peroxidase (GPX) activities and malondialdehyde (MDA) levels in the temporal lobe rather than in the frontal lobe homogenates. Our results provide further support for the toxic effects of 6-OHDA-induced memory impairment and oxidative stress with relevance for Parkinson’s disease.


2017 ◽  
Author(s):  
Silvia Maggi ◽  
Adrien Peyrache ◽  
Mark D. Humphries

AbstractThe prefrontal cortex is implicated in learning the rules of an environment through trial and error. But it is unclear how such learning is related to the prefrontal cor-tex’s role in short-term memory. Here we asked if the encoding of short-term memory in prefrontal cortex was used by rats learning decision rules in a Y-maze task. We found that a similar pattern of neural ensemble activity was selectively recalled after reinforcement for a correct decision. This reinforcement-selective recall only reliably occurred immediately before the abrupt behavioural transitions indicating successful learning of the current rule, and faded quickly thereafter. We could simultaneously decode multiple, retrospective task events from the ensemble activity, suggesting the recalled ensemble activity had multiplexed encoding of prior events. Our results suggest that successful trial-and-error learning is dependent on reinforcement tagging the relevant features of the environment to maintain in prefrontal cortex short-term memory.


2019 ◽  
Vol 2019 ◽  
pp. 1-14 ◽  
Author(s):  
Harquin Simplice Foyet ◽  
Eglantine Keugong Wado ◽  
Hervé Hervé Ngatanko Abaissou ◽  
Emmanuel Acha Assongalem ◽  
Oben Kenneth Eyong

Ziziphus mucronata Willd, also known as “buffalo thorn,” belongs to the family Rhamnaceae. Its bark and leaves are used in folk medicine for the treatment of various deficiencies related to nociception, inflammation, mood, and depression. Still, there is a lack of scientific data regarding its potential effect on learning and memory process. The present study was designed to investigate the neuroprotective potential of Ziziphus mucronata (ZM) on learning and memory impairment in a scopolamine-induced model of dementia in mice. The phytochemical analysis revealed five cyclopeptide alkaloids (sanjoinines) in the extract from Ziziphus Mucronata leaves using LC-HRMS, and the structural characterization of these compounds was determined via MS/MS. Alzheimer-type amnesia was induced by an intraperitoneal injection of scopolamine (1 mg/kg) to mice for 7 consecutive days. ZM (150 mg/kg, 300 mg/kg, and 600 mg/kg) and piracetam (150 mg/kg) were orally administrated to mice daily for a period of 14 days. Memory-related behavioural parameters were evaluated using the radial arm maze task for 7 days, Y-maze, and novel object recognition task. At the end of protocol schedule, animals were sacrificed, and the levels of acetylcholinesterase, malondialdehyde, catalase, and superoxide dismutase were determined in brain homogenates. Histological studies of the hippocampus were subsequently performed. The long-term scopolamine-injected group decreased the spontaneous alternation (Y-maze), the discrimination index, and the time taken to explore the new object (novel object recognition task). These effects were significantly reversed by ZM at all the doses tested. In the radial arm maze task, ZM (300 and 600 mg/kg) significantly decreased the working and reference memory errors when compared with the demented group. Scopolamine-mediated changes in AChE activity were also attenuated by ZM in mice. In addition, extract-treated groups showed a significant increase in the level of CAT and SOD activity and decreased levels of MDA in the mice brains, as compared with the control group. The present study suggests that ZM could have an important role in neuroprotection on this scopolamine-induced model of Alzheimer-type dementia.


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