Acute hypermethioninemia impairs redox homeostasis and acetylcholinesterase activity in the hippocampus, striatum, and cerebellum of young rats

2021 ◽  
Author(s):  
Bernardo Moraes Meine ◽  
Natália Pontes Bona ◽  
Karina Pereira Luduvico ◽  
Luiza Spohr ◽  
Nathalia Stark Pedra ◽  
...  
Keyword(s):  
Redox Homeostasis ◽  
Acetylcholinesterase Activity ◽  
Young Rats

Carcinogen sodium arsenite disrupts antioxidant and redox homeostasis in Drosophila melanogaster

2021 ◽  
Vol 0 (0) ◽  
Author(s):  
Aghogho Oyibo ◽  
Amos O. Abolaji ◽  
Oyeronke A. Odunola
Keyword(s):  
Oxidative Stress ◽  
Drosophila Melanogaster ◽  
Sodium Arsenite ◽  
Environmental Contaminants ◽  
Redox Homeostasis ◽  
Exposure Period ◽  
Acetylcholinesterase Activity ◽  
Glutathione S Transferase ◽  
Emergence Rate ◽  
Antioxidant Markers

Abstract Objectives The inadvertent exposure to environmental contaminants has been reported to induce cancer in different animal models. Here, we investigated the toxicity of Sodium Arsenite (SA), a Class I Carcinogen in Drosophila melanogaster. Methods Harwich fly strain (1–3 days old) of both sexes were orally exposed to SA (0, 0.0312, 0.0625 and 0.125 mM) for 14 days for survival study. Thereafter, 5 days exposure period was selected to assess the toxic effects of SA on oxidative stress and antioxidant markers. Results The results indicated that SA induced significant reduction in survival and emergence rate of flies. Furthermore, SA significantly increased Nitric Oxide (NO, nitrite and nitrate) and Hydrogen Peroxide (H2O2) levels in flies compared with control (p<0.05). In addition, SA inhibited catalase and glutathione-S-transferase (GST) activities, and depleted total thiol and glutathione (GSH) contents. Moreover, acetylcholinesterase activity significantly increased in flies treated with SA when compared with control. Conclusions Sodium arsenite-induced reduction in survival and emergence rates of flies occurred via the disruption of oxidative stress-antioxidant homeostasis in D. melanogaster.

The efficacy of donepezil administration on acetylcholinesterase activity and altered redox homeostasis in Alzheimer’s disease

2017 ◽  
Vol 90 ◽  
pp. 786-795 ◽  
Author(s):  
Pinar Atukeren ◽  
Mahir Cengiz ◽  
Hakan Yavuzer ◽  
Remise Gelisgen ◽  
Esma Altunoglu ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Redox Homeostasis ◽  
Acetylcholinesterase Activity

scholarly journals Decoding Aging: Understanding the Complex Relationship among Aging, Free Radicals, and GSH

2020 ◽  
Vol 2020 ◽  
pp. 1-11
Author(s):  
María E. López-Navarro ◽  
Mariana Jarquín-Martínez ◽  
Luis A. Sánchez-Labastida ◽  
Daniel Ramírez-Rosales ◽  
Marycarmen Godínez-Victoria ◽  
...  
Keyword(s):  
Free Radicals ◽  
Ex Vivo ◽  
Redox Homeostasis ◽  
Adult Rats ◽  
Paramagnetic Resonance ◽  
Young Rats ◽  
Male Wistar Rats ◽  
Michael Type Addition ◽  
Old Rats ◽  
In Cells

N-aryl maleimides can undergo a 1,4-Michael-type addition reaction with reduced glutathione (GSH), leading to a decreased concentration of GSH and an increased concentration of free radicals (FRs) in cells. GSH is a critical scavenging molecule responsible for protecting cells from oxidation and for maintaining redox homeostasis. N-aryl maleimides disturb redox homeostasis in cells because they scavenge thiol-containing molecules, especially GSH. This study aimed at measuring the concentrations of GSH and FRs by electronic paramagnetic resonance (EPR), in the brain and liver tissue of male Wistar rats (ex vivo) at different ages and after treatment with 3,5-dimaleimylbenzoic acid (3,5-DMB). Our results showed a relationship between age and the concentrations of GSH and FRs in cells. In young rats, the concentration of GSH was higher than in old rats, while the concentration of FRs was higher in adult rats than in young rats, suggesting an inverse relationship between GSH and FRs. On the other hand, the reaction of 3,5-DMB (an electrophilic maleimide) with cellular GSH increased the FR content. The results of this study contribute to the awareness that the process of aging implies not only a loss of tissue function but also essential changes in the molecular contents of cells, especially the concentrations of FRs and GSH.

Formation of New Sites of Acetylcholinesterase Activity in Denervated Muscles of Young Rats

Nature ◽  
1966 ◽  
Vol 210 (5031) ◽  
pp. 39-41 ◽  
Author(s):  
LILIANA LUBIŃSKA ◽  
JIŘINA ZELENÁ
Keyword(s):  
Acetylcholinesterase Activity ◽  
Young Rats ◽  
Denervated Muscles

Increased susceptibility of brain acetylcholinesterase activity to methylmalonate in young rats with renal failure

2013 ◽  
Vol 28 (3) ◽  
pp. 493-500 ◽  
Author(s):  
André C. Affonso ◽  
Daniele G. Machado ◽  
Fernanda Malgarin ◽  
Daiane B. Fraga ◽  
Fernando Ghedim ◽  
...  
Keyword(s):  
Renal Failure ◽  
Acetylcholinesterase Activity ◽  
Young Rats ◽  
Increased Susceptibility ◽  
Brain Acetylcholinesterase

scholarly journals Acute administration of fenproporex increased acetylcholinesterase activity in brain of young rats

2015 ◽  
Vol 87 (2 suppl) ◽  
pp. 1389-1395 ◽  
Author(s):  
BRENA P. TEODORAK ◽  
GABRIELA K. FERREIRA ◽  
GISELLI SCAINI ◽  
LETÍCIA B. WESSLER ◽  
ALEXANDRA S. HEYLMANN ◽  
...  
Keyword(s):  
Young Male ◽  
Synaptic Cleft ◽  
Acetylcholinesterase Activity ◽  
Acute Administration ◽  
Pathophysiological Mechanism ◽  
Dependent Manner ◽  
Posterior Cortex ◽  
Young Rats ◽  
The Brain

Fenproporex is the second most commonly amphetamine-based anorectic consumed worldwide; this drug is rapidly converted into amphetamine, in vivo, and acts by increasing dopamine levels in the synaptic cleft. Considering that fenproporex effects on the central nervous system are still poorly known and that acetylcholinesterase is a regulatory enzyme which is involved in cholinergic synapses and may indirectly modulate the release of dopamine, the present study investigated the effects of acute administration of fenproporex on acetylcholinesterase activity in brain of young rats. Young male Wistar rats received a single injection of fenproporex (6.25, 12.5 or 25mg/kg i.p.) or vehicle (2% Tween 80). Two hours after the injection, the rats were killed by decapitation and the brain was removed for evaluation of acetylcholinesterase activity. Results showed that fenproporex administration increased acetylcholinesterase activity in the hippocampus and posterior cortex, whereas in the prefrontal cortex, striatum and cerebellum the enzyme activity was not altered. In conclusion, in the present study we demonstrated that acute administration of fenproporex exerts an effect in the cholinergic system causing an increase in the activity of acetylcholinesterase in a dose-dependent manner in the hippocampus and posterior cortex. Thus, we suggest that the imbalance in cholinergic homeostasis could be considered as an important pathophysiological mechanism underlying the brain damage observed in patients who use amphetamines such as fenproporex.

Chemically Contaminated Eel Fed to Pregnant and Lactating Mouse Dams Causes Hyperactivity in Their Offspring

2016 ◽  
Vol 86 (1-2) ◽  
pp. 36-47 ◽  
Author(s):  
Imen Dridi ◽  
Nidhal Soualeh ◽  
Torsten Bohn ◽  
Rachid Soulimani ◽  
Jaouad Bouayed
Keyword(s):  
Open Field ◽  
Early Life ◽  
Home Cage ◽  
Anguilla Anguilla ◽  
Acetylcholinesterase Activity ◽  
Female Offspring ◽  
Significant Inhibition ◽  
Standard Diet ◽  
Early Life Exposure ◽  
Cage Test

Abstract.This study examined whether perinatal exposure to polluted eels (Anguilla anguilla L.) induces changes in the locomotor activity of offspring mice across lifespan (post-natal days (PNDs) 47 – 329), using the open field and the home cage activity tests. Dams were exposed during gestation and lactation, through diets enriched in eels naturally contaminated with pollutants including PCBs. Analysis of the eel muscle focused on the six non-dioxin-like (NDL) indicator PCBs (Σ6 NDL-PCBs: 28, 52, 101, 138, 153 and 180). Four groups of dams (n = 10 per group) received either a standard diet without eels or eels (0.8 mg/kg/day) containing 85, 216, or 400 ng/kg/day of ϵ6 NDL-PCBs. The open field test showed that early-life exposure to polluted eels increased locomotion in female offspring of exposed dams but not in males, compared to controls. This hyperlocomotion appeared later in life, at PNDs 195 and 329 (up to 32 % increase, p < 0.05). In addition, overactivity was observed in the home cage test at PND 305: exposed offspring females showed a faster overall locomotion speed (3.6 – 4.2 cm/s) than controls (2.9 cm/s, p <0.05); again, males remained unaffected. Covered distances in the home cage test were only elevated significantly in offspring females exposed to highest PCB concentrations (3411 ± 590 cm vs. 1377 ± 114 cm, p < 0.001). These results suggest that early-life exposure to polluted eels containing dietary contaminants including PCBs caused late, persistent and gender-dependent neurobehavioral hyperactive effects in offspring mice. Furthermore, female hyperactivity was associated with a significant inhibition of acetylcholinesterase activity in the hippocampus and the prefrontal cortex.

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