Oxidative stress and prevention of the adaptive response to chronic iron overload in the brain of young adult rats exposed to a 150 kilohertz electromagnetic field

Neuroscience ◽  
2011 ◽  
Vol 186 ◽  
pp. 39-47 ◽  
Author(s):  
K. Maaroufi ◽  
E. Save ◽  
B. Poucet ◽  
M. Sakly ◽  
H. Abdelmelek ◽  
...  
2021 ◽  
Vol 22 (10) ◽  
pp. 5272
Author(s):  
Débora Coimbra-Costa ◽  
Fernando Garzón ◽  
Norma Alva ◽  
Tiago C. C. Pinto ◽  
Fernando Aguado ◽  
...  

Background: Exposure to intermittent hypoxia has been demonstrated to be an efficient tool for hypoxic preconditioning, preventing damage to cells and demonstrating therapeutic benefits. We aimed to evaluate the effects of respiratory intermittent hypobaric hypoxia (IHH) to avoid brain injury caused by exposure to acute severe hypoxia (ASH). Methods: biomarkers of oxidative damage, mitochondrial apoptosis, and transcriptional factors in response to hypoxia were assessed by Western blot and immunohistochemistry in brain tissue. Four groups of rats were used: (1) normoxic (NOR), (2) exposed to ASH (FiO2 7% for 6 h), (3) exposed to IHH for 3 h per day over 8 days at 460 mmHg, and (4) ASH preconditioned after IHH. Results: ASH animals underwent increased oxidative-stress-related parameters, an upregulation in apoptotic proteins and had astrocytes with phenotype forms compatible with severe diffuse reactive astrogliosis. These effects were attenuated and even prevented when the animals were preconditioned with IHH. These changes paralleled the inhibition of NF-κB expression and the increase of erythropoietin (EPO) levels in the brain. Conclusions: IHH exerted neuroprotection against ASH-induced oxidative injury by preventing oxidative stress and inhibiting the apoptotic cascade, which was associated with NF-κB downregulation and EPO upregulation.


1983 ◽  
Vol 20 (1) ◽  
pp. 49-56 ◽  
Author(s):  
G.L. Coleman ◽  
R.O. Jacoby ◽  
P.N. Bhatt ◽  
A.L. Smith ◽  
A.M. Jonas

A lethal disease characterized by hemorrhage and necrosis of the brain, testes, and epididymides developed in young adult rats housed in specific pathogen free quarters. Morphological, virological, and serological investigations of the outbreak indicated that the probable causative agent was rat virus (Kilham), a common parvovirus of rats that usually Induces persistent, asymptomatic infection in adult rats.


2018 ◽  
Vol 18 ◽  
pp. 60-73 ◽  
Author(s):  
Alexandra Badea ◽  
Alaa Kamnaksh ◽  
Robert J. Anderson ◽  
Evan Calabrese ◽  
Joseph B. Long ◽  
...  

2016 ◽  
Vol 2016 ◽  
pp. 1-9 ◽  
Author(s):  
Alfonso Díaz ◽  
Samuel Treviño ◽  
Jorge Guevara ◽  
Guadalupe Muñoz-Arenas ◽  
Eduardo Brambila ◽  
...  

Energy drinks (EDs) are often consumed in combination with alcohol because they reduce the depressant effects of alcohol. However, different researches suggest that chronic use of these psychoactive substances in combination with alcohol can trigger an oxidative and inflammatory response. These processes are regulated by both a reactive astrogliosis and an increase of proinflammatory cytokines such as IL-1β, TNF-α, and iNOS, causing cell death (apoptosis) at the central and peripheral nervous systems. Currently, mechanisms of toxicity caused by mixing alcohol and ED in the brain are not well known. In this study, we evaluated the effect of chronic alcohol consumption in combination with ED on inflammatory response and oxidative stress in the temporal cortex (TCx) and hippocampus (Hp) of adult rats (90 days old). Our results demonstrated that consuming a mixture of alcohol and ED for 60 days induced an increase in reactive gliosis, IL-1β, TNF-α, iNOS, reactive oxygen species, lipid peroxidation, and nitric oxide, in the TCx and Hp. We also found immunoreactivity to caspase-3 and a decrease of synaptophysin in the same brain regions. The results suggested that chronic consumption of alcohol in combination with ED causes an inflammatory response and oxidative stress, which induced cell death via apoptosis in the TCx and Hp of the adult rats.


1998 ◽  
Vol 17 (7) ◽  
pp. 380-386 ◽  
Author(s):  
A Belmadani ◽  
G Tramu ◽  
A M Betbeder ◽  
E E Creppy

1. Ochratoxin A (OTA) is a mycotoxin produced by several fungi, especially Aspergillus and Penicillium species. Many food and foodstuffs can be contaminated by ochratoxin A, which is consequently found in blood of animals and humans. 2. The distribution into the brain of young adult rats fed OTA for 1 to 6 weeks and some consequences have been investigated in the present study. 3. Our results on rats given OTA (289 mg/kg/48 h) indicated that OTA accumulated in the whole brain as function of time according to a regression curve, Y=78.723 a+16.72 with a correlation coefficient of r=0.989, where Y-axis is the OTA concentration in ng/ g of brain and X-axis is the duration of the treatment in weeks. The brain OTA contents was 11.95+2.2, 23.89+4.4, 39.9+4.5, 50.3+7.3, 78.8+6.3, 94+16 ng/g of brain in the mycotoxin-treated animals for respectively 1, 2, 3, 4, 5 and 6-weeks treatment. OTA induced modifications of free amino-acid concentrations in the brain, mainly, Tyrosine (Tyr) and phenylalanine (Phe). Tyr decreased significantly as compared to control (p50.05). Phe increased signifi-cantly as compared to control (p<50.05). 4. Aspartame, (25 mg/kg/48 h) a structural analogue of OTA largely modified the distribution and prevented the accumulation of OTA in the brain since the respective brain OTA contents decreased respectively to 9.6+7.9, 19.2+3.0, 26.8+4.2, 19.7+1.9, 13.7+5.6 and 11.0+6.0 ng/g of tissue, for the same duration of treatment. It also prevented the modifications of Tyr and Phe levels. 5. The histological investigations showed several necrotic cells with pyknotic nucleus, detected in OTA treated animals with higher frequency as compared to the controls and Aspartame treated ones. Aspar-tame appeared to significantly prevent this nuclear effect as well, the meaning of which is discussed.


Author(s):  
Mansour Ataei ◽  
Arash Khaki ◽  
Yagoob Garedaghi

Introduction: Toxoplasmosis is caused by a protozoan named Toxoplasma gondii. This protozoan is a parasite of cats that can spread among other animals and birds around the world and cause a disease that varies from mild to severe. The disease is seen in the forms of acquired toxoplasmosis and congenital toxoplasmosis. Many studies have shown that there is a relationship between reproductive function and toxoplasmosis. T. gondii has led to decreased reproductive performance of males and females in many experimental animals. The aim of this study was to investigate the protective effect of hydroalcoholic extract of Solanum surattense on the brain tissue damage and brain oxidative stress induced by T. gondii in adult rats. Methods: For this purpose, 32 adult female rats were randomly divided into 4 groups. In group 1, 8 healthy rats received IP saline for 3 weeks. In group 2, 8 rats with T. gondii received IP saline for 3 weeks. In group 3, 8 rats with T. gondii received the hydroalcoholic extract of S. surattense for 3 weeks. In group 4, 8 healthy rats received the hydroalcoholic extract of S. surattense for 3 weeks. Then, brain tissue resection was performed to evaluate histological damage and levels of antioxidant enzymes. Results: Histological and biochemical studies showed that T. gondii had a deleterious effect on the brain tissue of rats and increased the level of tumor necrosis factor-α (TNF-α) and interferon-γ (IFN-γ). The administration of hydroalcoholic extract of S. surattense improved these effects due to its high antioxidant properties. Conclusion: The administration of the appropriate dose of hydroalcoholic extract of S. surattense for three consecutive weeks had a protective effect on brain tissue exposed to T. gondii.


2018 ◽  
Vol 9 (5) ◽  
pp. 2891-2901 ◽  
Author(s):  
Mayara Queiroga Barbosa ◽  
Rita de Cássia Ramos Egypto Queiroga ◽  
Camila Carolina de Menezes Santos Bertozzo ◽  
Daline Fernandes de Souza Araújo ◽  
Louise Iara Gomes Oliveira ◽  
...  

Goat milk fat induced anxiolytic effect in sedentary animals; exercise promoted lipid peroxidation in the brain; exercise induced anxiety.


Sign in / Sign up

Export Citation Format

Share Document