Maternal ethanol exposure induces behavioral deficits through oxidative stress and brain‐derived neurotrophic factor interrelation in rat offspring

2021 ◽  
Author(s):  
Rahebeh Mahdinia ◽  
Iran Goudarzi ◽  
Taghi Lashkarbolouki ◽  
Mahmoud Elahdadi Salmani
Keyword(s):  
Oxidative Stress ◽  
Neurotrophic Factor ◽  
Brain Derived Neurotrophic Factor ◽  
Ethanol Exposure ◽  
Behavioral Deficits ◽  
Rat Offspring

Evaluation of oxidative stress and brain-derived neurotrophic factor levels related to crack-use detoxification

2018 ◽  
Vol 670 ◽  
pp. 62-68 ◽  
Author(s):  
Gabriela Elisa Hirsch ◽  
Mônica Jaskulski ◽  
Henrique Morais Hamerski ◽  
Ferando Garcez Porto ◽  
Brenda da Silva ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Neurotrophic Factor ◽  
Brain Derived Neurotrophic Factor ◽  
Crack Use

scholarly journals Increased oxidative stress as a mechanism for decreased BDNF levels in acute manic episodes

2008 ◽  
Vol 30 (3) ◽  
pp. 243-245 ◽  
Author(s):  
Flávio Kapczinski ◽  
Benício N Frey ◽  
Ana C Andreazza ◽  
Márcia Kauer-Sant'Anna ◽  
Ângelo B M Cunha ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Bipolar Disorder ◽  
Neurotrophic Factor ◽  
Thiobarbituric Acid ◽  
Brain Derived Neurotrophic Factor ◽  
Oxidative Status ◽  
Control Group ◽  
Healthy Controls ◽  
Thiobarbituric Acid Reactive Substances ◽  
Low Levels

OBJECTIVE AND METHOD: There is a growing amount of data indicating that alterations in brain-derived neurotrophic factor and increased oxidative stress may play a role in the pathophysiology of bipolar disorder. In light of recent evidence demonstrating that brain-derived neurotrophic factor levels are decreased in situations of increased oxidative stress, we have examined the correlation between serum thiobarbituric acid reactive substances, a measure of lipid peroxidation, and serum brain-derived neurotrophic factor levels in bipolar disorder patients during acute mania and in healthy controls. RESULTS: Serum thiobarbituric acid reactive substances and brain-derived neurotrophic factor levels were negatively correlated in bipolar disorder patients (r = -0.56; p = 0.001), whereas no significant correlation was observed in the control group.. CONCLUSION: These results suggest that alterations in oxidative status may be mechanistically associated with abnormal low levels of brain-derived neurotrophic factor observed in individuals with bipolar disorder.

Effect of brain-derived neurotrophic factor on sperm function, oxidative stress and membrane integrity in human

Andrologia ◽  
2016 ◽  
Vol 49 (2) ◽  
pp. e12601 ◽  
Author(s):  
A. Najafi ◽  
F. Amidi ◽  
M. A. Sedighi Gilani ◽  
A. R. Moawad ◽  
E. Asadi ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Neurotrophic Factor ◽  
Membrane Integrity ◽  
Brain Derived Neurotrophic Factor ◽  
Sperm Function

scholarly journals Neuroprotective effects of dehydroepiandrosterone (DHEA) in rat model of Alzheimer's disease.

2011 ◽  
Vol 58 (4) ◽  
Author(s):  
Hanan F Aly ◽  
Fateheya M Metwally ◽  
Hanaa H Ahmed
Keyword(s):  
Oxidative Stress ◽  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Body Weight ◽  
Rat Model ◽  
Neurotrophic Factor ◽  
Intraperitoneal Administration ◽  
Brain Derived Neurotrophic Factor ◽  
Ovariectomized Rats ◽  
Antioxidant Enzyme Activities

The current study was undertaken to elucidate a possible neuroprotective role of dehydroepiandrosterone (DHEA) against the development of Alzheimer's disease in experimental rat model. Alzheimer's disease was produced in young female ovariectomized rats by intraperitoneal administration of AlCl(3) (4.2 mg/kg body weight) daily for 12 weeks. Half of these animals also received orally DHEA (250 mg/kg body weight, three times weekly) for 18 weeks. Control groups of animals received either DHAE alone, or no DHEA, or were not ovariectomized. After such treatment the animals were analyzed for oxidative stress biomarkers such as hydrogen peroxide, nitric oxide and malondialdehyde, total antioxidant capacity, reduced glutathione, glutathione peroxidase, glutathione reductase, superoxide dismutase and catalase activities, antiapoptotic marker Bcl-2 and brain derived neurotrophic factor. Also brain cholinergic markers (acetylcholinesterase and acetylcholine) were determined. The results revealed significant increase in oxidative stress parameters associated with significant decrease in the antioxidant enzyme activities in Al-intoxicated ovariectomized rats. Significant depletion in brain Bcl-2 and brain-derived neurotrophic factor levels were also detected. Moreover, significant elevations in brain acetylcholinesterase activity accompanied with significant reduction in acetylcholine level were recorded. Significant amelioration in all investigated parameters was detected as a result of treatment of Al-intoxicated ovariectomized rats with DHEA. These results were confirmed by histological examination of brain sections. These results clearly indicate a neuroprotective effect of DHEA against Alzheimer's disease.

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