Anxiety- and depression-like behaviors are accompanied by an increase in oxidative stress in a rat model of fetal alcohol spectrum disorders: Protective effects of voluntary physical exercise

2012 ◽  
Vol 62 (4) ◽  
pp. 1607-1618 ◽  
Author(s):  
Patricia S. Brocardo ◽  
Fanny Boehme ◽  
Anna Patten ◽  
Adrian Cox ◽  
Joana Gil-Mohapel ◽  
...  
Author(s):  
Marco Fiore ◽  
Carla Petrella ◽  
Giovanna Coriale ◽  
Pamela Rosso ◽  
Elena Fico ◽  
...  

Background: Fetal Alcohol Spectrum Disorders (FASD) are the manifestation of the damage caused by alcohol consumption during pregnancy. Children with Fetal Alcohol Syndrome (FAS), the extreme FASD manifestation, show both facial dysmorphology and mental retardation. Alcohol consumed during gestational age prejudices brain development by reducing, among others, the synthesis and release of neurotrophic factors and neuroinflammatory markers. Alcohol drinking induces also oxidative stress. Hypothesis/Objective : The present study aims at investigating the potential association between neurotrophins, neuroinflammation and oxidative stress in 12 prepubertal male and female FASD children diagnosed as FAS or partial FAS (pFAS). Methods: Accordingly, we analyzed, in the serum, the level of BDNF and NGF and the oxidative stress, as free oxygen radicals test (FORT) and free oxygen radicals defense (FORD). Moreover, serum levels of inflammatory mediators (IL-1α, IL-2, IL-6, IL-10, IL-12, MCP-1, TGF-β and TNF-α) involved in neuroinflammatory and oxidative processes have been investigated. Results: We demonstrated in pre-pubertal FASD children low serum levels of NGF and BDNF, respect to healthy controls. These changes were associated with higher serum presence of TNF-α and IL-1α. Quite interestingly, an elevation in the FORD was also found despite normal FORT levels. Moreover, we found a potentiation of IL-1α, IL-2, IL-10 and IL-1α1 in the analyzed female compared to male children. Conclusion: The present investigation shows an imbalance in the peripheral neuroimmune pathways that could be used in children as early biomarkers of the deficits observed in FASD.


2011 ◽  
Vol 67 (1-2) ◽  
pp. 209-225 ◽  
Author(s):  
Patricia S. Brocardo ◽  
Joana Gil-Mohapel ◽  
Brian R. Christie

2021 ◽  
Vol 22 (13) ◽  
pp. 7083
Author(s):  
Malgorzata Lopatynska-Mazurek ◽  
Lukasz Komsta ◽  
Ewa Gibula-Tarlowska ◽  
Jolanta H. Kotlinska

Fetal alcohol spectrum disorders (FASDs) are one of the most common consequences of ethanol exposure during pregnancy. In adulthood, these disorders can be manifested by learning and memory deficits and depressive-like behavior. Ethanol-induced oxidative stress may be one of the factors that induces FASD development. The mammalian target of the Rapamycin (mTOR) signaling pathway that acts via two distinct multiprotein complexes, mTORC1 and mTORC2, can affect oxidative stress. We investigated whether mTOR-dependent or mTOR-independent mechanisms are engaged in this phenomenon. Thus, Rapamycin—a selective inhibitor of mTORC1, Torin-2—a non-selective mTORC1/mTORC2 inhibitor, and FK-506—a drug that impacts oxidative stress in an mTOR-independent manner were used. Behavioral tests were performed in adult (PND60-65) rats using a passive avoidance (PA) task (aversive learning and memory) and forced swimming test (FST) (depressive-like behaviors). In addition, the biochemical parameters of oxidative stress, such as lipid peroxidation (LPO), as well as apurinic/apyrimidinic (AP)-sites were determined in the hippocampus and prefrontal cortex in adult (PND65) rats. The rat FASD model was induced by intragastric ethanol (5 g/kg/day) administration at postnatal day (PND)4–9 (an equivalent to the third trimester of human pregnancy). All substances (3 mg/kg) were given 30 min before ethanol. Our results show that neonatal ethanol exposure leads to deficits in context-dependent fear learning and depressive-like behavior in adult rats that were associated with increased oxidative stress parameters in the hippocampus and prefrontal cortex. Because these effects were completely reversed by Rapamycin, an mTORC1 inhibitor, this outcome suggests its usefulness as a preventive therapy in disorders connected with prenatal ethanol exposure.


2019 ◽  
Vol 111 (12) ◽  
pp. 714-748 ◽  
Author(s):  
Shama Bhatia ◽  
Danielle M. Drake ◽  
Lutfiya Miller ◽  
Peter G. Wells

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