Background:
Developmental ethanol (EtOH) exposure can cause lifelong behavioral hyperactivity,
cognitive deficits, emotional dysregulation, and more. However, co-treatment with lithium
(Li) on the day of EtOH exposure prevents many of the impairments.
Methods:
Experimental groups of pregnant mice were exposed to EtOH (20% v/v solution at a dose of
2.5 g/kg) in their drinking water and the animals were treated with Li (15 and 30 mg/kg) through IP
injection on gestational days14, 16, 18, and 20, and post-natal days (PD) 3, 5, 7, and 9. All treatments
with EtOH and exposure to Li doses to pregnant mice started on gestational day 14 and continued until
post-natal day 9 (PD9). The effects on some developing morphological indices, nerve reflexes during
weaning age, and various cognitive dysfunctions at adolescent ages and biochemical changes in the
brain tissue indices of below-mentioned neurotransmitters and oxidative stress in post-natal developing
offspring at adolescent age, were studied.
Results:
Perinatal exposure to EtOH in pregnant mice resulted in several postnatal developing and
morphological indices in the developing male pups during their weaning period, like gain in their body
weight, delay in appearance of their body hair fuzz and opening of their eyes, and disruptions in their
developing motor reflexes.
Discussion:
During adolescent age, a significant deficit in their learning capability and cognitive behavior,
decline in the neurochemical DA and 5-HT in their brain and some indices of oxidative stress
TBARS, GSH, GST, CAT, and SOD was observed.
Conclusion:
These results indicate that Li ameliorates significantly and dose-dependently EtOH induced
developmental toxicities like morphological developments and dysfunctions in cognitive retention
and oxidative stress on a long-term basis in brain tissue. However, further detailed studies are required
for the clinical use of as an ameliorating agent for perinatal EtOH induced dysfunctions.
Lysophosphatidylcholine Offsets the Protective Effects of Bone Marrow Mesenchymal Stem Cells on Inflammatory Response and Oxidative Stress Injury of Retinal Endothelial Cells via TLR4/NF-κB Signaling
