Repeated Cycles of Binge-Like Ethanol Intake in Adolescent Female Rats Induce Motor Function Impairment and Oxidative Damage in Motor Cortex and Liver, but Not in Blood

Abstract

Moderate ethanol consumption (MEC) is increasing among women. Alcohol exposure usually starts in adolescence and tends to continue until adulthood. We aimed to investigate MEC impacts during adolescence until young adulthood of female rats. Adolescent female Wistar rats received distilled water or ethanol (3 g/kg/day), in a 3 days on-4 days off paradigm (binge drinking) for 1 and 4 consecutive weeks. We evaluate liver and brain oxidative damage, peripheral oxidative parameters by SOD, catalase, thiol contents, and MDA, and behavioral motor function by open-field, pole, beam-walking, and rotarod tests. Our results revealed that repeated episodes of binge drinking during adolescence displayed lipid peroxidation in the liver and brain. Surprisingly, such oxidative damage was not detectable on blood. Besides, harmful histological effects were observed in the liver, associated to steatosis and loss of parenchymal architecture. In addition, ethanol intake elicited motor incoordination, bradykinesia, and reduced spontaneous exploratory behavior in female rats.

Behavioral and neuronal interactions between exercise and alcohol: Sex and genetic differences

“…These studies also highlight a critical sex disparity in this body of literature, since only a handful included female rodents . This is especially relevant given reported sex differences in the response to binge‐like alcohol consumption and metabolism, in which hormonal factors may contribute to the apparent selective vulnerability of the female brain to alcohol . For example, alcohol consumption causes females to display greater susceptibility to innate oxidative stress, neuroinflammation and anatomical and histological alterations due to alcohol consumption .…”

“…For example, heavy alcohol consumption causes neuronal damage by increasing oxidative stress and neuroinflammation . After ingestion, alcohol metabolism generates two toxic by‐products: acetaldehyde and reactive oxygen species.…”

“…The long‐term consequences of repeated neuroinflammation and oxidative stress include a decline in cognitive function . In contrast, regular exercise has been shown to increase reaction time, nonspatial memory, object recognition, spatial learning and overall cognitive performance .…”

“…[34][35][36][37][38][39] For example, heavy alcohol consumption causes neuronal damage by increasing oxidative stress and neuroinflammation. 37,[40][41][42] After ingestion, alcohol metabolism generates two toxic by-products: acetaldehyde and reactive oxygen species. This process leads to a reduction of antioxidant enzymes and eventually oxidative tissue damage.…”

“…36,44,46 This is especially relevant given reported sex differences in the response to binge-like alcohol consumption and metabolism, in which hormonal factors may contribute to the apparent selective vulnerability of the female brain to alcohol. 40,46 For example, alcohol consumption causes females to display greater susceptibility to innate oxidative stress, neuroinflammation and anatomical and histological alterations due to alcohol consumption. [46][47][48] While more research is needed in the female population, together these studies suggest that physical exercise may be used as a preventative and therapeutic tool, particularly in females, to ameliorate some of the pathological neuronal effects caused by alcohol consumption.…”