European Journal of Biomedical and Pharmaceutical Sciences

COMPREHENDING THE ROLE OF AAS ON THE AChE ACTIVITY AND ANTIOXIDANT SYSTEM IN THE BRAIN OF POSTNATAL FEMALE MICE

Praveenkumar S. Kondaguli, Laxmi S. Inamdar (Doddamani)*

ABSTRACT

Abuse of Anabolic-androgenic steroids (AAS) by professional and recreational athletes for endurance
performance is increasing globally. Supraphysiological doses of AAS exert profound effects on mental state and
behavior viz., depression, anxiety, and oxidative stress. Present investigation elucidates chronic impact of one of
the AAS Stanozolol (ST) on acetylcholinesterase (AChE) enzyme activity and oxidative stress in the brain of
postnatal female mice Mus musculus. 20 animals (21-days-old) were randomly assigned into four experimental
groups (n=5) and ST was administered subcutaneously for 30 days: [Low-dose (LD)-0.5mg/kg, medium-dose
(MD)-5.0mg/kg and high-dose (HD)-7.5mg/kg bwt or 1% alcohol-baseline control]. Acetylcholinesterase enzyme
activity was determined by Ellman’s method. Oxidative stress marker Malondialdehyde (MDA), enzymatic
antioxidant Superoxide Dismutase (SOD) and non-enzymatic antioxidant Glutathione (GSH) were assayed, and
absorbance was recorded. Results demonstrate a notable reduction in the AChE enzyme activity in the entire
treatment group, subsequently leading to the accumulation of ACh level in synaptic clefts. This results in
impairment of neuronal transmission, which in turn affects the efficiency of cholinergic neurotransmission. An
elevation in oxidative stress marker MDA level (in MD & HD) and a decline in anti-oxidant levels of SOD (in
MD & HD) and GSH (in HD) ST-treated groups were observed. The results reveal that ST causes an imbalance
between antioxidants and free radicals, which may lead to oxidative damage by attenuating antioxidant enzymes.
It is inferred that Prolonged ST-treatment interferes with neuronal transmission, subsequently resulting in neuronal
disorders, viz., stress-related anxiety, memory loss, and other cognitive behavioral abnormalities. Prolonged STtreatment
elevates oxidative stress marker MDA and a decline in antioxidants, leading to an imbalance in the local
antioxidant system thereby disrupting cellular redox balance in the brain.

Keywords: AChE activity, anti-oxidant levels, brain, stanozolol, Mus musculus.