Owumi_2025_Toxicon__108552

Aflatoxin B(1) (AFB(1)) is a mycotoxin known for its liver toxicity and cancer risk, as well as neurotoxic effects causing motor and cognitive issues in humans and animals. Ongoing research into protecting against AFB(1) damage has recently focused on antioxidant and anti-inflammatory agents. Gallic acid (GA), a low molecular weight triphenolic acid, demonstrates notable anti-oxidative and anti-inflammatory activities. Furthermore, Azithromycin (AZT), an antibiotic, has shown promise in mitigating inflammatory stress in experimental models. GA and AZT may help protect against AFB(1)-induced neurobehavioral deficits in rats. This experiment involved thirty-five rats randomly assigned to seven cohorts (n=5), over a 28-day treatment period. The study consisted of a control group given corn oil, a group exposed only to AFB(1), and groups that received GA, AZT, or combinations of these substances with AFB(1). The neurobehavioral status of the experimental rats was assessed using the Open Field Test (OFT) and Novel Object Recognition Test (NORT) on days 26 and 27, respectively. On day 28 following treatment, the Elevated Plus Maze (EPM), Y-maze, and Forced Swim Test (FST) were conducted. After behavioural evaluation, the rats were euthanised. The hippocampus and prefrontal cortex were dissected for biochemical analysis. Antioxidant enzyme activities (SOD, CAT, GPx, GST), GSH and TSH levels, acetylcholinesterase, and markers of oxidative stress (RONS, LPO) and inflammation (NO, MPO) were measured. AFB(1) exposure raised oxidative stress markers, MPO, and AChE activity, while lowering antioxidant enzymes in the hippocampus and prefrontal cortex, indicating notable neurotoxicity and signalling disruptions. Combined GA and AZT treatment improved antioxidant defence, reduced inflammation, and restored AChE activity. Neurobehavioral tests indicated better motor and cognitive function after AFB(1) exposure. These results suggest that GA and AZT together offer strong protection against AFB1-induced neurotoxicity via their antioxidant and anti-inflammatory effects.