Lutein and Zeaxanthin abated neurobehavioral, neurochemical and oxido-inflammatory derangement in rats intoxicated with aflatoxin B1

Toxicon. 2025 Apr 5:108345. doi: 10.1016/j.toxicon.2025.108345. Online ahead of print.

ABSTRACT

Aflatoxin B₁ (AFB₁), a mycotoxin commonly present in feed, has several toxic effects. AFB₁ seems to have a neurotoxic effect that leads to neurobehavioral impairment. On the other hand, Lutein and Zeaxanthin (LUT/ZEA) have antioxidant and anti-inflammatory effects. Here, we aimed to compare the effects of AFB₁ and the co-treatment with LUT/ZEA on neurobehavioural and biochemical changes viz-a-viz oxido-inflammatory response in male rats’ hippocampal and pre-frontal cortexes. Experimental rats of the Wistar strain (n= 40) were randomly grouped into treatment cohorts: Control (corn oil 2mL/Kg), AFB₁ (75 μg/kg), LUT/ZEA only (100 mg/kg), AFB₁ + LUT/ZEA (75 μg/kg + 100mg/kg), and AFB₁ + LUT/ZEA (75 μg/kg + 200 mg/kg). All groups were administered their respective treatment orally for 28 days, while behavioural tests were conducted using open field tests (OFT), Y-maze, novel object tests (NORT), and forced swim tests (FST) 1 hour after treatment on day 26-28. The animals were euthanized on day 29. In the hippocampal and pre-frontal cortex, antioxidant indicators (SOD, CAT, GSH, GST, GPx, TSH), inflammatory mediators (XO, NO, MPO), and acetylcholinesterase activity were measured. Our finding presents the anti-oxidant effect of lutein/Zeaxanthin in the brains of AFB₁-intoxicated rats, indicating better cognitive and spatial memory capacity in Y-maze and NORT, an improvement in locomotive and explorative behaviour in OFT and reduction in anxio-depressive-like behaviour in LUT/ZEA co-treated rats. Acetylcholinesterase activity was enhanced in LUT/ZEA co-treated rats. LUT/ZEA co-treatment dampened oxido-inflammatory mediators by decreasing XO, NO, and MPO levels and increasing antioxidant activities (SOD, CAT, GSH, GST, GPx, TSH) in the prefrontal and hippocampal cortices. We surmise that mechanistically, co-treatment with LUT/ZEA effectively lessened AFB₁ neurotoxicity through anti-inflammatory and antioxidant pathways and essentially improved the experimental rats’ neurobehavioural outcomes.

PMID:40194634 | DOI:10.1016/j.toxicon.2025.108345