Thymoquinone Mitigates Behavioural Deficit, Oxidative Stress, and Neurohistological Changes in the Brain of Wistar Rats Triggered by Exposure to Lead Acetate

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Lead is an environmental toxicant with adverse effects on the nervous system. This study evaluated the effect of thymoquinone (TQ) on learning, memory, motor coordination, oxidative stress, and neurohistology in lead acetate (PbA)-exposed male Wistar rats. Thirty rats (120–160 g) were randomly assigned to six groups (n = 5). The control group received distilled water (0.2 mL/day, p.o.), the PbA group received 15 mg/kg of PbA (i.p./week), and the TQ group received 5 mg/kg of TQ (p.o.), while the three remaining groups concurrently received PbA+TQ (5 mg/kg), PbA+TQ (3.75 mg/kg), and PbA+TQ (2.5 mg/kg), for 56 days. Rats were subjected to memory (novel object recognition and step-down latency) and motor coordination (rotarod and prehensile studies) tests. Twenty-four hours after the last administration, they were euthanised by cervical dislocation. The supernatants of the hippocampal and cerebellar tissue homogenates were spectrophotometrically analysed for indications of oxidative stress, while the haematoxylin and eosin staining technique was used to examine the histomorphology of the hippocampus, cerebellum, and prefrontal cortex. TQ protected memory and locomotor activities and maintained hippocampal and cerebellar malondialdehyde concentration while maintaining glutathione, catalase, and superoxide dismutase activities from PbA-induced deficits. The co-administration of TQ also preserved the cytoarchitecture of the hippocampus, prefrontal cortex, and cerebellar cortex. In conclusion, TQ at 5 mg/kg improved learning, memory, motor coordination, oxidative status, and neurohistology in male Wistar rats that had been exposed to PbA

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