Oxidant handling by hippocampus and Hebb‑William maze performance in aluminum‑exposed albino Wistar rats

Prasunpriya Nayak; Shiv Bhushan Sharma; Nadella Vijaya Subbaraya Chowdary

Prasunpriya Nayak Department of Physiology, NRI Medical College and General Hospital, Chinakakani, Mangalagiri Mandal, Guntur District, Andhra Pradesh‑522 503, India.
Shiv Bhushan Sharma Department of Physiology, Chettinad Hospital and Research Institute, Kelambakkam, Tamil Nadu, India
Nadella Vijaya Subbaraya Chowdary Department of Biochemistry, NRI Medical College and General Hospital, Chinakakani, Mangalagiri Mandal, Guntur, Andhra Pradesh, India

Keywords: Aluminum, Hebb‑William maze, Hippocampus, Neuro‑degeneration, Oxidative stress, Superoxide and peroxide handling capacity

Abstract

Background and Aim: Extensive use of aluminum in modern life made its exposure unavoidable. Hippocampus, a crucial brain structure involved in cognitive function is one of the preferred sites of aluminum accumulation. Oxidative stress was a common observation in neurodegenerative disorder (NDD) and aluminum toxicity. Therefore, the present study was planned to evaluate the association between oxidant handling capacity of hippocampus and aluminum‑induced neurotoxicity. Methods: Groups of 6 Wistar rats were administered with aluminum and concomitant exposure to different doses of pro‑oxidant (ethanol) for 4 weeks. Neurobehavioral performances in Hebb‑William Maze (HWM) were evaluated weekly. Oxidative stress and oxidant handling capacity of hippocampus were evaluated biochemically. Degenerative changes and deposition of aluminum in hippocampus was studied histologically. Two‑way analysis of variance (ANOVA) with replication and Tukey’s honest significant difference (HSD) test were performed for intergroup differences. Results: Progressive deterioration of HWM performances was noted during the study period. Degenerative changes were boosted by aluminum and ethanol exposure but there was no indication of ethanol‑induced enhancement of aluminum accumulation. No significant alteration in hippocampal oxidative stress parameter was observed upon exposure to either aluminum alone or in presence of pro‑oxidant dominance. Conclusion: The current dose and duration of aluminum exposure neither altered the oxidant status of rat hippocampus nor its oxidant handling capacity. Presence of concomitant exposure to ethanol caused decrement of superoxide and peroxide handling capacity (SPHC), in lower doses but not in higher doses, which demonstrated higher degree of degenerative changes. Therefore, the oxidative stress is not the only mechanism leading to hippocampal degeneration; in fact it might be a signaling mechanism to prevent oxidative stress faced by hippocampus.