Abstract

The effects of acrylamide (ACR), a synthetic neurotoxic chemical compound on non-enzymatic and enzymatic stress markers and brain histopathology, were studied in Wistar rats. ACR (50 mg/300 ml) was ingested through drinking water on alternative days, and brain tissues were collected on the 13th and 27th days post-ingestion for analysis. Results revealed that ACR causes significant increase in non-enzymatic stress markers such as lipid peroxidation (P < 0.05) and nitric oxide (P < 0.05), but depletion of glutathione (P < 0.05). Enzymatic stress markers, glutathione peroxidase, and glutathione s-transferase activities significantly increased (P < 0.05) at the 13th day post-ingestion, but decreased at the 27th day. However, acetylcholine esterase activity dropped significantly (P < 0.05) at the 13th and 27th days post-ingestion. In addition, ACR induced histological changes in brain such as degeneration of pyramidal and glial cells, mild vacuolation of pyramidal cells, and spongiosis in glia cells on 13th day post-ingestion. On the 27th day, brain tissue necrosis and pyknosis, necrosis of neurons and neurophagia, focal gliosis, and demyelination of nerve fibers were observed. In conclusion, ACR influences non-enzymatic and enzymatic stress markers in brain tissue and induces neurodegeneration in Wistar rats.

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