Abstract
Although the precise mechanism is unknown, neuron apoptosis is believed to participate in neuropathy caused by acrylamide (ACR). Telomerase reverse transcriptase (TERT) exhibits an anti-apoptotic function, but its contribution to the pathogenesis of ACR neurotoxicity is unclear. We investigated adult male rats that were given 30, 40 and 50 mg/kg ACR three times/week for 4 weeks. We found that ACR treatment caused significant deficits in sensory/motor function as measured by gait score, landing foot spread distance, movement initiation test and tail immersion test. Histological examination showed that the cerebral cortex in all ACR treated animals exhibited fewer neurons and more condensed nuclei than normal cortex. A significant increase in apoptosis was found in the cerebral cortex of rat brains subjected to ACR treatment in a dose-dependent manner. The expression of TERT in the brain was significantly reduced by ACR treatment. The pro-apoptotic cleaved caspase-3 protein level was increased, while the anti-apoptotic Bcl-2 protein level was decreased by 30 − 50 mg/kg ACR. Our findings indicate that TERT and its downstream regulators of neuron apoptosis, including Bcl-2 and cleaved caspase-3, were involved in ACR neurotoxicity.
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