Abstract
The aim of this study was to evaluate the effect of chronic formaldehyde (FA) exposure on the hippocampus in the chronic cerebral hypoperfusion rat model. Seventy-two male Sprague-Dawley rats were randomly divided into four groups: (A) sham-operated bilateral common carotid artery occlusion (BCCAO) with room air inhalation, (B) BCCAO with room air inhalation, (C) sham-operated BCCAO with FA inhalation at a concentration of 10 mL vapor m−3, 1 h per day for 90 days, and (D) BCCAO with FA inhalation. Decreased mobility, injected conjunctivae, and overreaction were observed in groups C and D rats after 30 days of FA exposure. The level of malondialdehyde (MDA) increased significantly in group D at 90 days after FA exposure. The expression of Bax protein increased, while Bcl-2 and NR2B proteins decreased significantly in group D compared to group B or C. Neuronal nuclear antigen (NeuN) positive cells decreased significantly in group D. Neuronal loss, oxidative stress, and the expression of proteins were more prominent at 90 days after FA exposure, especially in group D. Oxidative stress-induced neuronal damages in the hippocampus may be a possible mechanism of neurotoxicity as a result of chronic FA exposure. Chronic exposure of FA caused more neuronal damage in the chronic cerebral hypoperfusion rat model.
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