The Role of Histone H2B Acetylation Modification in Aluminum-Induced Cognitive Dysfunction.

Abstract

Aluminum (Al) is a low toxic trace element that can accumulate in the nervous system and induce cognitive disorders characterized by reduced learning and memory ability. Neuroepigenetic effects are structural changes in cellular function by the brain in response to environmental stimuli by altering the expression of specific genes and repressing normal cellular transcription, leading to abnormalities in a variety of biological processes within the nervous system and affecting neurobehavioral responses. One of the most important mechanisms of epigenetic control on chromatin shape is histone modification. In the present study, we established an offspring rat model of Al intoxication to investigate the changes in spatial learning and memory retention abilities and the relationship with histone H2B acetylation modification in rats exposed to different doses of Al over a long period of time. The results demonstrated that long-term AlCl3 staining resulted in decreased CBP gene and protein expression, increased HDAC3 gene and protein levels, as well as decreased histone H2B and acH2BK20 protein expression levels in the hippocampus of rats. In conclusion, long-term exposure to Al may vary the expression of histone H2B and acH2BK20 through the regulation of enzymes that specifically regulate histone acetylation, hence hastening the deterioration of the nervous system that impairs cognitive function.