Epidemiological studies have correlated arsenic exposure to various learning deficits and cognitive impairment in children in Bangladesh, West Bengal, and Mexico, as well as in adults in Texas, USA. Despite clear evidence that arsenic is a developmental neurotoxicant, the molecular mechanisms for the increased risk of cognitive and memory impairment remains unclear. A number of animal studies have focused on explaining neurotoxic effects of arsenic from prenatal exposure, as well as exposure in young adults. However, some may be questionable due to exposures greatly exceeding possible human exposures. In rats, prenatal and early life exposure to 100 mg/L arsenic in drinking water decreased neuromotor reflexes and produced deficits in learning. Studies in adult rats fed 20 mg/kg of arsenic in chow or exposed to 68 mg/L of the toxicant in water, demonstrated impaired learning and memory, changes in dopamine levels and alteration of ultra-structural brain morphology. A study in mice that used human relevant perinatal exposures, demonstrated arsenic increased learned helplessness and reduced performance in forced swim tests. In addition, in utero exposure to 50 mg/L impaired learning and memory of adult offspring. However, few molecular details have been provided to explain the pathogenic mechanisms resulting from in utero or adult exposure to arsenic. There is currently an intense focus on epigenetic regulation of phenotypes to identify chronic enhancement of disease risk resulting from arsenic exposure during discrete developmental windows. Arsenic is the only environmental toxicant that Reversine side effects causes changes in all three epigenetic markers �C DNA methylation, histone modifications and expression of noncoding RNAs. Since arsenic is extensively methylated during its metabolism, numerous studies have addressed changes in DNA and histone methylation with confounding results. Interestingly, in a report on global changes in histone modifications, a decreased acetylation of H3K9 was observed in peripheral mononuclear cells of workers exposed to arsenic. The link, however, Z-VAD-FMK between changes in epigenetic signals from arsenic exposure and changes in phenotypes linked to disease later in life are not well defined. In this report we present the results of a study undertaken to reveal arsenic-induced changes in enrichment of epigenetic marks in brain samples of offspring with in utero arsenic exposures. Chromatin immunoprecipitation followed by massive parallel sequencing using an antibody against acetylated lysine 9 of histone 3 was applied to evaluate the differences in H3K9 acetylation pattern genome-wide and to compare Gene Ontology terms and functional annotations of affected genes between exposed and control pups. We also present the results of behavioral testing conducted with young adult C57BL/6J mice exposed to human-relevant levels of arsenic. We performed a battery of tests which included three separate behavioral paradigms, novel object recognition and contextual fear conditioning) to test cognitive changes due to arsenic treatment. These tasks are widely applied for evaluation of cognitive and memory changes associated with therapeutic treatments and/or evaluation of neurotoxicity in rodents, particularly in young adults. We utilized the RWM to assess spatial learning and working memory function.