Objective: Although copper is an essential micronutrient involved in a variety of biological processes indispensable for sustaining life yet it can be toxic when administered in excess. Material and Methods: Thirty six adult male albino rats were equally divided into three groups; the first group was used as a negative control, the second group   received normal saline intraperitoneal (positive control group) and the third group received copper chloride 7mg/kg twice weekly intraperitoneal for 8 weeks (treated group). At the end of the experimental period, blood was withdrawn for measuring serum malondialdhyde (MDA) and catalase (CAT), then the rats were sacrificed and the brain was examined by light microscope for detecting histopathological changes. Brain sections were examined immunohistochemically for the detection of the apoptotic BaX protein and finally, the bone marrow was examined for detection of chromosomal aberrations. Results:  In Cu chloride treated group (group III), there was a significant elevation in serum malondialdehyde & a significant decrease in serum catalase.  Histopathological changes were in the form of increased cellularity of astrocytes, swelling of astrocytes that showed dense eosinophilic cytoplasm, with pyknotic nuclei and multiple apoptotic bodies. Also, there were degenerated neurons with deep eosinophilc cytoplasm using light microscope and BaX showed strong immunoreactions in the brain. Bone marrow showed significant increase in all types of chromosomal aberrations after 8 weeks of Cu chloride treatment. Conclusion: From the previous results, it can be concluded that Cu chloride exposure can induce oxidative stress changes in the form of a significant increase in MDA and significant decrease in CAT enzyme as well as histopathological changes in the brain and genotoxicity in adult male albino rats after short term exposure.