Cytotoxicity and genotoxicity reveal the link between acute cadmium exposure and Alzheimer’s disease

Abstract

Abstract Environmental hazards of heavy metals impact living organisms greatly. This study aimed at investigating the cytogenotoxicity exerted by cadmium chloride (Cd) on Alzheimer’s disease (AD). Forty rats were classified into 2 equal sets: the first received normal saline i.p. for 7 days, then equally sub-classified, one group served as normal control, while the other served as Cd only, received 3.5 mg/kg b. wt. i.p. once, one hour after their last saline injection. The second set was allocated for AD induction, done by i.p. injection of lipopolysaccharide (LPS) 250 µg/kg b. wt. for 7 days, then equally sub-classified, one group served as AD control, while the other served as AD rats with Cd, 3.5 mg/kg b. wt. i.p. once, one hour after their last LPS injection. Four hours later, open field test was performed for all rats. Twenty-four hours after their last injection, rats were sacrificed to collect their brain hippocampi to study histopathological structure, acetylcholinesterase (AChE) gene expression, malondialdehyde (MDA) content and catalase (CAT) activity. Femoral bone marrow cells were harvested to undergo in-vivo micronucleus (MN) and chromosomal aberration assays. The outcomes entailed that Cd injection to AD rats significantly disturbed their locomotor activity, damaged the hippocampal histology, vanished neuronal survival count, increased AChE gene expression, MDA content and CAT activity when compared to other groups. Furthermore, Cd significantly elevated frequency of MN and elevated different types of chromosomal aberrations in AD rats. In conclusion, the study results evidenced that acute Cd exerted a tremendous harm to the AD case.