Influence of cadmium chloride acute exposure on Alzheimer’s disease in rats: cytotoxicity and genotoxicity aspects

Abstract

<title>Abstract</title> Exposure to heavy metals poses grave environmental threats, with cadmium (Cd) being a particular concern. This study aimed to investigate the cytogenotoxicity effects of cadmium chloride (CdCl2) in an Alzheimer's disease (AD) rat model. Forty rats were divided into four groups: normal control, Cd-only, AD control, and AD + Cd. The AD groups received lipopolysaccharide (LPS) injections to induce the disease, while the Cd-only and AD + Cd groups received a single CdCl2 injection (3.5 mg/kg body weight). Behavioural, biochemical, and genetic analyses were conducted, along with histopathological examination of the hippocampus and cytogenetic assays on bone marrow cells. The results revealed that Cd exposure significantly impaired locomotor activity, increased acetylcholinesterase (AChE) gene expression, and elevated malondialdehyde (MDA) and catalase (CAT) levels in the AD + Cd group compared to the other groups. Histopathological analysis showed substantial hippocampal damage in the AD + Cd group. Furthermore, Cd significantly increased the frequency of micronuclei and chromosomal aberrations in the AD + Cd group, indicating heightened cytogenotoxicity. In conclusion, acute Cd exposure in an AD context can have detrimental effects at multiple levels, including behavioural, biochemical, histological, and genetic. These findings underscore the importance of understanding the interactions between environmental toxicants and neurodegenerative diseases to develop effective preventive and therapeutic strategies.