Acute aluminum chloride toxicity revisited: Study on DNA damage and histopathological, biochemical and neurochemical alterations in rat brain

Abstract

Aims: Due to rapid increase in industrialization in the last few years, use of aluminum (Al) and its alloys have been increased in different industrial fields. Ample evidence supports the neurotoxic effects of chronic aluminum chloride (AlCl3) administration in rats but acute Al toxicity has been less described so the present study was aimed to investigate the neurotoxic effects of acute AlCl3. Main methods: To investigate such effects 12 male albino Wistar rats were randomly divided into control and test rats. AlCl3 at a dose of 150 mg/kg was intraperitoneally injected to test rats for 7 days. Rats were subjected to behavioral assessments 24 h after last dose and after behavioral assessment rats were sacrificed to collect brain samples for further neurochemical, biochemical and histopathological examinations. Key findings: In the present study acute administration of AlCl3 resulted in noticeable behavioral deficits. Cognitive deficits and neuropsychiatric disturbances were evident in AlCl3 injected rats. Test rats also exhibited marked antioxidant enzymes, cholinergic, serotonergic and dopaminergic dysfunctions and DNA fragmentation. Histopathological alterations were observed in hippocampus and cortex of rats injected with AlCl3. Significance: The observed effects may be due to pro‐oxidant nature of Al and its participation in free radical mediated cellular injury. Al by promoting oxidative stress, impairing antioxidant defense system and altering brain neurochemistry may act as a potent neurotoxic agent as evident from observed histopathological alterations in brain of test rats. This investigation may further confirm and shed some more light on deleterious effects of acute Al intoxication on brain.