Sustained Functioning Impairments and Oxidative Stress with Neurobehavioral Dysfunction Associated with Oral Nicotine Exposure in the Brain of a Murine Model of Ehrlich Ascites Carcinoma: Modifying the Antioxidant Role of Chlorella vulgaris

SIMPLE SUMMARY: Nicotine is the major psychoactive component considered to underlie tobacco’s addictive nature, and its dependence has been linked to several drawbacks on behavior and brain health. The purpose of this study was to investigate the mechanisms triggered by oral nicotine that cause brain tissue damage, as well as the supportive role of Chlorella vulgaris microalgae supplementation in Ehrlich ascites carcinoma in mice. The results revealed pronounced neurobehavioral alterations, increased mortality rate, oxidative stress, DNA damage, and augmented inflammatory response in the brain tissue alongside the microstructural alteration caused by nicotine. Chlorella vulgaris was quite successful in reducing the negative effects of nicotine. It acts as an antioxidant anti-inflammatory and restores nearly normal tissue architectures. As a result, we believe it should be supplemented to cancer patients consuming regular nicotine doses. ABSTRACT: Background: This study provides a model for studying the mechanism(s) responsible for the nervous tissue damage and misfunctioning that occurred due to oral nicotine exposure, considered a stress factor, during the presence of Ehrlich ascites carcinoma bearing in the mouse model (EAC). The mitigating role of Chlorella vulgaris (CV) against nicotine-induced brain damage was evaluated. Methods: Eighty Swiss female mice were classified into four groups, these were the control, the CV group, the nicotine group(100 µg/kg), and the combination group. Oxidant/antioxidant status, proinflammatory cytokines levels, DNA damage, quantitative microscopical lesions, and Caspase 3, Bcl-2 proteins were assessed in the current study. Levels of dopamine (DA) and gamma-aminobutyric acid (GABA) were also evaluated. Results: Nicotine was found to cause pronounced neurobehavioral alterations, increase the mortalities oxidative stress DNA damage, and augment the inflammatory response in brain tissue alongside the microstructural alteration. The administration of CV with nicotine in EAC-bearing mice rescued the detrimental effects of nicotine. Conclusions: CV aids in reducing the harmful effects of nicotine and returns the conditions caused by nicotine to near-control levels. Thus, we are in favor of giving it to cancer patients who are taking daily dosages of nicotine even by smoking cigarettes or being exposed to second-hand smoke.