The Protective Effect of Physalis peruviana L. Against Cadmium-Induced Neurotoxicity in Rats Ahmed E. Abdel Moneim & Amira A. Bauomy & Marwa M. S. Diab & Mohamed Tarek M. Shata & Ebtesam M. Al-Olayan & Manal F. El-Khadragy Received: 20 May 2014 /Accepted: 3 July 2014 /Published online: 15 July 2014 # Springer Science+Business Media New York 2014 Abstract The present study was carried out to investigate the protective effect of Physalis peruviana L. (family Solanaceae) against cadmium-induced neurotoxicity in rats. Adult male Wistar rats were randomly divided into four groups. Group 1 was used as control. Group 2 was intraperitoneally injected with 6.5 mg/kg bwt of cadmium chloride for 5 days. Group 3 was treated with 200 mg/kg bwt of methanolic extract of Physalis (MEPh). Group 4 was pretreated with MEPh 1 h before cadmium for 5 days. Cadmium treatment induced marked disturbances in neurochemical parameters as indicat- ing by significant (p <0.05) reduction in dopamine (DA), serotonin (5-HT), and 5-hydroxyindoleacetic acid (5-HIAA) in cerebellum, hippocampus, and cerebral cortex and en- hanced significantly (p <0.05) the levels of lipid peroxidation and nitric oxide in the brain. Cadmium treatment also de- creased the amount of nonenzymatic and enzymatic antioxi- dants significantly (p <0.05). Pretreatment with MEPh result- ed in significant (p <0.05) decreases in lipid peroxidation and nitric oxide levels and restored the amount of glutathione successfully. Although, preadministration of MEPh also brought the activities of cellular antioxidant enzymes, namely superoxide dismutase, catalase, glutathione peroxidase, and glutathione reductase significantly (p <0.05) to the control levels, as well as the levels of Ca 2+ , Cl - , DA, 5-HT, and serotonin metabolite, 5-HIAA. These data indicated that Physalis has a beneficial effect in ameliorating the cadmium- induced oxidative neurotoxicity in the brain of rats. Keywords Physalis peruviana L. . Cadmium . Neurotoxicity . Oxidative stress . Rats Introduction Cadmium (Cd) is a major toxic metal and represents an increasing risk for cancer as a pollutant of the environment at large. Inhalation of Cd fumes or dust is the main route in occupational exposure to Cd. It is widely used in industry as anticorrosive in plating metals and manufacturing stor- age batteries, alloys, stabilizer, and pigments. Also, it is absorbed in significant quantities from cigarette smoke. Therefore, Cd concentration has been widely increased in the environment [1, 2]. Cadmium accumulation in the human body is dangerous and may also be linked to osteomalacia, infertility, hepatotox- icity, and nephrotoxicity [1]. Due to its high blood-brain barrier permeability [3], neurological disorders such as learn- ing disabilities and hyperactivity in children may occur after Cd exposure [4]. Parkinsonism has been noticed by Okuda et al. [5] after acute exposure to Cd. The mechanism by which Cd induces neurological damage is partially known. Cd in- duces oxidative stress, which produces protein damage in neuronal cells [4] and subsequently neurodegeneration [5]. Cd is also known to enhance the production of free radicals A. E. Abdel Moneim Department of Biochemistry and Molecular Biology, Asturias Institute of Biotechnology, University of Oviedo, Oviedo, Spain A. E. Abdel Moneim (*) : A. A. Bauomy : M. F. El-Khadragy Department of Zoology and Entomology, Faculty of Science, University of Helwan, Cairo, Egypt e-mail: aest1977@hotmail.com M. M. S. Diab Department of Molecular Drug Evaluation, National Organization for Drug Control and Research (NODCAR), Giza, Egypt M. T. M. Shata Department of Internal Medicine, Division of Digestive Diseases, University of Cincinnati College of Medicine, Cincinnati, OH, USA E. M. Al-Olayan : M. F. El-Khadragy Department of Zoology, Faculty of Science, King Saud University, Riyadh, Saudi Arabia Biol Trace Elem Res (2014) 160:392–399 DOI 10.1007/s12011-014-0066-9