198 F. MANNAA ET AL. Copyright © 2006 John Wiley & Sons, Ltd. J. Appl. Toxicol. 2006; 26: 198–206 JOURNAL OF APPLIED TOXICOLOGY J. Appl. Toxicol. 2006; 26: 198–206 Published online 3 January 2006 in Wiley InterScience (www.interscience.wiley.com). DOI: 10.1002/jat.1128 Protective role of Panax ginseng extract standardized with ginsenoside Rg3 against acrylamide-induced neurotoxicity in rats Fathia Mannaa, 1 Mosaad A. Abdel-Wahhab, 2, * Hanaa H. Ahmed 3 and Myung H. Park 4 1 Medical Physiology Department, National Research Centre, Dokki, Cairo, Egypt 2 Food Toxicology and Contaminants Department, National Research Centre, Dokki, Cairo, Egypt 3 Hormones Department, National Research Centre, Dokki, Cairo, Egypt 4 Ambo Institute, Seoul, Korea Received 4 March 2005; Revised 14 June 2005; Accepted 29 September 2005 ABSTRACT: Acrylamide (ACR) is an industrial neurotoxic chemical that has been recently found in carbohydrate-rich foods cooked at high temperatures. ACR was designated as a probable human carcinogen by IARC (1994) and USEPA (1988). Panax ginseng extract has efficacies such as anticancer, antihypertension, antidiabetes and antinociception. The objective of the current study is to evaluate the protective effects of Panax ginseng extract against ACR-induced toxicity in rats. Sixty adult Sprague Dawley female rats were divided into six groups included a control group, a group treated orally with ACR (50 mg kg -1 body weight; b.w.) for 11 days, a group treated orally with Panax ginseng extract (20 mg kg -1 b.w.) for 11 days and groups treated orally with Panax ginseng for 11 days before, during or after 11 days of ACR treatment. The results indicated that treatment with ACR alone resulted in a significant increase in lipid peroxidation level and LDH activity in brain homogenate as well as in serum CK activity, whereas it caused a significant decrease in SOD activity and a small but statistically insignificant decrease in Na + K + -ATPase activity in brain homogenate. Serum serotonin, corticosterone, T3, T4, TSH, estradiol, progesterone and plasma adrenaline were significantly decreased in ACR-treated rats. Treatment with Panax ginseng before, during or after ACR treatment reduced or partially antago- nized the effects induced by ACR towards the normal values of controls. It could be concluded that Panax ginseng extract exhibited a protective action against ACR toxicity and it is worth noting that treatment with Panax ginseng extract before or at the same time as ACR treatment was more effective than when administered after ACR treatment. Copyright © 2006 John Wiley & Sons, Ltd. KEY WORDS: acrylamide; Panax ginseng extract; ginsenoside; neurotoxicity; hormones; antioxidant; chemoprevention * Correspondence to: Dr M. A. Abdel-Wahhab, Department of Food Toxicology and Contaminants, National Research Centre, Dokki, Cairo, Egypt. E-mail: mosaad_attia@yahoo.com Introduction Acrylamide (ACR) is a water-soluble, vinyl monomer that has multiple chemical and industrial applications: e.g. waste water management, or processing. In addition, ACR is used extensively in molecular laboratories for gel chromatography (Tareke et al., 2002). In 2002 the Swedish National Food Authority reported the presence of elevated levels of ACR in certain types of food pro- cessed at high temperature (SNFA, 2002). Since then ACR has been found in a range of cooked and heat- processed foods in other countries, including Netherlands, Norway, Switzerland, United States, United Kingdom (Shelby, 2004). ACR is a well-documented neurotoxicant in both humans and laboratory animals. Subchronic, low-level occupational exposure of humans to ACR produces neurotoxicity characterized by ataxia, skeletal muscle weakness and numbness of the hands and feet (He et al., 1989; Deng et al., 1993). Early morphological studies suggested that both human and experimental neurotoxicities were mediated by cerebellar purkinje cell injury and by degeneration of distal axons in the PNS and CNS (Spencer and Schaumburg, 1974, 1977a, 1977b, 1979; Cavanagh, 1982). In addition to neurotoxicity, there are considerable experimental data from rodent studies that ACR produces reproductive toxicity (e.g. reduced litter size) and genotoxic effects (e.g. DNA strand breaks, dominant lethal mutation) (Working et al., 1987; Sega et al., 1989; Tyl et al., 2000a,b). Furthermore, studies of ACR-exposed laboratory animals have revealed an increased incidence of tumors in certain tissues, e.g. mammary gland fibroadenomas in female rats and tunica vaginalis mesotheliomas in male rats (Bull et al., 1984a,b; Johnson et al., 1986; Friedman et al., 1995).