BIOMEDICAL AND ENVIRONMENTAL SCIENCES 21, 144-149 (2008) www.besjournal.com Impacts of Passive Smoking on Learning and Memory Ability of Mouse Offsprings and Intervention by Antioxidants JIE YANG # , LI-NA JIANG + , ZHEN-LI YUAN + , YU-FEI ZHENG + , LU WANG # , MIN JI * , ZHI-QIANG SHEN * , XIN-WEI WANG * , QIANG MA * , ZHU-GE XI * , AND JUN-WEN LI *,1 # Chinese Center for Disease Control and Prevention, Beijing 100050, China; + School of Public Health, Jilin University, Changchun 130021, Jilin, China; * Medical Institute of Environment and Health, Tianjin 300050, China Objective To determine the impact of passive smoking and the protective effect of antioxidants such as vitamin E and quercetin on learning and memory ability of mouse offsprings. Methods A passive smoking model of pregnant mice was established. Learning and memory ability was evaluated by the water maze test and long term potentiation (LTP). Nitric oxide (NO), content, nitric oxide synthase (NOS), acetylcholinesteras (Ache) activity in brain, vitamin E concentration, and reactive oxygen species (ROS) in serum were determined. The latency period (the time during which the mice swim from the starting position to the ending position) and errors (the number of mice entering the blind end) in control and antioxidant intervention groups were compared with those in the smoke exposure group after 6 days. Results The latency period as well as errors in the air, control diet, tobacco smoke (TS), and vitamin E diet groups were decreased significantly as compared with the TS and control diet groups (P<0.05). LTP was restrained in the TS and control diet groups. LTP in all the antioxidant diet groups was significantly increased compared with the TS and control diet groups. In addition, NOS and acetylcholinesteras (Ache) activitiy was significantly higher in the TS and control diet groups than in the air and control diet group. NO content was not significantly different among the different groups, and significantly lower in the TS and vitamin E diet groups than in the TS group, control diet group, quercetin diet group, and mixture diet group (P<0.05). Vitamin E concentration and ROS activity in serum were correlated with the outcome of water maze and LTP. Conclusion Passive smoking reduces LTP formation by disturbing the hippocampus function of mice, by decreasing NOS and Ache activity and increasing NO content. Antioxidants (especially vitamin E) partially improve the learning and memory ability of offsprings whose mothers are exposed to tobacco smoke during pregnancy. Key Word: Passive smoking; Mice offspring, Learning and memory ability; Long term potentiation; Antioxidant intervention REFERENCES 1. Perera F P, Jedrychowski W, Rauh V, et al. (1999). Molecular epidemiologic research on the effects of environmental pollutants on the fetus. Environ Health Perspect 107, 451-460. 2. Roy T S, Seidler F J, Slotkin T A (2002). Prenatal Nicotine Exposure Evokes Alterations of Cell Structure in Hippocampus and Somatosensory Cortex. JPET 300, 124-133. 3. WHO. Global tobacco treaty enters into force with 57 countries already committed. 2005, GENEVA.http//www.who.int/tobacco, 2005-2-24. 4. Yang G H, Ma J M, Liu N, et al. (2005). Smoking and passive smoking in Chinese, 2002. Chin J Epidemiol 26, 77-83. (In Chinese) 5. Yang W R, Wang Z Z (2003). The relationship of infant respiration infection and family smoke in Wu Han China. Maternal and Child Health Care of China 18, 108-110. (In Chinese) 6. Cui G C, Ye G L (2002). Recent advances in the study of long-term potentiation (Part I). Nervous Diseases and Mental Hygiene 2, 179-182. 7. Brenda M, Larry R S, Eric P K (1998). Cognitive neuroscience and the study of memory. Neuron 20, 445-468. 8. Geddes D M, LaPlaca M C, Cargill R S (2003). Susceptibility of hippocampal neurons to mechanically induced injury. Experimental Neurology 184, 420-427. 9. Squire L R (1992). Memory and the hippocampus: a synthesis from findings with rats, monkeys and humans. Psychol Rev 99, 195-231. 10. Siwinska E, Mielzynska D, Bubak A, et al. (1999). The effect of coal stoves and environmental tobacco smoke on the level of urinary 1-hydroxypyrene. Mutat Res 445, 147-153. 11. Coyle J T, Puttfarcken P (1993). Oxidative stress, glutamate, and neurodegenerative disorders. Science 262, 689-695. 12. Xie Z, Sastry B R (1995). Impairment of long-term potentiation in rats fed with vitamin E deficient diet. Brain Res 681, 193-196. 13. WANG X R (2003). Experimental method and technology of Toxicology. People’ Medicine Publishing House, Beijing, pp, 1 Correspondence should be addressed to Dr. Jun-Wen LI, Medical Institute of Environment and Health, Tianjin 300050, China. Tel: 86-22-84655418. Fax: 86-22-23328809. E-mail: jlccyangjie@yahoo.com.cn Biographical note of the first author: Jie YANG, male, born in 1965, M. D., majoring in environmental health. 0895-3988/2008 CN 11-2816/Q Copyright © 2008 by China CDC 144