Protective effects of pre-germinated brown rice diet on low levels of Pb-induced learning and memory deficits in developing rat.
Lead (Pb) is a known neurotoxicant in humans and experimental animals. Numerous studies have provided evidence that humans, especially young children, and animals chronically intoxicated with low levels of Pb show learning and memory impairments. Unfortunately, Pb-poisoning cases continue to occur in many countries. Because the current treatment options are very limited, there is a need for alternative methods to attenuate Pb toxicity. In this study, the weaning (postnatal day 21, PND21) rats were randomly divided into five groups: the control group (AIN-93G diet, de-ionized water), the lead acetate (PbAC) group (AIN-93G diet, 2g/L PbAC in de-ionized water), the lead acetate+WR group (white rice diet, 2g/L PbAC in de-ionized water; PbAC+WR), the lead acetate+BR group (brown rice diet, 2g/L PbAC in de-ionized water; PbAC+BR) and the lead acetate+PR group (pre-germinated brown rice diet, 2g/L PbAC in de-ionized water; PbAC+PR). The animals received the different diets until PND60, and then the experiments were terminated. The protective effects of pre-germinated brown rice (PR) on Pb-induced learning and memory impairment in weaning rats were assessed by the Morris water maze and one-trial-learning passive avoidance test. The anti-oxidative effects of feeding a PR diet to Pb-exposed rats were evaluated. The levels of reactive oxygen species (ROS) were determined by flow cytometry. The levels of 8-hydroxy-2-deoxyguanosine (8-OHdG), gamma-aminobutyric acid (GABA) and glutamate were determined by HPLC. Our data showed that feeding a PR diet decreased the accumulation of lead and decreased Pb-induced learning and memory deficits in developing rats. The mechanisms might be related to the anti-oxidative effects and large amount of GABA in PR. Our study provides a regimen to reduce Pb-induced toxicity, especially future learning and memory deficits in the developing brain.
Zhang
Rong
R
Department of Occupational Health and Environmental Health, School of Public Health, Hebei Medical University, Zhongshan East Road 361, Shijiazhuang 050017, Hebei, People's Republic of China.
Lu
Hongzhi
H
Tian
Su
S
Yin
Jie
J
Chen
Qing
Q
Ma
Li
L
Cui
Shijie
S
Niu
Yujie
Y
D000080242:8-Hydroxy-2'-Deoxyguanosine; D000818:Animals; D001921:Brain / Q000187:drug effects / Q000378:metabolism; D003849:Deoxyguanosine / Q000031:analogs & derivatives / Q000032:analysis; D004032:Diet; D005260:Female; D018698:Glutamic Acid / Q000032:analysis; D005979:Glutathione Peroxidase / Q000378:metabolism; D007854:Lead / Q000097:blood; D007855:Lead Poisoning / Q000517:prevention & control*; D008297:Male; D008315:Malondialdehyde / Q000032:analysis; D018782:Maze Learning / Q000187:drug effects*; D008568:Memory / Q000187:drug effects*; D012275:Oryza; D051381:Rats; D017207:Rats, Sprague-Dawley; D017382:Reactive Oxygen Species / Q000378:metabolism; D013482:Superoxide Dismutase / Q000378:metabolism; D005680:gamma-Aminobutyric Acid / Q000032:analysis
D017382:Reactive Oxygen Species; D007854:Lead; D018698:Glutamic Acid; D008315:Malondialdehyde; D005680:gamma-Aminobutyric Acid; D000080242:8-Hydroxy-2'-Deoxyguanosine; D005979:Glutathione Peroxidase; D013482:Superoxide Dismutase; D003849:Deoxyguanosine