|LIM, SUN-YOUNG - BUSAN, KOREA
|DOHERTY, JOHN - USEPA, WASH. D.C.
|MCBRIDE, KATHLEEN - NIH, BETHESDA, MD
|CARMONA, GILBERTO - NIH, BETHESDA, MD
|STARK, KEN - NIH, BETHESDA, MD
|SALEM, JR, NORMAN - NIH, BETHESDA, MD
Submitted to: Journal of Nutrition
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 2/17/2005
Publication Date: 2/17/2005
Citation: Lim, S., Doherty, J.D., Mcbride, K., Miller-Ihli, N.J., Carmona, G.N., Stark, K.D., Salem, Jr, N. 2005. Lead exposure and (n-3) fatty acid deficiency during rat neonatal development affect subsequent spatial task performance and olfactory discrimmination. Journal of Nutrition. 135(5): 1019-26.
Interpretive Summary: We were asked to collaborate on this project because NIH did not have the expertise in-house to do low-level lead determinations of very small samples. We provided specialized analytical expertise needed for this project determining very low levels of lead in water and reagents used for the study and also analyzing both baseline levels of lead as well as elevated levels of lead in very (mg) small samples. All work was done in a clean laboratory using graphite furnace atomic absorption spectrometry (GFAAS). Only half a brain was received for each analysis and careful handling was required to ensure the integrity of the sample and avoid sample contamination. This work shows that the lead concentration of brains were approximately equal for rats at weaning and at maturity, regardless of whether or not they received docosahexanoic acid (22:6n-3, DHA) with their lead treatment. Both lactational lead exposure and n-3 deficiency led to behavioral deficits. This is important when considering risks associated with lead exposure for children since not only can lead produce neurological deficits but they can be magnified by a fatty acid deficiency (low DHA). This work is important to nutritionists and those interested in characterizing neurological effects of lead exposure and/or fatty acid deficiency on children.
Technical Abstract: Docosahexaenoic acid (22:6n-3, DHA) is important for optimal infant central nervous system development and Pb exposure during development can produce neurological deficits. The effect of Pb exposure on behavioral deficits and evaluation whether n-3 fatty acid deficiency exacerbates these effects was studied. Rats were fed either an n-3 deficient (DEF) diet or an adequate (ADQ) diet through two generations. At the birth of the second generation, the dams were subdivided into four groups and supplied drinking water containing either 1100 ppm lead (Pb) or sodium (Na) acetate until weaning. Rats were sacrificed at weaning and maturity for brain Pb and fatty acid analysis. The DEF group rats had a 78% lower content of brain DHA as compared to the ADQ group with no effect of Pb exposure. At weaning, the lead content of the brains for the ADQ group and the DEF-Pb group were similar (1400 ng Pb/g brain) and that was also true at maturity (250 ng Pb/g brain). In behavioral testing, significant effects of Pb were observed in the Morris Water Maze probe trial and in two odor olfactory acquisition and olfactory-based reversal learning tasks. Significant effects of n-3 content in the diet were observed for olfactory based tasks. Both lactational lead exposure and n-3 deficiency led to behavioral deficits.