Prenatal malnutrition and lead intake produce increased brain lipid peroxidation levels in newborn rats

Abstract

Objectives: Prenatal malnutrition (M) and lead intoxication (Pb) have adverse effects on neuronal development; one of the cellular mechanisms involved is a disruption of the pro- and anti-oxidant balance. In the developing brain, the vulnerability of neuronal membrane phospholipids is variable across the different brain areas. This study assesses the susceptibility of different brain regions to damage by quitar tissue oxidative stress and lead quitar concentrations to determine whether the combined effect of prenatal malnutrition (M) and lead (Pb) intoxication is worse than the effect of either of them individually.

Methods: M was induced with an isocaloric and hypoproteinic (6% casein) diet 4 weeks before pregnancy. Intoxication was produced with lead acetate in drinking water, from the first gestational day. Both the M and Pb models were continued until the day of birth. Four brain regions (hippocampus, cortex, striatum, and cerebellum) were dissected out to analyze the lipid peroxidation (LP) levels in four groups: normally nourished (C); normally nourished but intoxicated with lead (CPb); malnourished (M); and M intoxicated with lead (MPb).

Results: Dam body and brain weights were significantly reduced in the fourth gestational week in the MPb group. Their pups had significantly lower body weights than those in the C and CPb groups. The PbM group exhibited significant increases of lead concentration and LP in all areas evaluated. A potentiation effect of Pb and M on LP was found in the cerebellum.

Discussion: This study provides information on how environmental conditions (intoxication and malnutrition) during the intrauterine period could differentially affect the development of neuronal plasticity and, in consequence, alter adult brain functions such as learning and memory.

Keywords:

• Lead
• Prenatal malnutrition
• Lipid peroxidation
• Neonatal brain
• Hypoproteinic diet

Acknowledgements

This study was supported by DGAPA-UNAM and CONACYT. The authors wish to thank A. Aguilar and M. García for technical assistance. We are grateful to M. Salas and S. Castro-Chavira for their invaluable suggestions on the manuscript and to D. Pless for proofreading.

Disclaimer statements

Contributors Each of the authors contributed equally to this paper.

Funding None.

Conflicts of interest There are no conflicts of interest to declare.

Ethics approval This work was approved by the Bioethics Comittee of the Instituto de Neurobiología de la Universidad Nacional Autónoma de México.