Enhanced brain regional lipid peroxidation in developing rats exposed to low level lead acetate.
Neurotoxicity associated with lead exposure may be the result of a series of small perturbations in brain metabolism, and, in particular, of oxidative stress. Some studies have suggested a lead-induced enhancement on lipid peroxidation as a possible mechanism for some toxic effects of lead. However, there are no reports about the association between lipid peroxidation enhancement and brain lead content. In this study, we determined the concentration of lead and the formation of lipid fluorescence products in the blood, as well as in the parietal cortex, striatum, hippocampus, thalamus, and cerebellum of rats exposed prenatally and postnatally to variable concentrations of lead acetate through drinking water. Pregnant Wistar rats were intoxicated throughout gestation with solutions containing either 320 or 160 ppm of lead. The pups were treated after birth in the same way until 45 days of age. Control animals received deionized water for the same period of time. The developing rats were sacrificed at postnatal day 45 and lead level was assessed biochemically in the blood and different brain regions. Results showed that blood lead levels were increased in a dose-dependent manner. In the brain, lead accumulated preferentially in the parietal cortex, striatum, and thalamus as compared to the control group, while lipid fluorescence products were significantly increased in the striatum, thalamus, and hippocampus of the treated animals. These data suggest that in the brain of rats exposed to lead acetate, lead produces a neurotoxic effect with a complex correlation with both lead regional content and lipid peroxidation.
Villeda-Hernández
J
J
Laboratorio de Neuromorfología Celular, Instituto Nacional de Neurología y Neurocirugía "M. Velasco Suárez", Mexico City, Mexico.
Barroso-Moguel
R
R
Méndez-Armenta
M
M
Nava-Ruíz
C
C
Huerta-Romero
R
R
Ríos
C
C
D000818:Animals; D001921:Brain / Q000187:drug effects* / Q000196:embryology / Q000254:growth & development; D002648:Child; D004781:Environmental Exposure / Q000009:adverse effects; D005260:Female; D006801:Humans; D020264:Lead Poisoning, Nervous System, Childhood / Q000378:metabolism* / Q000503:physiopathology; D015227:Lipid Peroxidation / Q000187:drug effects* / Q000502:physiology; D009474:Neurons / Q000187:drug effects* / Q000378:metabolism; D009942:Organometallic Compounds / Q000097:blood / Q000493:pharmacokinetics / Q000633:toxicity*; D018384:Oxidative Stress / Q000187:drug effects / Q000502:physiology; D011247:Pregnancy; D011297:Prenatal Exposure Delayed Effects; D051381:Rats; D017208:Rats, Wistar; D014874:Water Pollutants, Chemical / Q000493:pharmacokinetics / Q000633:toxicity
D009942:Organometallic Compounds; D014874:Water Pollutants, Chemical; C008261:lead acetate