Morphometric analysis of brain lesions in rat fetuses prenatally exposed to low-level lead acetate: correlation with lipid peroxidation.
The effect of prenatal lead acetate exposure was studied microscopically together with the concentration of lead and lipid fluorescent products (LFP) in the brain of rat fetuses. Wistar rats were intoxicated with a lead solution containing either 160 or 320 ppm of lead acetate solution during 21 days through drinking water. The control group (ten rats) received deionized water for the same period. The rats were killed on gestation day 21 and fetuses were obtained; the placenta, umbilical cord and parietal cortex (Cx), striatum (St), thalamus (Th) and cerebellum (Ce) were collected for measuring tissue lead concentration, LFP as an index of lipid peroxidation and histopathologic examination. Lead contents were increased in placenta, umbilical cord, St, Th and Cx in both lead-exposed groups. Lead exposure increased (LFP) in placenta and umbilical cord, St, Th and Ce as compared to the control group. Histopathological examination showed severe vascular congestion in placenta, the Cx, St, Th and Ce with hyperchromatic and shrunken cells. Interstitial oedema was found in all regions studied of both lead exposed groups. The morphometric evaluation of the studied brain regions showed an absolute decrease in total cell number and increased number of damaged cells and interstitial oedema. Our results show that morphological changes in rat brain are correlated with increased lipid peroxidation, and the lead levels of the umbilical cord, however it is not clear whether oxidative stress is the cause or the consequence of these neurotoxic effects of lead.
Villeda-Hernández
J
J
Laboratory of Neurodegenerative Diseases, Instituto Nacional de Neurología y Neurocirugía Manuel Velasco Suarez, Mexico. villeda_2606@yahoo.com.mx
Méndez Armenta
M
M
Barroso-Moguel
R
R
Trejo-Solis
M C
MC
Guevara
J
J
Rios
C
C
D000818:Animals; D001921:Brain / Q000187:drug effects* / Q000196:embryology* / Q000378:metabolism / Q000473:pathology; D001923:Brain Chemistry / Q000187:drug effects; D001929:Brain Edema / Q000473:pathology; D002531:Cerebellum / Q000737:chemistry / Q000196:embryology / Q000378:metabolism / Q000473:pathology; D002540:Cerebral Cortex / Q000737:chemistry / Q000196:embryology / Q000378:metabolism / Q000473:pathology; D003342:Corpus Striatum / Q000737:chemistry / Q000196:embryology / Q000378:metabolism / Q000473:pathology; D005260:Female; D006651:Histocytochemistry; D007854:Lead / Q000032:analysis / Q000097:blood; D015227:Lipid Peroxidation / Q000187:drug effects*; D008055:Lipids / Q000032:analysis; D009942:Organometallic Compounds / Q000633:toxicity*; D010920:Placenta / Q000737:chemistry / Q000378:metabolism / Q000473:pathology; D011247:Pregnancy; D011297:Prenatal Exposure Delayed Effects; D049188:Prenatal Injuries / Q000139:chemically induced / Q000378:metabolism / Q000473:pathology*; D051381:Rats; D017208:Rats, Wistar; D013788:Thalamus / Q000737:chemistry / Q000196:embryology / Q000378:metabolism / Q000473:pathology; D014470:Umbilical Cord / Q000737:chemistry / Q000378:metabolism / Q000473:pathology
D008055:Lipids; D009942:Organometallic Compounds; D007854:Lead; C008261:lead acetate