Low level developmental lead exposure decreases the sensitivity, amplitude and temporal resolution of rods.
Electroretinographic (ERG), morphometric and biochemical studies on retinas from monkeys or rats reveal that moderate level developmental lead (Pb) exposure produces long-term selective rod deficits and degeneration. The present studies determined whether similar alterations occur following low level developmental Pb exposure. Long-Evans rats, exposed to Pb only via dam's milk from parturition to weaning, had mean blood Pb of 18.8 micrograms/dl at weaning and 6.6 micrograms/dl at 90 days of age. Morphometric and ultrastructural studies revealed no signs of rod loss or degeneration although the presence of glycogen in some rod mitochondria suggests the occurrence of a metabolic dysfunction. Retinal sensitivity and rhodopsin content per eye were decreased in a manner such that, they followed the established log-linear relationship. A- and b-wave voltage- and latency-log intensity functions, generated from single-flash ERGs in fully dark-adapted rats, revealed that low level Pb exposure caused a 25% and 15% decrease in mean amplitude, a 0.5 and a 0.5 log unit decrease in absolute sensitivity, and a 23% and 16% increase in mean latency, respectively. Scotopic (rod-mediated) and photopic (cone-mediated) flicker fusion frequency measures revealed selective rod deficits. Adult rats had a 15% inhibition of retinal cGMP-phosphodiesterase resulting in a 19% and 12% increase in cGMP in dark- and light-adapted states, respectively. The above data confirm and extend our previous studies conducted in rats with blood lead levels of 59 micrograms/dl during development. The rhodopsin and cyclic nucleotide metabolism data, as well as our recent data showing an inhibition of retinal Na+, K(+)-ATPase, are entirely consistent with the observed ERG changes. The fact that rat rods are similar to monkey and human rods suggests the relevance and applicability of these data to low level pediatric Pb poisoning. Thus, these data suggest that alterations in rod sensitivity and temporal processing may occur in children exposed to low levels of lead during perinatal development.
Fox
D A
DA
College of Optometry, Department of Biochemical and Biophysical Sciences, University of Houston, Texas 77204-6052.
Katz
L M
LM
Farber
D B
DB
D000818:Animals; D006152:Cyclic GMP / Q000378:metabolism*; D004596:Electroretinography; D005260:Female; D007855:Lead Poisoning / Q000378:metabolism* / Q000473:pathology; D008854:Microscopy, Electron; D010786:Photoreceptor Cells / Q000187:drug effects* / Q000254:growth & development / Q000648:ultrastructure; D051381:Rats; D012243:Rhodopsin / Q000378:metabolism*; D012374:Rod Cell Outer Segment / Q000187:drug effects* / Q000254:growth & development / Q000648:ultrastructure; D012680:Sensitivity and Specificity; D013997:Time Factors
D012243:Rhodopsin; D006152:Cyclic GMP