Lead and mercury toxicity and the rod light response

Lead and mercury have been reported to alter selectively the rod component of the electroretinogram, and to inhibit the phosphodiesterase in rod outer segments which may be responsible for generating the rods' light response. The authors have investigated the effect of lead and mercury on the voltage response to light of rods, and compared these effects with those of the phosphodiesterase inhibitor papaverine. Lead and mercury, like papaverine, slow the light response. In addition, papaverine increases the light response amplitude while lead decreases it. Mercury initially increases and then decreases the amplitude. The late decrease in amplitude produced by mercury is associated with rod degeneration: an effect which may mimic degenerative diseases in which the rod phosphodiesterase is insufficiently active. These results demonstrate that the changes of electroretinogram induced by lead and mercury can be accounted for by the changes in receptor potential these heavy metals produce. The changes in receptor potential seen are consistent with mercury inhibiting the rod phosphodiesterase, and with lead having an action in addition to phosphodiesterase inhibition.