ABSTRACT
The organolead compounds of prime concern from the standpoint of the pathological changes that they cause are the short-chain tetraalkylleads (R4Pb) used as antiknocking agents in petrol, namely, tetraethyllead, tetramethyllead, and various mixed tetraalkyls. The R4Pb compounds are intrinsically nontoxic and have to be converted in the liver by the microsomal mixed-function oxygenase system to the active trialkyl forms for toxicity to occur. Neuronal necrosis characterized by eosinophilia and pyknosis was first observed in the pyriform cortex within 24 hr after administration and before the appearance of hypermotility and hypersensitivity. Since the original description of the model, many workers have reproduced the encephalopathy caused by dietary supplementation of the young rat with inorganic lead salts. The action of the triethyltin, therefore, appears to be specifically on the oligodendroglial cell, while that of the trimethyltin is essentially on groups of neurons in specific regions of the forebrain.
