Hepatic plasma-membrane modifications in disease.

The idea that aberrant cell behaviour can be pinpointed to critical molecular modifications has gained elegant experimental support in studies showing specific nucleic and corresponding amino acid changes in inherited disorders in haemoglobin synthesis and structure. The realization that many physiological processes are membrane mediated, coupled with progress in knowledge of the structure and function of biological membranes, has encouraged many investigators to study membrane pathology. The plasma membrane is positioned strategically for modification by intraand extracellular factors. The easy availability and relative simplicity of erythrocyte membranes has already led to the demonstration of membrane changes in genetic and infectious diseases, and two recent examples include those detected in haemoglobinuria (Banga, Pinder, Gratzer, Linch & Huehns, 1979) and aRcr infection by malaria sporozoites (Wallach, 1979). The plasma membrane of nucleated cells, and especially those constituting tissues and organs, is a far more complex organelle. In addition to its various transport functions, the plasma membrane has been shown to be a primary site of action of polypeptide hormones, viruses, drugs and toxins. The plasma membrane’s outer surface is also a key component in controlling cell-cell interactions, as well as cell, organ and tissue specificity. The metabolic versatility of the hepatocyte is reflected at its cell surface, where the plasma membrane is differentiated into at least three major anatomical and functional regions. The plasma membrane at the blood-interfacing sinusoidal and bile-interfacing canalicular regions forms microvilli and these two regions are separated by smooth