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The mechanism responsible for the changes in serum and liver γ-glutamyl transpeptidase (γ-GT) activity was studied in a model of experimental hexachlorobenzene porphyria in rabbits. Porphyria followed the administration of hexachlorobenzene in doses of 280 μmol • kg^-1 body weight, which were given daily through a gastric tube over a 20-day period. Serum γ-GT activity and the activities of the lysosomal enzymes β-N-acetylglucosaminidase and α-mannosidase were increased, whereas L-aspartate: 2-oxoglutarate aminotransferase and L-alanine: 2-oxoglutarate aminotransferase remained unaltered. There was a considerable increase in liver microsomal protein, γ-GT, cytochrome P-450, anilinehydroxylase, aminopyrine-demethylase and δ-aminolevulinic acid synthase. In the liver γ-GT was detected in the microsomes as well as in the cytoplasm where enzymatic activity was higher. The high correlation coefficient between liver γ-GT, cytochrome P-450 and δ- aminolevulinic acid synthase witnesses a hexachlorobenzene-induced γ-GT formation in the liver. A statistically significant correlation between serum and liver γ-GT activity was also found. These data strongly suggest that the increase in serum γ-GT activity may result from the induction of the enzyme in the liver.

The subjection of rats with body weight 150 +/- 10 g to complete starvation for a period of four days leads to a diminution of total protein, total lipids, blood sugar, body weight and liver weight. Lipid dystrophy develops in the liver, as well as deposition of lipofuscin-like pigment and atrophy. Lipid dystrophy and desposition of pigment increase during the first three days and abruptly decrease during the fourth. Atrophy is a progressive process. The delineation of three phases in the atrophic - dystrophic process is possible with the application of histological, enzyme-histochemical, morphometric, biochemical and electron microscopic methods: Phase I (first 24 hours) - a common adaptive phase. It engages both the liver, which must utilize the increased nutrients from the organism depots and the homeostatic mechanisms of the organism as a whole. Phase II - (second and third 24 hours) - alterative-restorative, manifested markedly at the liver parenchimal level and especially by autophagic lysosome function. Phase III - (fourth 24 hours) - alterative. Exhaustion of adaptive-restorative liver process (and the hepatocyte in particular), and the organism as a whole as well.