[Protein-calorie deficiency and the immune processes]. / Belkovo-kaloriinaia nedostatochnost' i immunnye protsessy.

The paper deals with issues that concern the influence of alimentary factors, of protein-caloric deficiency in particular, on the function of the immune system. Subject to a consecutive study was the pathogenesis of disorders in endocytosis of antigens, in humoral and cellular immunity and in reactions of hypersensitivity with proteinic deficiency. An inference is drawn to the effect that immunogenesis and a number of immune reactions are extrmely sensitive to alimentary effects and, above all, to the proteinic deficiency. Mention is also made of the fact that under certain conditions alimentary factors can direct favourably the course of a given immune process.

[Ultrastructural changes in the subcellular membranes of hepatocytes during the early periods of starvation]. / Ul'trastrukturnye izmeneniia subkletochnykh membran gepatotsitov na rannikh srokakh golodaniia

Ultrastructural changes in the membranes of subcellular structures of the liver in rats were studied with the help of electron microscopy at early periods (48 hours) of fasting. In the hepatocytes of fasting animals the authors found a disrupted structure of the nuclear membranes (an increased lumen between membranes and enlargement of pores) and of mitochondria (changed shape and a significant diminution in the number of cristae) along with vacuolization and degranulation of the rough endoplasmatic reticulum. At the same time, the hepatocytes demonstrated a drastic hypertrophy of the GERL zone characterized by a rising number of the Golgi apparatus dictyosomata, of the smooth endoplasmatic reticulum cysterns and of primary lysosomes. All this was accompanied by a sharp intensification of the processes of autophagy, finding its expression in a significantly increased numbers of secondary lysosomes of the autophagic type. Emphasis is laid upon the fact that while the revealed ultrastructural changes in the cellular and mitochondrial membranes, as well as in the endoplasmatic reticulum may with high degree of probability, be interpreted as manifestations indicative of functional disorders occurring in these organelles, the hypertrophy of the Golgi apparatus, a rise in the number of primary and secondary lysosomes and their activation appear as an adaptation reaction of the cell to conditions created by the organism switching over to a forced endogenous alimentation.

Effect of long-term starvation on the rat liver lysosomes.

The effect of 120- and 240-h starvation on rats hepatocytes ultrastructure and particularly the changes of the lysosomes were studied. Eelectronmicroscopically and cytochemically there have been observed diminution of the number of mitochondria and degranulation and vacuolzation of the ER. At the same time Golgi complex was hypertrophied and the number of lysosomes was much increased, mainly those of the autophagic type. Biochemically was shown, that the activity of some acid hydrolases (beta-glucosidase, alpha- and beta-galactosidases, beta-N-acetylglucosaminidase, beta-glucuronidase and arylsulphatases A and B) in the liver of starved rats was markedly expressed. The sedimentation properties of the lysosomes and the lysosomal membrane stability was damaged as well. The data received have been discussed in the light of the reconstructive role of lysosomes.

Histochemical, biochemical and ultrastructural studies on the liver of fasted rats.

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.