title: [Morphometry of hepatocyte mitochondrial apparatus in normal and cirrhotic rat liver].
abstract: Morphometric electron microscopy study of the hepatocyte mitochondrial apparatus and morphofunctional analysis of the degree of pathological alterations were carried out on the liver of rats with CCL4-cirrhosis (experimental group). Chronic poisoning of rats with CCL4 for 6 months led to a 4.2-fold increase in proportion of connective tissue and to a decrease in the number of hepatocytes in the liver by 21.8 %. Dry mass and ploidy of hepatocytes in the cirrhotis liver rose as compared with norm by 20.6 and 9.3%, respectively. Activities of alanine and aspartate aminotransferases in blood of rats of experimental group exceeded normal ones 2.0 and 1.4 times, respectively. Concentration of total bilirubin in blood of the cirrhotic animals increased 1.7 times, while concentration of total protein decreased by 22%. Concentration of diene conjugates in the liver of rats of experimental group increased 2.1 times as compared with normal one, while the level of malonic dialdehyde - by 34%. Activities of superoxide dismutase and catalase in the cirrhotic liver were lower than in the normal liver were lower than in the normal liver by 16 and 23 %, respectively. Morphometry of the hepatocyte mitochondrial apparatus has shown that in spite of an increase in the voluminous density of mitochondria in hepatocytes of the cirrhotic liver (by 28 %), concentration of internal mitochondrial membranes in the cells was reduced almost 1.5 times, while the total length of internal membrane in a single mitochondrion was reduced about twice as compared with norm. Thus, despite compensation of the partial loss of hepatocytes because of their polyploidization and hypertrophy, the specific synthetic activity of cells in the case of cirrhosis is decreased due to deterioration of the antioxidant system and electron transport chain of the mitochondrial apparatus.
authors.forename: N N
authors.initials: NN
authors.lastname: Bezborodkina
authors.forename: S V
authors.initials: SV
authors.lastname: Okovityĭ
authors.forename: M V
authors.initials: MV
authors.lastname: Kudriavtseva
authors.forename: O V
authors.initials: OV
authors.lastname: Kirik
authors.forename: I V
authors.initials: IV
authors.lastname: Zarubina
authors.forename: B N
authors.initials: BN
authors.lastname: Kudriavtsev
mesh_terms: D000410:Alanine Transaminase / Q000097:blood; D000818:Animals; D001219:Aspartate Aminotransferases / Q000097:blood; D002251:Carbon Tetrachloride / Q000009:adverse effects; D002908:Chronic Disease; D022781:Hepatocytes / Q000378:metabolism / Q000473:pathology* / Q000648:ultrastructure; D008099:Liver / Q000473:pathology / Q000648:ultrastructure*; D008106:Liver Cirrhosis, Experimental / Q000139:chemically induced / Q000378:metabolism / Q000473:pathology; D008297:Male; D008928:Mitochondria / Q000473:pathology / Q000648:ultrastructure*; D008930:Mitochondria, Liver / Q000473:pathology / Q000648:ultrastructure*; D051336:Mitochondrial Membranes / Q000648:ultrastructure; D011003:Ploidies; D051381:Rats
chemical_list: D002251:Carbon Tetrachloride; D001219:Aspartate Aminotransferases; D000410:Alanine Transaminase