Sialic acids are essential constituents of many glycoproteins, glycopeptides and glycolipids. This widespread occurrence in glycoconjugates of different origin indicates that a variety of biological functions should be associated with this sugar. There are vahd indications that siahc acids influence or even determine the recognition of low and high molecular-weight compounds, the action of certain hormones, physicochemical and catalytic properties of enzymes, hemostasis, cellular adhesiveness, antigenicity, transport processes and synaptic transmission. Despite this apparently heterogenous spectrum of biological actions, four main functions—according to the concept of Schauer (1982)—can be attributed to sialic acid: (1) Endowment of glycoconjugates and cellular membranes with a negative charge, (2) Influence on the macromolecular structure of certain glycoproteins, (3) Information transfer, (4) Protection of glycoconjugates and cells from recognition and degradation. This rather physicochemical classification could be of use when starting to elucidate the biological significance of sialoglycoconjugates. Reviews on siahc acids have recently been published by Rosenberg and Schengrund 1976, Neufeld and Ashwell 1980, and Schauer 1982. The aim of this contribution, however, is to emphazise the important role of sialic acids in the occurrence of pathobiochemical alterations found in animals and human beings.

Biological Significance of Sialic Acids

We investigated the hepatoprotective effect of purple potato extract (PPE) against D-galactosamine (GalN)-induced liver injury in rats. PPE (400 mg) was administered once daily for 8 d, and then GalN (250 mg/kg of body weight) was injected at 22 h before the rats were killed. Serum tumor necrosis factor alpha (TNF-α), lactate dehydrogenase (LDH), alanine aminotransferase (ALT), and asparate aminotranferase (AST) levels increased significantly after injection of GalN, but PPE inhibited GalN-induced alterations in serum TNF-α, LDH, ALT, and AST levels. Hepatic lipid peroxide and glutathione levels in the control + GalN group were higher and lower respectively than those in the control group, and those in the PPE + GalN group did not differ from that in the control group. The lipid peroxide level in hepatic microsomes treated with 2,2′-azobis (2-amidinopropane) dihydrochloride in the PPE group was significantly lower than that in the control group. This suggests that PPE has hepatoprotective effects against ...

https://www.tandfonline.com/doi/pdf/10.1271/bbb.50670

Hepatoprotective Effects of Purple Potato Extract against D-Galactosamine-Induced Liver Injury in Rats

Acute intoxication of the rat liver with a single dose of 100 mg thioacetamide (TAA)/kg body weight causes within 48 h a fatty liver and a heterogeneous reaction in the hepatocytes. This affects principally the centrilobular liver parenchymal cells (zone 3) and to a lesser extent the periportal ones (zone 1). Ultrastructural analysis was performed to determine to what extent the formation of lipid-carrying particles of the very low density type (VLDL) is changed in affected hepatocytes in zones 1 and 3. Being morphologically the most conspicuous site of VLDL processing, the Golgi complex was chosen for quantitation by measuring its volume, VLDL content and particle size. The concentration and composition of the liver lipids were determined, biochemically. After TAA treatment of the liver the number of Golgi-VLDL particles is significantly reduced to about 50% in both the lobular zones examined. In addition, distinct classes of size-modified Golgi-VLDL particles appear which show an abnormally wide size distribution pattern. In periportal hepatocytes the size distribution of Golgi-VLDL particles shows a clear shift towards smaller particles homogeneous in size (mean diameter 39 nm). In contrast, centrilobular hepatocytes contain particles of very heterogeneous size, the mean diameter of which is nearly doubled (77 nm). The decrease in VLDL particle number and their size modification induced by TAA is not accompanied by significant changes in the volume of the Golgi complex. Biochemical analysis showed that the accumulation of lipids in the TAA-treated liver, mainly evident morphologically as drop-like deposits in the central area of the liver lobules, is due to an increase in triglycerides (TG) by 23 μmol/g liver wet weight, which represents nearly 95% of the accumulated lipids. Despite the striking elevation of the absolute cholesterol ester (CHOL-E) content (2μmol/g liver wet weight), this corresponds to only 5% of the newly accumulated lipids.

Qualitative and quantitative changes in hepatic lipoprotein particles following acute injury of the rat liver induced by thioacetamide.

The effect of an acute liver injury induced by thioacetamide (TAA) on hepatic and serum lipoprotein metabolism in rats was studied using biochemical and ultrastructural methods. A single dose of 100 mg TAA/kg body weight caused within 48 h a decrease of hepatic triglyceride (TG) output into the serum by about 50% in comparison to the controls. The steady state of serum TG concentration from 24 to 96 h after TAA treatment implies that the clearance of TG from serum must be diminished to the same extent as the hepatic TG output was found to decrease. Moreover, the TAA treatment caused changes in the electrophoretic mobility as well as in the concentration and composition of circulating serum-lipoproteins. The electrophoresis revealed a decrease in the alpha-band, which can be explained by the decrease in the high density lipoproteins (HDL) total lipid concentration. The pre-beta-migrating band disappeared, whereas a broad beta-mobility band appeared, which most likely consists of a mixture of very low density lipoproteins (VLDL) and low density lipoproteins (LDL) as can be concluded from the changes in concentration and composition of lipids in both fractions. For a better visualization of the VLDL-forming capability in perilobular and centrolobular liver parenchymal cells of the TAA-treated animals the VLDL secretion blocking agent colchicine was used. It was shown that in comparison with colchicine-treated controls the VLDL secretory products are accumulated at a considerably lower rate manifested in a diminution of VLDL clusters, secretory vesicle size and the number of intravesicular VLDL particles.(ABSTRACT TRUNCATED AT 250 WORDS)

Biochemical and substructural studies on hepatic and serum lipoprotein metabolism after acute liver injury induced by thioacetamide in rats

Effect of d-galactosamine in vitro on [U-14C]palmitate oxidation, triacylglycerol synthesis and secretion in isolated hepatocytes

The effect of galactosamine administration on the concentration and composition of plasma lipoproteins was studied in female rats. After a single intraperitoneal injection of 3.48 mmol galactosamine/kg the following alterations occurred within 24 h: Disappearance of alpha-lipoproteins as shown by agarose electrophoresis, increase of abnormal lipoproteins in the beta- and pre-beta-region. These changes corresponded to a two- to three-fold increase of VLDL and LDL and a decrease of HDL to 20-30% of normal after sequential ultracentrifugation. When compared to control animals, galactosamine-treated rats exhibited an abnormal chemical composition of their plasma lipoproteins: A nearly total loss of cholesterol esters, but an increase of free cholesterol and phospholipids, particularly in the LDL and HDL density classes. Moreover, polyacrylamide gel electrophoresis in 8M urea revealed a clear diminution of all C-apoproteins in the VLDL and HDL density class and a complete disappearance of the A II band in the HDL fraction 24-48 h after galactosamine administration. These lacking apoprotein bands reappeared 72-168 h after galactosamine treatment. The same effects could be obtained by lower doses of galactosamine (2.32 and 1.16 mmol/kg, respectively) which led only to slight increases of hepatocellular enzymes in the plasma. It is concluded therefore, that galactosamine administration in experimental animals leads to profound, but reversible alterations in the synthesis and/or secretion of plasma lipoproteins.

Lipoproteins and apolipoprotein patterns in rat plasma after liver injury induced by D-galactosamine.

The total carbohydrate content and the monosaccharide composition of plasma apolipoproteins isolated from normal and D-galactosamine-treated rats were investigated. In the lipoprotein classes VLDL, LDL and HDL of control animals, the carbohydrate content was 5,5%, 3,4% and 2,9% of dry weight apolipoprotein, respectively. 24 h after galactosamine treatment, these values dropped to 1.8%, 1.6% and 2.3%. The reduction of the carbohydrate content in VLDL and LDL was mainly due to a decrease of the following monosaccharides: Mannose, galactose, N-acetylglucosamine and sialic acid. Minor changes were observed in the fucose, glucose and N-acetylgalactosamine content. Particularly, the mannose/galactose ratio in the LDL fraction fell from 2.3 in control animals to 1.0 in the galactosamine-treated animals. In another series of experiments, the time course of these carbohydrate alterations in the LDL apolipoprotein was studied. As early as 3 h after galactosamine application, we found a reduction of the mannose, galactose and N-acetylglucosamine levels, with the absolute minimum at 24 h, and later on a normalization at 48 and 72 h.

Decreased Carbohydrate Content of Rat Plasma Apolipoproteins in Galactosamine Hepatitis

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Lipoproteins and apolipoprotein patterns in rat plasma after liver injury induced by D-galactosamine.

Decreased Carbohydrate Content of Rat Plasma Apolipoproteins in Galactosamine Hepatitis