Liver pathologies and infection with Toxoplasma gondii (Nicolle et Manceaux, 1908) are widespread among HIV-infected patients. However, a possible contribution of toxoplasmosis to the development of various forms of liver diseases in HIV-infected individuals has not yet been determined. This research is a retrospective cohort study. Medical cards of 907 HIV-positive patients, including 119 individuals who died, were studied. The patients were divided into two groups: 531 patients were seropositive to T. gondii and 376 seronegative. General liver pathology was more widespread among patients seropositive to T. gondii than in seronegative patients (63.1 ± 2.1% and 51.9 ± 2.6%, respectively, p < 0.001). The association of seropositive to T. gondii with general liver pathology is weak both in the whole cohort (Pearson's contingency coefficient C = 0.112), and among the deceased patients (C = 0.228). and Chronic HBV-HCV coinfection was more common in the seropositive than in seronegative individuals as it was found both in entire cohorts (26.0 ± 1.9% and 18.6 ± 2.0%, respectively, p = 0.010) and in died patients (31.0 ± 5.5% and 14.6 ± 5.1%, respectively, p = 0.041). Toxoplasma gondii had a weak role in distributing of HBV-HCV coinfection between cohorts (C = 0.187). In both cohorts in patients with chronic hepatitis, regardless of its etiology, there was no significant difference in alanine transaminase activity (ALT). Cirrhosis of the liver occurred 4.5 times more often in deceased seropositive patients than in the entire seropositive cohort (23.9 ± 5.1 and 5.3 ± 2.0, respectively, p = 0.0006) whereas it no significantly increased in seronegative cohort (10.4 ± 4.4 against 4.8 ± 1.1, p > 0.05). In them T. gondii is weakly involved in cirrhosis formation (C = 0.168). Thus, in HIV-infected patients, T. gondii is a weak nonspecific adjunct that supports chronic liver inflammation and progression of cirrhosis, regardless of etiology, but does not influence the degree of hepatitis activity. The increased prevalence of HBV-HCV coinfection in patients seropositive for T. gondii may be related to their risk factor behaviour associated with uncontrolled blood contacts.
We have observed a significantly increased content of fats and decreased content of proteins in the liver of experimental rats fed a diet supplemented with 25 % casein proteins in comparison with the application of de-fatted soy flour. Casein proteins have a higher content of methionine in relation to cystine than baked soy flour. But the soy diet in contrast to the casein diet has a high content of free aminoacids which are not present in casein at all: aspartic acid, asparagine, a-aminoadipic acid, methionine, norleucine, lysine, phenylalanine, /3-alanine, ethanolamine, histidine, proline, y-aminobutyric acid, taurine. Differences in free valine, alanine, arginine, glycine, ornithine and cysteic acid are also significant. The content of free aminoacids in the liver of experimental animals fed a soy diet is high in the content of cystine, cystathionine, ornithine, /3-aminoisobutyric acid, /3-alanine, y-aminobutyric acid, leucine. We have also found accumulation of methionine, glycine, a-aminobutyric acid, taurine and cytrulline in free aminoacids from the liver of animals fed a casein diet. Citrulline and glycine in free aminoacids from the liver of animals fed a soy protein supplement were not recorded. Our investigations have shown that the application of a soy diet enriched with cystine acts protectively on methionine and that methionine is preferentially utilized for protein synthesis. The catabolic pathway of methionine prevails in animals on a casein diet.
Mitochondria as an energy generating cell device are very sensitive to oxidative damage. Our previous findings obtained in hepatocytes demonstrated that Complex I of the respiratory chain is more sensitive to oxidative damage than other respiratory chain complexes. We present additional data on isolated mitochondria showing that palmityl carnitine oxidation is strongly depressed at a low (200 μM) tert-butyl hydroperoxide (tBHP) concentration, while oxidation of the flavoprotein-dependent substrate - succinate is not affected and neither is ATP synthesis inhibited by tBHP. In the presence of tBHP, the respiratory control index for palmityl carnitine oxidation is strongly depressed, but when succinate is oxidized the respiratory control index remains unaffected. Our findings thus indicate that flavoprotein-dependent substrates could be an important nutritional factor for the regeneration process in the necrotic liver damaged by oxidative stress., Z. Červinková, H. Rauchová, P. Křiváková, Z. Drahota., and Obsahuje bibliografii a bibliografické odkazy
K+-p-nitrophenylphosphatase (K+pNPPase) is the enzyme, which is considered to be involved in K+-dependent hydrolysis of the phosphoenzyme in the reaction cycle of Na+, K+-ATPase. The aim of our present study was to characterize some features of K+pNPPase in homogenates of the rat brain and liver. We determined p-nitrophenylphosphatase (pNPPase) activity in the presence of various ion combinations (Mg 2++K+, Mg2+, K+). We found a higher total pNPPase activity in the brain (0.8±0.079 nkat/mg protein) than in the liver (0.08±0.01 nkat/mg protein). Contrary to the liver, the main part of the total brain activity was K+-dependent. The activity of K+pNPPase was significantly higher in cerebral cortex homogenates (0.86±0.073 nkat/mg protein) in comparison to those of the whole brain (0.57±0.075 nkat/mg protein). The specific K+pNPPase activity was two times higher in the isolated pellet fraction (0.911±0.07 nkat/mg protein), rich in synaptosomes, compared to the whole brain homogenate (0.57±0.075 nkat/mg protein). Our results demonstrate the high activity of K+pNPPase in the brain tissue and its distribution mainly into the pellet fraction, what might indicate a possible role of K+pNPPase in specific structures of the brain, e.g. in synaptosomes., M. Ďurfinová, M. Brechtlová, B. Líška, Ž. Barošková., and Obsahuje seznam literatury
Lipasin is a recently identified lipokine expressed predominantly in liver and in adipose tissue. It was linked to insulin resistance in mice and to type 1 and type 2 diabetes (T1D, T2D) in humans. No metabolic studies concerning lipasin were performed yet in rats. Therefore, we used rat model of T2D and insulin resistance, Goto-Kakizaki (GK) rats, to determine changes of lipasin expression in liver and in white adipose tissue (WAT) over 52 weeks in the relation to glucose tolerance, peripheral tissue insulin sensitivity and adiposity. GK rats were grossly glucose intolerant since the age of 6 weeks and developed peripheral insulin resistance at the age of 20 weeks. Expression of lipasin in the liver did not differ between GK and Wistar rats, declining with age, and it was not related to hepatic triacylglycerol content. In WAT, the lipasin expression was significantly higher in Wistar rats where it correlated positively with adiposity. No such correlation was found in GK rats. In conclusion, lipasin expression was associated neither with a mild age-related insulin resistance (Wistar), nor with severe genetically-based insulin resistance (GK)., M. Cahová, D. Habart, T. Olejár, Z. Berková, Z. Papáčková, H. Daňková, A. Lodererova, M. Heczková, F. Saudek., and Obsahuje bibliografii
The aim of the present study was to define the stress-induced pattern of cytosolic glucocorticoid receptor (GR) and Hsp70 protein in the liver of male Wistar rats exposed to different stress models: acute (2 h/day) immobilization or cold (4 °C); chronic (21 days) isolation, crowding, swimming or isolation plus swimming and combined (chronic plus acute stress). Changes in plasma levels of corticosterone were studied by radioimmunoassay (RIA). The results obtained by Western immunoblotting showed that both acute stressors led to a significant decrease in cytosolic GR and Hsp70 levels. Compared to acute stress effects, only a weak decrease in the levels of GR and Hsp70 was demonstrated in chronic stress models. Chronically stressed rats, which were subsequently exposed to novel acute stressors (immobilization or cold), showed a lower extent of GR down-regulation when compared to acute stress. The exception was swimming, which partially restores this down-regulation. The observed changes in the levels of these major stress-related cellular proteins in liver cytosol lead to the conclusion that chronic stressors compromise intracellular GR down-regulation in the liver., D. Filipović, L. Gavrilović, S. Dronjak, M. Demajo, M. B. Radojčić., and Obsahuje bibliografii a bibliografické odkazy
Male Wistar rats were maintained on a nutritionally adequate diet and diazepam was administered in a dose of 10 mg/kg/day. Control animals were pair-fed an adequate diet. Feeding was continued for 180 days, and the effects on the liver, plasma and erythrocyte phospholipid content were studied. It was found that the contents of sphingophospholipids and phosphatidylinositol + phosphatidylserine were significantly reduced in the erythrocytes of diazepam-treated rats. There was a significantly increased content of phosphatidylcholine in the liver and erythrocytes after 180 days of diazepam treatment. Such treatment did not cause statistically significant changes in the plasma of diazepam-treated rats. These investigations are in agreement with the hypothesis that extended or chronic use of drugs such as diazepam may alter membrane-dependent processes.
The effects of octadecylamide of alginic acid (amidated alginate) and tetrahydrolipstatin on serum and hepatic cholesterol, and the faecal output of fat and sterols, were investigated in rats. Amidated alginate is a sorbent of lipids, tetrahydrolipstatin is an inhibitor of pancreatic lipase. Rats were fed diets containing cholesterol and palm fat at 10 and 70 g/kg, respectively. Palm fat was provided by coconut meal. Amidated alginate at 40 g/kg diet significantly decreased serum total cholesterol, low-density lipoprotein and hepatic cholesterol, and hepatic lipids and increased the faecal output of fat and coprostanol. Tetrahydrolipstatin at 300 mg/kg diet significantly decreased low-density lipoprotein cholesterol and hepatic lipids and increased the faecal output of fat. The intake of feed was not significantly influenced; however, the weight gains in rats fed amidated alginate were lower than in rats of the control group. Both amidated alginate and tetrahydrolipstatin modified the fatty acid profile in excreta lipids. Concentrations of saturated fatty acids were decreased and those of unsaturated fatty acids increased. Despite different modes of action, amidated alginate and tetrahydrolipstatin were equally efficient in removing the dietary fat from the body.
Xenomas caused by Microgemma vivaresi Canning, Feist, Longshaw, Okamura, Anderson, Tsuey Tse et Curry, 2005 were found in liver and skeletal muscle of sea scorpions, Taurulus bubalis (Euphrasen). All muscle xenomas examined were in an advanced stage of destruction. In developing xenomas found in liver, parasites were restricted to the centre of the cell, separated from a parasite-free zone by a nuclear network formed by branching of the host cell nucleus. Although xenomas were able to reach a size of several hundred microns, the surface remained a simple plasma membrane. Host reactions took the form of penetration by phagocytes and isolation by fibroblasts. Once the xenoma had been attacked, the nuclear profiles became pycnotic and the barrier between parasitized and parasite-free zones was lost. Parasite antigens cannot be exposed at the surface of intact xenomas, as the host does not recognise the enlarging cell as foreign. Breaches in the plasma membrane of the xenoma and leakage of parasite antigens are thought to be the stimuli for phagocyte entry into the cell, its isolation by fibroblasts and eventual granuloma formation.
The aim of this work was to study the effects of low energy parenteral diets with different lipid/glucose ratios on rat liver and jejunal mucosa protein synthesis. The studied diets were: LO (100 % glucose, control diet), L25 (25 % lipids: 75 % glucose), L50 (50 % lipids: 50 % glucose) and L75 (75 % lipids: 25 % glucose). All diets were isoenergetic and isonitrogenated, with a standard amino acid content. The diets were assayed in 93 rats with open femoral fracture immobilized by Kirschner pin insertion. The diets were administered for 4 days. On the fifth day, liver and jejunal mucosa protein synthesis were determined. Highest liver protein synthesis rates were obtained with the diet compositions: lipid/carbohydrate ratio: 25 % lipids and 75 % carbohydrates (expressed as energy ratio). A higher proportion of lipids significantly decreases liver protein synthesis (p<0.05). Jejunal mucosa protein synthesis followed the same pattern, with the same statistical differences.