Endogenic non-enzymatic antioxidative system of polyester grafts during their healing.

OBJECTIVE: Non-enzymatic low-molecular antioxidants are one of the important mechanisms which protect cells against the toxic effect of oxygen. The aim of the present study was to determine the content of glutathione, glutathione reductase, and ascorbic acid in the principal layers of polyester grafts. INTERVENTIONS AND MEASURES: The experiments were carried out on 24 mongrel dogs, in which polyester double velour DALLON grafts were implanted. Seven days, 1, 4, and 12 months after the operation the grafts were excised. The following were determined: glutathione content by use of a GSH-400 system, glutathione reductase activity by the method of Langdon and Mize, and ascorbic acid content by the Kyaw method. RESULTS: It was found that the glutathione content in the graft neointima was 33% lower, in the graft neomedia higher during the first 4 months, in the neoadventitia 50% lower after 4 months than in the corresponding layers of the aorta (p < 0.01). The activity of glutathione reductase was significantly higher in all the graft layers during 12 months' observation than in the normal aorta layers. The ascorbic acid content of the graft layers was lowest 7 days after the implantation, and then in time increased so that 12 months after the operation it reaches its highest values. CONCLUSIONS: Our study shows that low non-enzymatic antioxidative potential is not capable of proteoting the newly forming graft layers, particularly the neointima, against oxygen toxicity. Thus, it would be beneficial to administer antioxidants (vitamin C, vitamin E, and N-acetylcysteine).

Activity and distribution of superoxide dismutase in the layers of polyester grafts.

The aim of the present study was to evaluate superoxide dismutase (Cu, Zn-SOD) activity in the principal layers of polyester grafts implanted into the abdominal aorta of dogs. The grafts were examined 7 days and 1, 4 and 12 months after the operation. It was found that SOD activity occurred in all polyester graft layers during the whole experiment. The neointima activity ws 1.5-fold lower during the 1st month; with the passage of time, it became 2-fold lower than in the normal aorta (p < 0.01). SOD activity in the medial and outer graft layers behaved similarly: it was lowest after 7 days, increased after 1 month and significantly decreased after 4 and 12 months (p < 0.01). Our study shows that the activity of SOD is low in polyester grafts and it can thus be inferred that protection against the superoxide anion is inadequate.

The role of free oxygen radicals in children with chronic viral hepatitis B.

Lipid peroxidation of polyunsaturated fatty acids, being important components of cellular membranes, caused by free oxygen radicals is considered to be one of the main causes of hepatocyte injury. The aim of this study is to estimate the malondialdehyde (MDA) level in the red blood cells of children with chronic viral hepatitis B. The decrease of MDA concentration along with the clinical and serological improvement in children with chronic hepatitis B was observed. We also noticed a correlation of MDA with HBeAg-anti HBe seroconversion and obliteration of HBV DNA polimerase activity.

Ethanol ingestion decreases superoxide dismutase activity and diminishes -SH compounds in the liver and red blood cells in rats.

SOD activity and -SH compounds in the liver and RBCs, and some hematological parameters were investigated in control rats and in those submitted to chronic (3 months) intoxication with ethanol. We found significantly lower SOD activity and a decrease in -SH groups in the liver and RBCs of ethanol-treated rats in comparison with the control group. The hemoglobin content and mean corpuscular hemoglobin concentration were reduced, while mean corpuscular volume of RBCs was increased when compared with the control group.

The 21-aminosteroid U-74389G protects the antioxidant enzymes in the ischemia/reperfusion-induced rat brain damage.

The antioxidant enzymatic system in the ischemia/reperfusion induced brain injury in rats after U-74389G administration was evaluated. Ischemia/reperfusion caused a decrease in the activities of superoxide dismutase and glutathione reductase, as well as of total and free sulfhydryl groups, while thiobarbituric acid-reactive substances became elevated. Administration of U-74389G lead to restoring to normal values of all above parameters. Protective effect of the drug in ischemia/reperfusion induced brain injury has been suggested.

Accumulation of ammonia and changes in the activity of some ammonia metabolizing enzymes during brain ischemia/reperfusion injury in rats.

The ammonia concentration and changes in the activity of ammonia metabolizing enzymes in the brain tissue during ischemia/reperfusion were investigated in rats. During ischemia (0.5 h) we found a statistically significant increase in brain ammonia concentration and a significant decrease in glutamate dehydrogenase activity. After 1 h of reperfusion, a further accumulation of ammonia concentration was observed. Furthermore, the brain glutamine syntethase and glutamate dehydrogenase were decreased, whereas the brain glutaminase activity was increased. The causes for the changed activities of some ammonia metabolizing enzymes in brain after ischemia/reperfusion have been discussed.

Inhibition of non-enzymatic lipid peroxidation by 'Essentiale' a drug enriched in phosphatidylcholine in ethanol-induced liver injury.

The effect of 'Essentiale'--a drug, now clinically listed in European countries in the treatment of liver diseases was examined in ethanol-induced liver injury in rats (free access to a 20% ethanol solution for 3 months). The antioxidant enzymes, SOD (superoxide dismutase), CAT (catalase), GSH-R (glutathione reductase), non-protein and total SH groups as well as TBA-rs contents were investigated. Following treatment, we found beneficial effects in SOD and CAT activities. The above enzyme activities were restored after a 3-month drug administration. Furthermore, 'Essentiale' treatment normalized TBA-rs levels in the liver. These effects have been briefly discussed.

The effect of heparegen on antioxidant enzyme activities in ethanol-induced liver injury in rats.

SOD, CAT, GSH-Px, and sulfhydryl compounds MDA contents in liver of rats treated with heparegen for 7, 14, and 21 days after alcoholic liver injury have been investigated. After use of this drug, we found beneficial effects on GSH-Px activity, sulfhydryl compounds (total and nonprotein), and MDA content and a partially beneficial effect on SOD and CAT activities. These enzyme activities after 21 days of drug administration were restored. Furthermore, heparegen shortens the time necessary for the return of AIAT and GGTP to normal value. This enzymatic data are supported by histological studies in light microscopy.

The diminution of liver glutathione content and changes in activities of antioxidant enzymes in long-term acetaldehyde poisoning.

The effect of acetaldehyde administration for 4 weeks on antioxidant protection systems was investigated in liver of rats. Liver SOD activity was decreased from control value 542.4 U/g of tissue to 411.2 U/g of tissue in experimental group (24% decrease). GSH-Px activity was practically unchanged and liver CAT activity was significantly decreased (35%). Sulfhydryl compounds in liver non-proteins following ACH treatment were decreased from 4.22 mumol/g of tissue in control group to 2.86 mumol/g of tissue (23%). Furthermore acetaldehyde treatment caused significant increase in MDA level in liver (78% increase).

The decrease of superoxide dismutase activity and depletion of sulfhydryl compounds in ethanol-induced liver injury.

There appears to be increasing evidence that ethanol toxicity may be associated with an increased production of reactive oxygen intermediates. In rats we studied the effect of 4 weeks of ethanol ingestion on the liver cytosolic defense system against active oxygen species. Compared with the control rats, the ethanol-fed animals had a significantly higher liver malondialdehyde content and significantly lower reduced glutathione level. Moreover, ethanol feeding resulted in a decrease of superoxide dismutase and catalase activities while glutathione peroxidase activity was only slightly diminished. Thus, prolonged ethanol administration profoundly modified the hepatic status of the enzymatic defense system leading to lipid peroxidation that may disrupt vital functions of liver cells.

Products of lipid peroxidation and changes in sulfhydryl compounds in pancreatic tissue of rats with caerulein-induced acute pancreatitis.

Acute edematous pancreatitis was induced in rats by iv infusion of caerulein (CR) in a supramaximal dose of 7.5 x 10(-6)g x kg-1 x hr-1 during 6 hr. The most important finding of our study was the marked decrease of protein and nonprotein thiol content in pancreatic tissue of rats with CR-induced acute pancreatitis (AP). Oxygen radicals as well as 4-hydroxyalkenals resulting from lipid peroxidation are believed to be at least partly responsible for this phenomenon. Covalent binding of excessive amounts of 4-hydroxyalkenals to pancreatic tissue protein sulfhydryl groups has been documented. Presented data suggest a serious disturbance of sulfhydryl compounds metabolism in pancreatic tissue of rats with CR-induced AP which may be of importance in the pathogenesis of the disease.

The effect of immunostimulatory drugs on sulfhydryl compounds in plasma, liver and brain after ethanol-induced liver injury in rats.

Sulfhydryl compounds in plasma, liver and brain of rats treated with two immunostimulant drugs, isoprinosine and levamisole, after alcoholic liver injury have been investigated. After use of both drugs for 6 days we found partially beneficial effect on the SH-groups in plasma and liver. No changes in nonprotein SH compounds were observed in rat brain after treatment with isoprinosine, levamisole or ethanol. Furthermore, levamisole shortens the time necessary for the return of AlAT activity to normal value.

The effect of Heparegen and D-penicillamine on the activity of some ammonia metabolizing enzymes in liver and brain of rats intoxicated with ethanol.

This paper reports data on the effect of two drugs: Heparegen (thiazalidine-4-carboxylic acid) and D-penicillamine on the blood ammonia concentration and on some ammonia metabolizing enzymes in liver and brain of rats intoxicated with ethanol. It seems, that both drugs decrease ammonia concentration and simultaneously elevate liver and brain glutamine synthetase activity. The effect of D-penicillamine on the nitrogen metabolism in the damaged liver appears to be more favorable than that of Heparegen.

Oxygen radicals mediate depletion of pancreatic sulfhydryl compounds in rats with cerulein-induced acute pancreatitis.

Acute edematous pancreatitis was induced in conscious rats by intravenous infusion of cerulein at a supramaximal dose of 7.5 micrograms/kg/h during 6 h. The most important finding of our study was a marked decrease in the protein and non-protein content of sulfhydryl groups parallel to an evident elevation in the malondialdehyde concentration in pancreatic tissue. The presented data suggest that in cerulein-induced acute pancreatitis in rats, oxygen radicals mediate increased peroxidation reactions which are accompanied by depletion of nonenzymatic sulfhydryl-containing free radical scavengers. The above phenomenon contributes to a disturbance in thiol metabolism resulting in serious diminution of pancreatic protein sulfhydryl compounds.

Branched-chain amino acid enriched diet given simultaneously with ethanol partially prevents morphological and biochemical changes in the liver.

Morphological examination of the liver and biochemical studies of the serum were carried out on rats fed: a) ethanol p.o. in the daily dose of 6 g/kg for 4 weeks and maintained on standard diet (Et-OH) and b) ethanol in the same doses but fed the BCAA enriched diet (to amount of 1.174 mM/day/rat) were carried out. It can be concluded that BCAA enriched diet given simultaneously with ethanol prevent in part the morphological and ultrastructural changes in liver and improve positive body weight gain of experimental animals.

Ethanol decreases the level of sulfhydryl compounds in red blood cells and changes their hematological pattern in rats.

The level of sulfhydryl compounds in red blood cells (RBCs) and plasma and some haematological parameters were investigated in rats treated with ethanol for 4 weeks (daily dose of 6g/kg, 30% w/v, p.o.). After ethanol ingestion, the significant decrease of non-protein - SH groups were observed in RBCs and plasma. In treated rats, the mean corpuscular haemoglobin concentration (MCHC) was decreased and the mean corpuscular volume (MCV) was increased. There is a positive correlation between these two parameters and decreased content of sulfohydryl groups in RBCs.

Changes in activities of some ammonia-metabolizing enzymes in the rat liver and the brain after chronic ethanol administration.

The changes in the activities of ammonia-metabolizing enzymes in liver and brain after ethanol intoxication has been investigated in rats. After administration of ethanol 30% (w/v) 6g kg-1 for 4 weeks we found an increase in liver glutamate dehydrogenase and glutaminase activity. In brain tissue the glutaminase activity was significantly higher and glutamate dehydrogenase was significantly lower. Glutamine synthetase activity in liver and brain was practically unchanged. The reasons for these changes in the activities of some ammonia-metabolizing enzymes in liver and brain after ethanol ingestion have been discussed.

Changes in sulfhydryl compounds in plasma, liver and brain after acute and chronic acetaldehyde administration in rats.

The content of sulfhydryl compounds in proteins and non-proteins of plasma, liver and brain after acute and chronic administration of acetaldehyde (ACH) was investigated in rats. After ACH 1.5% w/v ingestion for 1 and 4 weeks (0.3 ml/kg) daily, proteins and non-proteins in plasma and liver were decreased significantly. After acute ACH administration SH-groups in brain proteins were not significantly decreased, but in the brain non-proteins these groups were increased significantly.

The changes in sulfhydryl compounds in plasma, liver and brain after acute and chronic ethanol administration in rats.

The content of sulfhydryl compounds in proteins and non-proteins of plasma, liver and brain after acute and chronic ethanol administration was investigated in rats. After ethanol ingestion for 4 weeks (6 g/kg, day 30% w/v) significant changes were observed in plasma proteins and in liver proteins and non-proteins. In brain proteins and non-proteins we did not find any changes in sulfhydryl compounds content after acute and chronic ethanol administration.