[Hepatotoxic efects of acetaminophen. Protective properties of tryptophan-derivatives].

Rat intoxication with acetaminophen (APAP) (500-1500 mg/kg body weight intragastrically) caused a considerable dose-dependent decrease in reduced glutathione (GSH) level in both liver cellular cytoplasm and mitochondria (at the dose 1500 mg/kg body weight by 60% and 33%, respectively). The cytoplasmic GSH level decreased more pronounced by comparison with that in mitochondria. At the same time, we did not observe any inactivation of the mitochondrial enzymes: succinate dehydrogenase, alpha-ketoglutarate dehydrogenase, glutathione peroxidase despite of mitochondrial GSH consumption; also we did not observe any decrease in the respiratory activity of liver mitochondria isolated from APAP-intoxicated rats.

Structure, stability, and antiplatelet activity of O-acyl derivatives of salicylic acid and lipophilic esters of acetylsalicylate.

The anti-thrombotic activity of acetylsalicylic acid (ASA) has been shown to be due to specific irreversible acetylation of blood platelet cyclooxygenase. The aim of our study was to investigate the associations between the antiplatelet activities of derivatives of both ASA and salicylic acid (SA), as well as the structure, stability, and molecular properties of these compounds. Homologous series of O-acyl derivatives of salicylic acid (propionyl-, butyrylsalicylic acids, PSA, BSA) and lipophilic dodecyl (C12)-, hexadecyl (C16)-, and cholesteryl acetylsalicylates were synthesized and tested for structure-activity relationships.

Melatonin attenuates metabolic disorders due to streptozotocin-induced diabetes in rats.

Enhanced oxidative stress and impairments in nitric oxide synthesis and bioavailability are of considerable importance in the pathogenesis of diabetic vascular diseases. The aim of the present work was to evaluate the metabolic effects of pharmacological doses of the melatonin, a known antioxidant, on streptozotocin-induced diabetic damage in rats. We investigated the indolamine's influence on the cellular redox-balance, nitric oxide (NO) level, and the activities of antioxidative defence enzymes, as well as the activities of enzymes involved in phase II detoxication and NADPH-generating pentose phosphate pathway.

Protective effects of N-acetyl-L-cysteine against acute carbon tetrachloride hepatotoxicity in rats.

In recent years, N-acetyl-L-cysteine (NAC) has been widely investigated as a potentially useful protective and antioxidative agent to be applied in many pathological states. The aim of the present work was further evaluation of the mechanisms of the NAC protective effect under carbon tetrachloride-induced acute liver injuries in rats. The rat treatment with CCl4 (4 g/kg, intragastrically) caused pronounced hepatolysis observed as an increase in blood plasma bilirubin levels and hepatic enzyme activities, which agreed with numerous previous observations.

[Hypoclorous acid modifies rat liver and heart enzymes of the pentose phosphate pathway and antioxidative defence in vitro].

Hypoclorous acid is an effective biological oxidant produced by activated neutrophils. HOCl plays a role of the major inflammation mediator in mammalian tissues. The aim of the present study was to investigate the mechanisms of hypochlorous acid-induced modification of antioxidant enzymes, which defence the cell under oxidative stress, and enzymes of the pentose phosphate pathway, which supply reducing equivalents in the cell.