ABSTRACT
The participation of lipid peroxidation products in the mechanisms of paraquat toxicity in Ehrlich ascites tumor (EAT) cells was observed. Paraquat in a concentration 0.5-1.0 mmol increased the level of lipid peroxidation according to the Ohakawa TBARS (thiobarbituric acid-reactive substances) method. These changes in TBARS production in EAT cells correlated with paraquat toxicity on the cells registered by using the method for cell injury, which is based on changes in lactate dehydrogenase activity. The metal chelator DTA removed the effect of paraquat on TBARS production and on cell injury. The present data suggested that the increased level of lipid peroxidation and cell injury is a result of the paraquat action in EAT cells depending on iron.
Subject(s)
Carcinoma, Ehrlich Tumor/metabolism , Lipid Peroxidation/drug effects , Paraquat/toxicity , Animals , Chelating Agents/pharmacology , Drug Synergism , Edetic Acid/pharmacology , Ferric Compounds/toxicity , Male , Mice , Mice, Inbred BALB C , Neoplasm Transplantation , Thiobarbituric Acid Reactive Substances/metabolismABSTRACT
1. The effects of vanadium ions on the .OH radical production in the presence of and in the absence of dialuric acid were studied. 2. Dialuric acid enhanced deoxyribose degradation. 3. Vanadium ions and vanadium/EDTA complexes decreased the degradation of deoxyribose in the presence and in the absence of dialuric acid. 4. The question as to whether or not free .OH radicals are formed via reaction of vanadium ions with H2O2 in the presence of dialuric acid is discussed. 5. The results are interpreted with a view to the vanadium ability to decrease the toxic effects of dialuric acid.
Subject(s)
Barbiturates/pharmacology , Iron/pharmacology , Vanadium/pharmacology , Hydroxyl RadicalABSTRACT
Iron loading was associated with development of oxidative stress, viz, decrease in tocopherol content and an increase in amount of lipid peroxidation products but only slight, if any, decrease in cytochrome P-450 content. Combinations of iron loading with other stress-inducing treatments (exhaustive physical exercise and hyperoxia) caused marked decreases in cytochrome P-450 content. Thus, a combination of factors favoring development of oxidative stress, but insufficient to exert a damaging effect on the cytochrome P-450-dependent detoxification system when acting alone, may become quite potent when acting in concert.
