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PubMed1984

Mode of death effect on rat liver iodothyronine 5' deiodinase activity: role of adenosine 3',5' monophosphate.

Liver thyronine 5'-deiodinase activity assayed in crude homogenates in the absence of dithiothreitol (DTT) is increased in rats killed by asphyxia when compared to that of animals killed by phenobarbital injection or decapitation. The addition of cyclic adenosine monophosphate leads to a consistent decrease in observed deiodinase activity, suggesting the possible involvement of this nucleotide in the regulation of this enzyme. The addition of DTT eliminates this effect and suggest a dual regulation of the enzyme by cAMP and physiological sulfhydryl compounds.

1-Methyl-3-isobutylxanthine↗
PubMed1995

Effect of the pyrrolizidine alkaloid, monocrotaline, on bile composition of the isolated, perfused rat liver.

Monocrotaline is a hepatotoxic pyrrolizidine alkaloid, releasing high levels of metabolites into bile of isolated, perfused liver. Although perfusion of rat liver with 0.5 mM monocrotaline does not affect bile flow over a 1 hr study period, it markedly affects bile composition. Biliary release of conjugated and free GSH increases 30-fold. Marked increases are also observed in the biliary concentration of the related sulfur-containing substances, cysteine and cysteinylglycine. However, biliary release of the sulfur amino acids, taurine and methionine, is unaffected. Only two amino acids show mildly increased releases, 23% for glycine and 46% for aspartate. Release of bile acids, cholesterol and phospholipids also decrease, both in terms of mM concentration in bile and in terms of nmol secreted per g liver. Thus, exposure to monocrotaline causes disturbances in sulfur metabolism in the liver and in the composition of bile. The consequences of the digestive properties of bile and gastrointestinal toxicity remain to be established. As sulfhydryl compounds are involved in detoxification of monocrotaline metabolites, these findings indicate a mutual interaction of pyrrolizidine toxicity and sulfur metabolism. This suggests that dietary sulfur amino acid intake may influence susceptibility to pyrrolizidine poisoning.

Amino Acids↗
PubMed1992

Effects of antioxidants on induction of micronuclei in rat peripheral blood reticulocytes by potassium bromate.

Micronucleus induction in male F344 rat peripheral blood by potassium bromate (KBrO3), a rat renal carcinogen, and its inhibition by several antioxidants were studied using the acridine orange supravital staining method. The frequency of micronucleated reticulocytes (MNRETs) peaked 32 h after a single i.p. treatment of rats with KBrO3 at a dose of 60 mg/kg. Co-treatment with glutathione (GSH) or cysteine (Cys) i.p. at doses of 800 mg/kg and 400 mg/kg, respectively, 30 min before and 30 min after the KBrO3 treatment significantly inhibited the micronucleus induction by KBrO3. Daily i.g. administration of vitamin C for 5 days at a dose of 200 mg/kg/day was also effective in protecting against micronucleus induction by KBrO3 given on the 4th day. However, co-treatment with superoxide dismutase in liposome-encapsulated form by i.p. injection at a dose of 18,000 U/kg 30 min before and 30 min after the KBrO3 application exerted no effect. The results indicate that antioxidants, especially sulfhydryl compounds, have protective potential against the clastogenicity of KBrO3, also suggesting that active oxygen species may play an important role in its clastogenicity.

Acridine Orange↗
PubMed1991

The urotoxic effects of N,N'-dimethylaminopropionitrile. 2. In vivo and in vitro metabolism.

The urotoxicity and metabolism of N,N'-dimethylaminopropionitrile (DMAPN) were investigated in male Sprague-Dawley rats. Animals treated with 525 mg DMAPN/kg or equimolar doses of commercially available potential DMAPN metabolites showed varying levels of urinary retention. About 44% of the administered dose of DMAPN was excreted unchanged in 5 days. beta-Aminopropionitrile and cyanoacetic acid were identified as urinary metabolites. The urinary excretion of cyanoacetic acid was nonlinearly proportional to the volume of urine retained in the bladders. In vitro, the metabolism of DMAPN to cyanide, formaldehyde, and cyanoacetic acid was localized mostly in the microsomal fraction of liver, kidney, and urinary bladders. This reaction required NADPH and oxygen for maximal activity. Metabolism of DMAPN was increased in hepatic microsomes obtained from phenobarbital-treated rats (220% of control) and decreased following CoCl1 treatments (73% of controls). Addition of SKF 525-A to the incubation mixtures inhibited the metabolism of DMAPN to formaldehyde (47-64% of controls). Addition of sulfhydryl compounds (glutathione and cysteine) to the incubation mixtures did not affect the rate of these reactions. These findings indicate that DMAPN is primarily metabolized via a cytochrome P450-dependent mixed-function oxidase system and that the urotoxic effects of DMAPN may be related to this metabolism.

Acetates↗
PubMed1980

Restoration of impaired immune functions in aging animals. IV. Action of 2-mercaptoethanol in enhancing age-reduced immune responsiveness.

The enhancing effect of 2-mercaptoethanol (2-ME) on the immune responses of young and old unseparated spleen cells and purified populations of T-cells, B-cells and macrophages was studied. While 2-ME enhances both the normal responses of young cells and the age-reduced responses of old cells, the sulfhydryl compound has a relatively greater enhancing effect on old spleen cells in the humoral response to sheep red blood cells and the blastogenic response to concanavalin A (Con A). The greater enhancing effect in the humoral response appears to be due to 2-ME overcoming a suppressive effect of old T-cells which develops with increasing age. The greater enhancing effect in Con A stimulation appears to be an effect on the Con A responsive sub-population of T-cells and not on the synergistic effect of the presence of B-cells.

Aging↗
PubMed1991

Evidence for membrane protein oxidation during in vivo aging of human erythrocytes.

Oxidative lesions to membrane proteins were studied in human erythrocytes of different age and were evaluated on ghost membrane preparations by assaying thiol and methionine sulphoxide groups, and in situ on intact cells, after treating erythrocytes with the fluorochrome N-(7-dimethyl-amino-4-methyl-coumarinyl) maleimide (DACM). DACM reacts with thiol groups and the amount of this reagent bound by membrane proteins was quantified after SDS-PAGE separation. Results obtained show that during aging of normal cells the oxidative state of membrane proteins increases: this was better shown by the assay of methionine sulphoxide residues rather than by the thiol titration, when studies were carried out on ghost membranes. After separation of individual membrane proteins by SDS-PAGE, decreased accessibility of DACM to thiol groups of band 3 and of the main proteins of the membrane skeleton was evident in senescent erythrocytes. These results show that during aging, band 3 and membrane skeleton proteins undergo conformational changes and/or oxidation. Similar results were obtained when thiol distribution was studied in membrane proteins separated by SDS-PAGE in both reducing and non-reducing conditions.

Electrophoresis, Polyacrylamide Gel↗
PubMed1986

On the toxic effects of tetraethyl lead and its derivatives on the chrysophyte Poterioochromonas malhamensis. VII. Protective action of thiol compounds, vitamins, trace elements, and other agents.

The influence of 45 different substances on the growth inhibiting effects of triethyl lead chloride (TriEL) in cultures of the unicellular alga Poterioochromonas malhamensis was studied. Ten thiol or disulfide compounds, 9 vitamins, 12 trace elements, 14 miscellaneous agents, and 9 combinations of these agents were tested. The agents were applied to the algal cultures in three different concentrations simultaneously with 10 microM TriEL and incubated for 72 hr. While none of the tested thiol and disulfide compounds remarkably protected the algae from TriEL toxicity, two vitamins (tocopheryl acetate, ascorbic acid), one trace element (zinc), adenosine-5'-triphosphate Na2 salt, cyclic AMP, and concanavalin A as well as combinations of some of these agents were found to suppress markedly the growth inhibiting effects of TriEL. Zinc was the most effective agent; it increased algal growth in TriEL-treated cultures by about 70 times as compared with cultures containing TriEL alone. A combination of 10 essential trace elements was even more protective and almost completely suppressed TriEL toxicity. In contrast to this, some of the other agents potentiated the toxic effects of TriEL (e.g., magnesium, molybdenum, caffeine, deuteriumoxide, chlorpromazine, dimethylsulfoxide) in the tested concentration ranges. The most protective agents Zn, VitC, and VitE did not prevent the inhibitory effects of TriEL on microtubule (MT) assembly in vitro, suggesting that their in vivo protection is based on mechanisms other than direct protecting MTs from the attack of the lead compound. Zn had no direct influence on the stability and half life of TriEL in the growth medium. The lack of protection found by the thiol compounds used suggests that most probably general thiol interaction of TriEL is not its major toxic mechanism of action. It is postulated that the protective action of Zn, VitE, and VitC is directly or indirectly mediated by suppression of TriEL-induced peroxidation processes in the poisoned algae. The protective agents found provide a basis for further screening experiments in order to test their "therapeutic" potency in experimental animals poisoned with organolead.

Disulfides↗