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Protective effects of erdosteine against doxorubicin-induced cardiomyopathy in rats.

The usefulness of doxorubicin (DXR) is limited by its cardiotoxicity. In order to improve future DXR therapy by using a new antioxidant agent, an experimental study was designed. This study was undertaken to determine whether DXR-induced cardiotoxicity is prevented by erdosteine, a mucolytic agent showing antioxidant properties. Three groups of male Sprague-Dawley rats (60 days old) were used: one group was untreated as a control; the other groups were treated with DXR (single i.p. dosage of 20 mg kg(-1) body wt.) or DXR plus erdosteine (10 mg kg(-1) day(-1), orally), respectively. The DXR treatment without erdosteine increased antioxidant enzyme activities and also increased lipid peroxidation in myocardial tissue. The rats treated with DXR plus erdosteine produced a significant decrease in lipid peroxidation in comparison with control and DXR groups. Furthermore, erdosteine administration led to an increase in antioxidant enzyme activities in comparison with the control group. Erdosteine treatment also increased the activities of catalase (CAT) and glutathione peroxidase (GSH-Px) in comparison with the DXR group. There was no significant difference in lipid peroxidation of myocardial tissue between control and DXR plus erdosteine-treated rats. It was concluded that erdosteine caused an increase in the activities of antioxidant enzymes, especially GSH-Px and CAT, protecting the heart tissue sufficiently from oxidative damage to membrane lipids and other cellular components induced by DXR.

Animals↗
PubMed1992

Lipogenesis from n-butyrate in colonocytes. Action of reducing agent and 5-aminosalicylic acid with relevance to ulcerative colitis.

Cell membranes of colonic epithelial cells (CEC) in ulcerative colitis show structural abnormalities which are specific to the disease and which suggest impaired lipogenesis in CECs. Lipogenesis from [1-14C]-n-butyrate, the chief oxidative fuel of colonic epithelial cells, was measured in isolated CECs under control conditions, with or without glucose and in the presence of mercaptoacetate, a major reducing agent in the colonic lumen. Glucose significantly (p < 0.01) stimulated lipogenesis from [1-14C]-butyrate which was reversed by 5 mM mercaptoacetate. Mercaptoacetate significantly diminished CEC thiolase activity (EC 2.3.1.9). 5-Aminosalicylic acid reversed the adverse effects of mercaptoacetate in the saponifiable fraction of extracted lipids. Changes in lipogenesis due to colonic luminal reducing agents would affect the barrier function of CECs a feature relevant to the disease process of ulcerative colitis.

Aminosalicylic Acids↗
PubMed1998

Inhibitors of fatty acid oxidation (mercaptoacetate, R-3-amino-4-trimethylaminobutyric acid) stimulate feeding in mice.

Several lines of evidence indicate that fatty acid oxidation contributes to control of eating. We examined the effect of inhibitors of fatty acid oxidation (mercaptoacetate, R-3-amino-4-trimethylaminobutyric acid = emeriamine) on food intake in mice because fatty acid oxidation has been shown recently to increase the hepatic membrane potential in mouse liver, and this potential has been proposed to represent a signal for control of food intake. The effect of intraperitoneal injection of mercaptoacetate (200, 400, or 600 micromol/kg body weight) and emeriamine dihydrochloride (8.7, 17.4, 34.8, or 69.6 micromol/kg body weight) was investigated in mice fed a fat-enriched diet (18% fat). Both mercaptoacetate (400 or 600 micromol/kg) and emeriamine (34.8 or 69.6 micromol/kg) significantly increased food intake. These results suggest that fatty acid oxidation is also involved in feeding control in mice. Therefore, the pertinent mechanisms can be studied in mice.

Animals↗
PubMed1969

A new class of chromophoric organomercurials and their reactions with D-glyceraldehyde 3-phosphate dehydrogenase.

THE SYNTHESES OF THE FOLLOWING ORGANOMERCURIALS ARE DESCRIBED: 2-chloromercuri-4-nitrophenol, 2-chloromercuri-4,6-dinitrophenol, 4-chloromercuri-2-nitrophenol and 2,6-dichloromercuri-4-nitrophenol. All four organomercurials show large spectral changes in the visible spectrum when thiols displace a more weakly bound ligand such as EDTA from the mercury atom. These spectral changes are primarily associated with pK perturbation of the nitrophenols. The mercurials are therefore chromophoric probes for thiol groups in proteins and other thiols of biological interest. The enzyme d-glyceraldehyde 3-phosphate dehydrogenase from lobster muscle is used as a model system in which the properties of the organomercurials may be illustrated. In particular it is shown how d-glyceraldehyde 3-phosphate dehydrogenase carboxymethylated at the active site may be mercurated at a specific site. This mercurial derivative may be crystallized and shown to be isomorphous with the parent enzyme. The mercurials also act as ;reporter groups' by monitoring phosphate or pyrophosphate binding to the enzyme. The mercurials may also be used to estimate cations by an EDTA displacement method.

Chemical Phenomena↗
PubMed2001

Effects of mercaptoacetate on feeding, circulating glucose and lipids, and gastric emptying in rats fed a carbohydrate-free high-fat diet.

In the present study we investigated whether glucose deprivation contributes to feeding induced by mercaptoacetate (MA), an inhibitor of fatty acid oxidation, in Sprague-Dawley rats fed a carbohydrate-free, high-fat diet (HF-rats). The results show that inhibition of fatty acid oxidation by MA, reflected by a decrease in plasma beta-hydroxybutyrate, elicited eating in the HF-rats and that the eating response was not associated with a decrease in circulating glucose. The effect of MA on food intake was tested in two different substrains (Zur:SD and Ico:OFA SD) of Sprague-Dawley rats. The threshold dose of MA for eliciting eating was much higher in Zur:SD (between 800 and 1,600 micromol/kg) in comparison to Ico:OFA SD rats (between 200 and 400 micromol/kg). At a high dose of MA (1,200 micromol/kg), but not at a low dose (400 micromol/kg) the feeding response in the Ico:OFA SD rats was associated with hyperglycemia due to an increase in glycogenolysis. Unlike in Zur:SD, in Ico:OFA SD rats the higher doses of MA (800 and 1,200 micromol/kg but not 400 micromol/kg) produced a long-term suppression of feeding, which partly might be causally related to the observed inhibitory effect of MA on gastric emptying. The present results indicate that glucose deprivation does not contribute to feeding elicited by MA-induced inhibition of fatty acid oxidation in rats fed a carbohydrate-free, high-fat diet.

3-Hydroxybutyric Acid↗
PubMed1975

Carbon monoxide as a degradation product of cytochrome C and of ascorbic acid.

Cytochrome c has been incubated with 4 different reducing agents at 37 degrees C for 24 h at pH 7.0, and the spectral changes and the production of carbon monoxide have been followed. Only with hydrazine hydrate cytochrome c produced some carbon monoxide. Accidentally, carbon monoxide formation from ascorbic acid was found, amounting to about 0.1 mumol from 15 mumol of ascorbic acid in 24 h under the above conditions.

Acetates↗
PubMed1974

Nutritional features of Bacteroides fragilis subsp. fragilis.

Studies of three reference strains of Bacteroides fragilis subsp. fragilis showed that they grow well in a minimal defined medium containing glucose, hemin, vitamin B(12), minerals, bicarbonate-carbon dioxide buffer, NH(4)Cl, and sulfide. The vitamin B(12) requirement of 0.1 ng/ml was replaced with 7.5 mug of methionine. Cysteine or sulfide was an excellent source of sulfur, thioglycolate was a poor source, and thiosulfate, methionine, beta-mercaptoethanol, dithiothreitol, sulfate, or sulfite did not serve as sole sources of sulfur. Neither single amino acids, nitrate, urea, nor a complex mixture of L-amino acids or peptides effectively replaced ammonia as the nitrogen source. Comparative studies with a few strains of other subspecies of B. fragilis including B. fragilis subsp. vulgatus, B. fragilis subsp. thetaiotaomicron, and B. fragilis subsp. distasonis indicate that they exhibit similar growth responses in the minimal medium. A single strain of B. fragilis subsp. ovatus required other materials. The results indicate the great biosynthetic ability of these organisms and suggest that, in their ecological niche within the large intestine, many nutrients such as amino acids are in very low supply, whereas materials such as ammonia, heme, and vitamin B(12), or related compounds, must be available during much of the time.

Anaerobiosis↗
PubMed1979

Interaction of Chlamydia psittaci reticulate bodies with mouse peritoneal macrophages.

Noninfectious reticulate bodies of Chlamydia psittaci are readily phagocytized by thioglycolate-elicited mouse peritoneal macrophages in monolayer culture. The internalized reticulate bodies are rapidly destroyed as indicated by a 60 to 70% decrease in trichloroacetic acid-precipitable radioisotopic counts in the macrophage pellet by 10 h and a concomitant increase of the trichloroacetic acid-soluble radiolabeled chlamydial nucleic acid in the cytoplasm. This intracellular destruction of reticulate bodies in macrophages is independent of the multiplicity of infection. Reticulate bodies at a high multiplicity of infection, up to 1,000:1, are also incapable of inducing immediate cytotoxicity in macrophages as evidenced by the lack of early release of the host cell-soluble cytoplasmic enzyme lactic dehydrogenase. Thus, it appears that the virulence factors for (i) initiation or maintenance of intracellular survival via circumvention of phagolysosome formation and (ii) host cell damage are either missing or not expressed by the RB form of this bacterium.

Animals↗
PubMed1986

Control of food intake by fatty acid oxidation.

The role of fatty acid oxidation in the control of food intake was studied using mercaptoacetate (MA), an inhibitor of fatty acid oxidation. Food intake, plasma free fatty acids (FFA) and ketone bodies, and blood glucose were measured. Rats were fed either a low-fat (LF, 3.33% fat) or a medium-fat (MF, 18% fat) diet. At the onset of the dark phase of the lighting cycle, MA did not affect food intake in LF rats but increased it 74% in MF rats in comparison to control. Four hours after the injection the effect of MA on food intake disappeared. In the middle of the bright phase of the lighting cycle, MA increased food intake in MF rats approximately 120% up to 6 h postinjection. After MA, plasma FFA concentration was elevated, and plasma 3-hydroxybutyrate concentration was lowered, indicating that fatty acid oxidation had been successfully reduced. MA did not affect blood glucose. These results indicate fatty acid oxidation is involved in the control of food intake, at least when the dietary fat level is relatively high.

3-Hydroxybutyric Acid↗
PubMed1994

Hepatic vagotomy effects on metabolic challenges during parenteral nutrition in rats.

During parenteral nutrition (PN) glucoprivic-induced feeding appeared to be neutralized by the oxidation of infused fatty acids. With the use of a latin-square design, the feeding response to 2-deoxy-D-glucose (2-DG) and/or 2-mercaptoacetate (MA) was evaluated in male Sprague-Dawley rats with hepatic branch vagotomy (HV) or sham operations (SO). Rats received continuous infusions of 0.9% saline or PN providing 100% of daily caloric needs (PN-100) for four consecutive days. During PN-100, food intake was stimulated by 2-DG in HV rats and when fatty acid oxidation was simultaneously inhibited by MA. 2-DG-induced hyperglycemia was apparent under all conditions. Lipoprivic-induced feeding and increased plasma free fatty acid concentrations were absent in HV rats, whether MA was administered alone or with 2-DG. The feeding response to glucoprivic challenges is influenced by the relative availability of alternate energy sources. The lack of feeding response to 2-DG during PN-100 is mediated by vagal input of hepatic fatty acid oxidation status.

Animals↗
PubMed1997

Development of independent ingestive responding to blockade of fatty acid oxidation in rats.

The present studies examined the development of ingestive responsiveness to blockade of fatty acid oxidation in rat pups using 2-mercaptoacetate (MA), an inhibitor of mitochondrial acyl-coenzyme A dehydrogenases, or methyl palmoxirate (MP), an inhibitor of carnitine palmitoyltransferase I (CPT-I). Rat pups aged 6, 9, 12, or 15 days of age received an intraperitoneal injection of 0, 100, 200, 400, or 800 mumol/kg MA, and intake of a commercial half-and-half or 15% glucose diet from the floor of test containers was assessed in a 30-min test beginning 1 h after administration of MA. The results demonstrate that, although no dose of MA affected intake of either diet in pups 9 days or younger, low doses of MA increased intake and the highest dose suppressed intake of both diets in pups 12 days of age or older. Physiological measurements indicated that levels of beta-hydroxybutyrate were significantly lower following doses of 400 or 800 mumol/kg MA in 9-, 12-, and 15-day-old pups and that gastric emptying was inhibited in 12 and 15 day olds by 800 mumol/kg MA. Intake of a commercial half-and-half diet from the floor of test containers was also assessed in 12- to 18-day-old rat pups 6.5 h after they received a gavage load of 0, 1.25, 2.5, 5, or 10 mg/kg MP. Unlike MA, MP did not increase intake of a commercial half-and-half diet in rat pups 12 or 15-18 days of age; instead, the highest dose of MP suppressed intake in 15- to 18-day-old pups. The failure of MP to enhance intake in pups at the ages tested is likely related to composition of dam's milk; rat milk is high in medium-chain fatty acids that do not require CPT-I for entry into mitochondria. Thus it is likely that MP does not significantly block fatty acid oxidation in pups at the ages tested. On the other hand, blockade of fatty acid oxidation produced by MA significantly affects intake by 12 days of age, suggesting it may be the first metabolic signal that influences intake in rat pups.

3-Hydroxybutyric Acid↗
PubMed2000

Protective effect of erdosteine against hypochlorous acid-induced acute lung injury and lipopolysaccharide-induced neutrophilic lung inflammation in mice.

The effect of erdosteine, a mucoactive drug, on hypochlorous acid (HOCl)-induced lung injury, and the lipopolysaccharide (LPS)-induced increase in tumour necrosis factor-alpha (TNF-alpha) production and neutrophil recruitment into the airway, was investigated. Male BALB/c mice were orally administered erdosteine (3-100 mgkg(-1)), ambroxol hydrochloride (ambroxol) (3-30 mgkg(-1)), S-carboxymethyl-L-cysteine (S-CMC) (100-600 mgkg(-1)) or prednisolone (10 mgkg(-1)), 1 h before intratracheal injection of HOCl or LPS. In the HOCl-injected mice, erdosteine markedly suppressed increases in the ratios of lung wet weight to bodyweight and lung dry weight to bodyweight, whereas the other mucoactive drugs ambroxol and S-CMC had little effect. Erdosteine also inhibited the LPS-induced neutrophil influx, although it did not affect the increased level of TNF-alpha in the bronchoalveolar lavage fluid. The results suggest that attenuation of reactive oxygen species and neutrophil recruitment is involved in the clinical efficacy of erdosteine in the treatment of chronic bronchitis.

Administration, Oral↗
PubMed1999

Behavioral specificity of effects of 2-mercaptoacetate on independent ingestion in developing rats.

Blockade of fatty acid oxidation in rat pups using 2-Mercaptoacetate (MA) produces increases in independent ingestion by 12 days of age. In the present experiments, the behavioral specificity of the effects of MA on ingestion were examined. In the first experiment, administration of MA to pups aged 9 and 12 days of age failed to increase intake of an oral infusion of a milk diet. In the second experiment, administration of MA did enhance intake of a milk diet in a short-term test of consuming from the floor of a test container and the level of gastric fill appeared to determine intake during the test. Finally, administration of MA did not affect intake of water in 9- or 12-day-old pups. These results suggest that MA produces increases in intake through specific effects on selective ingestive responses and not through nonspecific behavioral arousal.

Animals↗