Disease relevance of AMMONIUM THIOGLYCOLATE

• On d 10 of each period, two animals per treatment were injected intravenously with either mercaptoacetate (300 mumol/kg body weight 0.75) or saline at 2 h postfeeding [1].
• The results of the present study show that centrally acting dopaminergic and serotoninergic anorectic drugs, the opiate receptor antagonist naloxone, the alpha-adrenoceptor blocking drug phentolamine, and peripherally administered 5-HT counteract the overeating induced by mercaptoacetate [2].
• In the main experiment, either 2DG or MA or the two drugs together was sufficient to induce a significant, temporary hypothermia [3].

Psychiatry related information on AMMONIUM THIOGLYCOLATE

• Further, no evidence was found to suggest that MA, either alone or in combination with 2-DG (100 mg/kg), produces interoceptive cues like 2-DG or 24-hr food deprivation [4].

High impact information on AMMONIUM THIOGLYCOLATE

• Carboxymethylation of mercaptoacetate-treated H4 with iodo[3H) acetate acid yielded 3H-labeled H4 and subsequent chymotryptic digestion showed that the only radioactive peptides were again those containing the lysines known to be the normal sites of enzymatic acetylation [5].
• In TG-elicited C3HeB/FeJ peritoneal macrophages, in contrast, expression of both caveolin-1 protein and mRNA is up-regulated in vitro in response to LPS stimulation [6].
• In contrast, Thio M phi s stimulated in vitro with gamma interferon (IFN-gamma), with or without lipopolysaccharide, resulted in cells that exhibited chlamydiastatic activity which was lost shortly after IFN-gamma was removed from the culture medium [7].
• Inhibition of fatty acid oxidation by mercaptoacetate stimulates food intake of rats fed dietary fat [1].
• Lesion and Fos studies have shown that the neural pathway for feeding stimulated by mercaptoacetate (MA)-induced blockade of fatty acid oxidation includes several structures rich in galanin cell bodies or terminals [8].

Chemical compound and disease context of AMMONIUM THIOGLYCOLATE

• 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) [9].

Biological context of AMMONIUM THIOGLYCOLATE

• GAL gene expression and peptide immunoreactivity in this area is enhanced by food deprivation; in contrast, it is reduced by injection of MA [10].
• MA treatment during hibernation affected thermoregulation after the animals aroused, including an increased duration of euthermia and maintenance of erratic patterns of Tb [11].
• 2DG given during hibernation significantly increased latency to regain euthermia, especially during the initial phase of rewarming (from first Tb > 10 degrees C to first Tb > 15 degrees C), without affecting the duration or other features of the ensuing euthermic period; MA did not affect rate of rewarming [11].
• Recent in vivo studies investigating the effects of mercaptoacetate on the hepatic membrane potential and on afferent activity of the hepatic vagus branch are consistent with this notion [12].
• Glucose homeostasis and sympathoadrenal activity in mercaptoacetate-treated rats [13].

Anatomical context of AMMONIUM THIOGLYCOLATE

• Mercaptoacetate induced Fos-li in the nucleus of the solitary tract (NTS), the central subnucleus of the lateral parabrachial nucleus (1PBN), the central nucleus of the amygdala (CNA, lateral part) and the dorsal motor nucleus of the vagus (DMV) [14].
• Both food deprivation and MA (600 micromol/kg), but not 2-DG, affected GAL in the hypothalamus, in one specific area [10].
• In contrast, MA-induced lipoprivation increased the outflow of NE from the sympathetic nerve endings without a significant effect on plasma E concentrations [15].
• This conclusion was reinforced by the use of inhibitors of fatty acid beta-oxidation, methyl palmoxirate or mercaptoacetate, exposure to which during oocyte maturation led to developmental failure post-fertilisation [16].

Associations of AMMONIUM THIOGLYCOLATE with other chemical compounds

• Furthermore, chymotryptic digestion of histone H4 from mercaptoacetate-treated cells and subsequent mercury-affinity chromatography revealed that the only peptides which bound to the column were the NH2-terminal peptides, the ones containing the lysines known to be the normal sites of in vivo acetylation [5].
• Results revealed that total destruction of the PVN does not impair either 2DG- or MA-induced food intake and suggest that this structure is not essential for these particular controls of feeding [17].
• The energy antimetabolites 2-deoxy-D-glucose (2-DG) and Na-2-mercaptoacetate (MA) both reliably augment food intake in rats [4].
• Rats were injected acutely with antimetabolites of either glucose (2 deoxy-D-glucose, 2DG), fat (methylpalmoxirate, MP or mercaptoacetate, MAC), or the combination of these agents, in dosages known to stimulate food intake [18].
• Inhibition of fatty acid oxidation with either mercaptoacetate (which blocks acetyl-CoA dehydrogenase) or methylpalmoxirate will increase food intake [19].

Gene context of AMMONIUM THIOGLYCOLATE

• Food deprivation which enhances aPVN GAL produces a marked increase in fat ingestion, whereas MA which reduces aPVN GAL causes a specific reduction in fat ingestion along with a stimulation of protein intake [10].
• Matrix-assisted laser desorption ionization time-of-flight mass spectrometric studies revealed that 2 mol of mercaptoacetate covalently bind to L1 upon incubation of the enzyme with N-benzylacetyl-d-alanylthioacetic acid; however, this covalently modified enzyme has the same activity as wild-type L1 [20].
• The antimetabolite mercaptoacetate, in contrast, which blocks fatty acid oxidation, produced no significant change and actually tended to reduce NPY levels in the ARC [21].
• There were, however, no significant effects of MA on free fatty acid, insulin, glucagon, epinephrine, and norepinephrine concentrations in both dietary conditions either at rest or after exercise [22].

Analytical, diagnostic and therapeutic context of AMMONIUM THIOGLYCOLATE

• Conversely, the antichlamydial activity of IB M phi s was stable over time but not through the production of autostimulatory cytokines, as evidenced by the lack of stimulation of Thio M phi s to restrict 6BC replication in coculture experiments [7].
• Mercaptoacetate or vagotomy had no effect on diet selection in rats fed unsaturated fat [23].
• Intravenous injection of mercaptoacetate decreased dry matter intake to 25% that of the control during 4 h postinjection [1].
• Responses of hepatic and celiac vagal afferents to intraportal mercaptoacetate in rats fed a high-fat or low-fat diet [24].
• Reversed-phase ion-pair high-performance liquid chromatography of mercaptoacetate and N-acetylcysteine after derivatization with N-(1-pyrene)maleimide and N-(7-dimethylamino-4-methyl-3-coumarinyl)maleimide [25].

References