Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Hydroxamic Acids”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 1,567 records · Page 87Linked to original sources
PubMed1982

Origin of excess urinary nitrate in the rat.

The ability of intestinal microorganisms to N-oxidize nitrogenous compounds to nitrite or nitrate was evaluated both in vivo and in vitro. Nitrate balance studies with germ-free and conventional rats indicated that the host and not the microbial flora is responsible for excess urinary nitrate. In vitro studies showed that most intestinal microorganisms are not able to N-oxidize nitrogenous compounds to nitrite. Although the metabolic pathway for endogenous nitrate formation remains unknown, the capacity of the rats to N-oxidize acetohydroxamate and hydroxylamine to nitrate indicates that such compounds could be intermediates in nitrate synthesis.

Amino Acids↗
PubMed1995

Pharmacologically distinct, pertussis toxin-resistant inward currents evoked by metabotropic glutamate receptor (mGluR) agonists in dorsolateral septal nucleus (DLSN) neurons.

We have reported previously that a selective metabotropic glutamate receptor (mGluR) agonist, (1S,3R)-1-aminocyclopentane-1,3-dicarboxylic acid (1S,3R-ACPD), caused a slow membrane depolarization in rat dorsolateral septal nucleus (DLSN) neurons. Using single electrode voltage-clamp recording methods, we now investigate the pharmacological properties of the receptor that mediates ACPD-induced membrane currents in DLSN neurons recorded from pertussis toxin (PTX)-treated rats. Two pharmacologically distinct inward currents, that is, the ACPD current and Qm current, have been identified based on their agonist preference and sensitivity to various antagonists. The ACPD current is blocked by L-2-amino-4-phosphonobutyric acid (L-AP4), but is insensitive to L-aspartic acid-beta-hydroxamate (L-AA beta H), (+)-alpha-methyl-4-carboxyphenylglycine (+)-MCPG), or L-2-amino-3-phosphonopropionic acid (L-AP3). The Qm current is blocked by L-AA beta H and (+)-MCPG, but is insensitive to L-AP3 or L-AP4. These two inward currents distribute differentially within subpopulations of DLSN neurons. The ACPD current is the only current observed in most DLSN "burster" neurons, while the Qm current is observed more frequently in DLSN "nonburster" neurons. The pharmacological profiles of these currents suggest that the Qm current is likely mediated by mGluR1 or mGluR5, while the ACPD current is mediated by receptors that are pharmacologically distinct from any of the currently cloned mGluRs.

Animals↗
PubMedDate not supplied

Induction of reporter gene expression by inhibitors of histone deacetylase.

The relationship between histone acetylation and induction of gene expression was studied in Ros 17/2.8 rat osteosarcoma cells transfected with the pCH110 plasmid. This plasmid is commonly used in cotransfections as a measure of transfection efficiency. Cells were incubated for 48 hours with sodium butyrate, phenylbutyrate, 3-bromopropionate or trichostatin A. There was an approximate relationship between the extent of beta-galactosidase induction and the degree of histone hyperacetylation. Trichostatin A was the most effective agent followed by sodium butyrate and then phenylbutyrate. The toxicity of 3-bromopropionate made it difficult to compare its action with the other agents. Phenylbutyrate was less effective than sodium butyrate in causing induction of gene expression and histone hyperacetylation but this action may be a factor in the growth-inhibitory and differentiating activity of phenylbutyrate which has also been attributed to glutamine depletion.

Animals↗
PubMed1990

Excitatory and inhibitory transmission from dorsal root afferents to neonate rat motoneurons in vitro.

Intracellular recordings were made from antidromically identified motoneurons in neonate (12-22 days) rat transverse spinal cord slices and the transmitters and receptors probably involved in initiating the excitatory (EPSP) and inhibitory (IPSP) postsynaptic potentials were investigated. Stimulation of dorsal roots elicited in motoneurons an EPSP, an IPSP, or an EPSP followed by an IPSP. EPSPs in 70% of motoneurons had a short latency (less than or equal to 1 ms) and in the remaining cells a latency longer than 1 ms. The IPSPs had a long latency (greater than or equal to 1 ms). Short- and long-latency EPSPs were enhanced by the acidic amino acid uptake inhibitor L-aspartic acid-beta-hydroxamate (AAH) and depressed by the non-selective glutamate receptor antagonists gamma-D-glutamylglycine (DGG) and kynurenic acid. Short-latency EPSPs were suppressed by the quisqualate/kainate (QA/KA) receptor antagonist 6,7-dinitroquinoxaline-2,3-dione (DNQX) but not by the N-methyl-D-aspartate (NMDA) receptor antagonists D-(-)-2-amino-5-phosphonovaleric acid (APV) and ketamine. Long-latency EPSPs were reduced by DNQX as well as by APV and ketamine. Superfusion of the slices with a Mg-free solution increased the EPSPs and unmasked a late, APV-sensitive component. The IPSP was reduced by the glycine antagonist strychnine as well as by APV and ketamine but resistant to DNQX. The results indicate that stimulation of dorsal roots elicited in motoneurons a monosynaptic EPSP mediated by glutamate/aspartate acting predominantly on the QA/KA subtype of glutamate receptors; an NMDA component can be unveiled in Mg-free solution.(ABSTRACT TRUNCATED AT 250 WORDS)

Action Potentials↗