Disease relevance of o-hydroxybenzoic acid

• Sulfasalazine and salicylate-induced exacerbation of ulcerative colitis [1].
• Decreased serum salicylate concentrations in children with rheumatic fever treated with antacid [2].
• When deficient erythrocytes from patients with severe hemolysis were incubated with salicylate (2 to 30 mg per deciliter), there was a marked decrease (25 to 75 percent) in ATP [3].
• Phenacetin abuse is known to produce kidney disease; salicylate use is supposed to prevent cardiovascular disease [4].
• Salicylate and mitochondrial injury in Reye's syndrome [5].

Psychiatry related information on o-hydroxybenzoic acid

• The presenting signs of salicylate poisoning, especially chronic (repeated administration of therapeutic or excessive doses for longer than 12 h), can include metabolic acidosis, hypoglycaemia, lethargy, and coma and fits [6].
• Salicylic acid potentiates an agonist-dependent gain control that amplifies pathogen signals in the activation of defense mechanisms [7].
• Seven men and one woman with primary affective disorder, mania, were given a slow intravenous infusion of physostigmine salicylate [8].
• It may lead to erroneous conclusions concerning patient compliance, unwarranted increases in salicylate dosage and resultant toxicity, and delay of appropriate therapeutic maneuvers [9].
• OBJECTIVE: A multicenter trial to evaluate the efficacy of controlled-release physostigmine salicylate, a cholinesterase inhibitor, was conducted in 1,111 mild-to-moderate Alzheimer's disease (AD) subjects [10].

High impact information on o-hydroxybenzoic acid

• This cell death requires salicylic acid, a plant immune system activator [11].
• These data provide a missing link between accumulation of SA and activation of NPR1 in the SAR signaling pathway [12].
• SAR induction results in accumulation of the signal molecule salicylic acid (SA), which induces defense gene expression via activation of NPR1 [12].
• Transposon inactivation of Arabidopsis MAP kinase 4 produced the mpk4 mutant exhibiting constitutive systemic acquired resistance (SAR) including elevated salicylic acid (SA) levels, increased resistance to virulent pathogens, and constitutive pathogenesis-related gene expression shown by Northern and microarray hybridizations [13].
• The effects of the controlled-release preparation on plasma levels of aspirin and salicylate, serum levels of thromboxane B2, and urinary dinor metabolites of prostacyclin and thromboxane B2 (measured by gas chromatography-mass spectrometry) were compared with those of conventional immediate-release aspirin in normal volunteers [14].

Chemical compound and disease context of o-hydroxybenzoic acid

• Salicylate other than 5-aminosalicylic acid ineffective in ulcerative colitis [15].
• With the glycine-rich protein gene, an upstream sequence of 645 base pairs was sufficient for tobacco mosaic virus and salicylate inducibility of the reporter gene, whereas constructs containing 400 base pairs or fewer of the glycine-rich protein promoter were largely inactive [16].
• Jasmonic acid (JA), but not SA, rapidly accumulates in phloem exudates of leaves challenged with an avirulent strain of Pseudomonas syringae [17].
• The salicylate-derived mycobactin siderophores of Mycobacterium tuberculosis are essential for growth in macrophages [18].
• Expression of the gene for a small GTP binding protein in transgenic tobacco elevates endogenous cytokinin levels, abnormally induces salicylic acid in response to wounding, and increases resistance to tobacco mosaic virus infection [19].

Biological context of o-hydroxybenzoic acid

• These results have implications for understanding how salicylic acid activates defense signaling in cells spatially removed from infection sites without causing cell death [11].
• Salicylate is known to uncouple mitochondrial oxidative phosphorylation [3].
• Fibrinolysis in blood, but not in plasma, increased 66 per cent after sodium salicylate [20].
• Sodium salicylate and aspirin also inhibited NF-kappa B-dependent transcription from the Ig kappa enhancer and the human immunodeficiency virus (HIV) long terminal repeat (LTR) in transfected T cells [21].
• Twelve lizards received identical injections of bacteria along with a nontoxic dose of sodium salicylate; five animals increased their mean body temperature at least 0.6 degrees C and survived the week, whereas seven did not develop a fever and died within 3 days [22].

Anatomical context of o-hydroxybenzoic acid

• Sodium salicylate increased fibrinolytic activities of blood and of purified polymorphonuclear leukocytes in vitro, whereas aspirin had little effect [20].
• To learn whether in vitro blastogenesis of lymphocytes is affected by in vivo salicylate ingestion, blood samples were obtained from 19 normal volunteers before and after therapeutic doses of aspirin [23].
• Marsupials, placentals and their close therian relatives possess complex (tribosphenic) molars that are capable of versatile occlusal functions [24].
• As salicylate blocks electromotility in cochlear outer hair cells at the same concentration, the role of prestin as a motor protein may need to be reassessed [25].
• Scanning electron micrographs of goats fed controlled diets demonstrate that cementum bands preserve variations in the relative orientation of collagen fibers that reflect changes in the magnitude and frequency of occlusal forces from chewing different quality diets [26].

Associations of o-hydroxybenzoic acid with other chemical compounds

• 1. The effects of phenacetin on morbidity and mortality, with adjustment for base-line salicylate excretion, were similar [4].
• Jasmonate and salicylate induce expression of herbivore cytochrome P450 genes [27].
• Other inducers of the heat shock response, including salicylate, dinitrophenol, ethanol, and arsenite, have no effect on HSF trimerization in vitro, indicating that these inducers act by indirect mechanisms [28].
• PURPOSE: Experiments were planned to determine the lowest dose of aspirin that can markedly suppress the levels of mucosal prostaglandins E2 and F(2alpha) in colorectal mucosa and to determine whether a relationship exists between these levels and plasma levels of both acetylsalicylic acid and its metabolite, salicylic acid [29].
• Experiments using radiolabeled chloramphenicol and salicylate demonstrated active efflux of both compounds in the presence of the gene cluster [30].

Gene context of o-hydroxybenzoic acid

• Insulin resistance was improved by systemic neutralization of IL-6 or salicylate inhibition of IKK-beta [31].
• EDS1 is essential for elaboration of the plant hypersensitive response, whereas EDS1 and PAD4 are both required for accumulation of the plant defence-potentiating molecule, salicylic acid [32].
• We are systematically investigating the role of individual TGA factors in the transcriptional control of pathogenesis-related (PR) defense genes, whose expression is stimulated in leaves by salicylic acid (SA) through a stimulus pathway involving NPR1 [33].
• In both responses, EDS1, assisted by its interacting partner, PHYTOALEXIN-DEFICIENT4 (PAD4), regulates accumulation of the phenolic defense molecule salicylic acid (SA) and other as yet unidentified signal intermediates [34].
• ACD6, a novel ankyrin protein, is a regulator and an effector of salicylic acid signaling in the Arabidopsis defense response [35].

Analytical, diagnostic and therapeutic context of o-hydroxybenzoic acid

• No correlation could be demonstrated between the plasma salicylic acid level and the degree of suppression of blastogenesis [23].
• Plasma concentrations of acetylsalicylic acid and salicylic acid were determined by use of high-performance liquid chromatography [29].
• Transcriptional analysis, fluorometry, and flow cytometry revealed evidence of salicylic acid-mediated activation of the stress-response gene sigB [36].
• After oral administration of aspirin, the plasma contained mostly salicylic acid (98%), whereas the gastric mucosa contained mostly aspirin (80%-85%) [37].
• These specimens were injected with silicon rubber compound, xerographed, cleared with methyl salicylate, and examined with transillumination before histologic sampling [38].

References