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PubMed1993

Dermal and underlying tissue pharmacokinetics of salicylic acid after topical application.

The time course of salicylic acid at a dermal application site and in local underlying tissues below the site in rats was examined using a physiologically based pharmacokinetic model assuming first-order diffusional mass transfer between the dermis and underlying tissues. The concentrations of salicylic acid in tissues below the applied site were measured and compared with plasma concentrations and concentrations in similar tissues on the contralateral side. The direct penetration of salicylic acid was dominant only to a depth of 3-4 mm below the applied site for the first approximately 2 hr after application. The time course of salicylic acid in individual rats was modeled using known tissue blood flows and tissue-tissue clearances by (i) numerical integration and nonlinear regression of a series of differential equations representing events in individual tissues, and (ii) numerical integration and nonlinear regression of a single differential equation representation of the concentration-time course in an individual tissue with a polynomial representation of salicylate concentrations in other input tissues and an exponential representation of the input from the solution. Tissue-tissue clearances were deduced by both nonlinear regression and mass balance analysis (only for underlying dermis) using area-under-the-curves from salicylic acid tissue penetration data in anesthetized rats. The relative importance of direct penetration and blood supply in determining the concentrations of salicylic acid in deeper tissues was assessed by simulations in which either no direct penetration occurred or there was zero input from blood. Simulations confirm that direct penetration is only evident in the superficial tissues for approximately 2 hr. An attempt was also made to examine the dermal pharmacokinetics of salicylic acid using statistical moments.

Administration, Topical↗
PubMed1992

Inhibition of Sucrose Enhancer Effect of the Potato Proteinase Inhibitor II Promoter by Salicylic Acid.

Effect of salicylic acid (SA) on the expression of the potato proteinase inhibitor (PI) II promoter was studied with transgenic tobacco plants (Nicotiana tabacum) carrying a gene fusion between the PI-II promoter and the chloramphenicol acetyltransferase (cat) reporter. As previously observed, the PI-II promoter was inducible by wounding and the promoter activity was further enhanced by sucrose. Addition of SA did not influence the wound induction of the PI-II promoter but significantly inhibited the sucrose response. The 5'-deletion mutant -573 was unable to respond to wounding but did respond to sucrose and SA. The 3'-deletion analysis indicated the presence of a sucrose-responsive element between -574 and -520. A study of the insertion mutants revealed the function of another sucrose-responsive element between -522 and -500. Enhancer effects of these sucrose-responsive elements were inhibited by SA. These studies suggest that SA inhibits PI-II promoter activity by decreasing the sucrose response. Analysis of SA-related chemicals revealed that only acetyl-SA showed a similar inhibitory effect, and other hydroxybenzoic acids had little or no effect on the sucrose enhancer activity. Therefore, it seems that the interaction between SA and the receptor molecule is specific.

Journal Article↗
PubMed1997

Salicylic Acid Interferes with Tobacco Mosaic Virus Replication via a Novel Salicylhydroxamic Acid-Sensitive Mechanism.

Salicylic acid (SA) induces resistance to all plant pathogens, including bacteria, fungi, and viruses, but the mechanism by which SA engenders resistance to viruses is not known. Pretreatment of tobacco mosaic virus (TMV)-susceptible (nn genotype) tobacco tissue with SA reduced the levels of viral RNAs and viral coat protein accumulating after inoculation with TMV. Viral RNAs were not affected equally, suggesting that SA treatment interferes with TMV replication. Salicylhydroxamic acid (SHAM), an inhibitor of the mitochondrial alternative oxidase, antagonized both SA-induced resistance to TMV in nn genotype plants and SA-induced acquired resistance in resistant (NN genotype) tobacco. SHAM did not inhibit induction of the PR-1 pathogenesis-related protein or induction of resistance to Erwinia carotovora or Botrytis cinerea by SA. This indicates that SA induces resistance to TMV via a novel SHAM-sensitive signal transduction pathway (potentially involving alternative oxidase), which is distinct from that leading to resistance to bacteria and fungi.

Journal Article↗
PubMed1985

Dose-dependent effect of calcium and magnesium etidronate on salicylic acid absorption in the rat.

Disodium etidronate affected salicylic acid absorption from the rat small intestine, in-situ, when instilled into a jejunal segment for different exposure times before the salicylic acid absorption was measured. At low etidronate concentrations and short exposure times, the salicylic acid absorption rate was significantly increased compared with saline controls. At high etidronate concentrations and longer exposure times, the absorption rate was reduced. Etidronate precomplexed with calcium or magnesium ions at low concentrations still enhanced salicylic acid absorption but at high concentrations absorption of salicylic acid was close to saline controls. Intestinal mucosa exposed to high etidronate concentrations showed a progressive structural destruction but with the complexes, there was no visible alteration. It is proposed that a solubilized etidronate complex, formed either in-situ or administered as such, is responsible for enhancing salicylic acid absorption. This effect is hidden at high etidronate concentrations because of the deterioration of the mucosal surface and at high complex concentrations because these decrease the absorbing surface area and increase the viscosity of the lumen contents.

Animals↗
PubMed1997

Influence of salicylic acid on H2O2 production, oxidative stress, and H2O2-metabolizing enzymes. Salicylic acid-mediated oxidative damage requires H2O2.

We investigated how salicylic acid (SA) enhances H2O2 and the relative significance of SA-enhanced H2O2 in Arabidopsis thaliana. SA treatments enhanced H2O2 production, lipid peroxidation, and oxidative damage to proteins, and resulted in the formation of chlorophyll and carotene isomers. SA-enhanced H2O2 levels were related to increased activities of Cu,Zn-superoxide dismutase and were independent of changes in catalase and ascorbate peroxidase activities. Prolonging SA treatments inactivated catalase and ascorbate peroxidase and resulted in phytotoxic symptoms, suggesting that inactivation of H2O2-degrading enzymes serves as an indicator of hypersensitive cell death. Treatment of leaves with H2O2 alone failed to invoke SA-mediated events. Although leaves treated with H2O2 accumulated in vivo H2O2 by 2-fold compared with leaves treated with SA, the damage to membranes and proteins was significantly less, indicating that SA can cause greater damage than H2O2. However, pretreatment of leaves with dimethylthiourea, a trap for H2O2, reduced SA-induced lipid peroxidation, indicating that SA requires H2O2 to initiate oxidative damage. The relative significance of the interaction among SA, H2O2, and H2O2-metabolizing enzymes with oxidative damage and cell death is discussed.

Arabidopsis↗
PubMed1984

[Effects of acetylsalicylic acid on partial functions of human thrombocytes are not inhibited in vivo by salicylic acid].

Acetylsalicylic acid inhibits platelet function. In plasma acetylsalicylic acid is rapidly deacetylated to salicylic acid which is slowly eliminated and has no direct inhibitory effects on platelet function. However, salicylic acid prevents the inhibition by acetylsalicylic acid of collagen-induced aggregation of human thrombocytes in vitro. It was suggested that salicylic acid might inhibit the antiplatelet effects of acetylsalicylic acid in vivo and therefore low-dose acetylsalicylic acid would be more effective for antithrombotic therapy. A 500-mg tablet of acetylsalicylic acid applied 90 min after oral administration of 500 mg salicylic acid to six healthy male volunteers led to the same inhibition of collagen-induced platelet aggregation and tissue-extract-induced platelet stimulation as 500 mg acetylsalicylic acid alone. These results cannot give additional support to the recommendation of low-dose acetylsalicylic acid in the prevention of thromboembolic disease.

Administration, Oral↗
PubMed1985

The effect of cimetidine on the pharmacokinetics of salicylic acid.

The pharmacokinetics of the interaction between salicylic acid and cimetidine was investigated in 11 healthy male and female volunteers. The plasma concentrations of total and free salicylic acid were measured. The kinetic disposition of salicylic acid after multiple administration of cimetidine (1 g per day) showed two modifications: the elimination rate was slower and plasma clearance was reduced. The corresponding area under concentration-time curves was always significantly greater. These differences were the same in both sexes. The rate of absorption, peak salicylate concentration and plasma protein binding of salicylic acid in the presence of cimetidine were not changed.

Adult↗
PubMed2001

Salicylic acid in soups prepared from organically and non-organically grown vegetables.

BACKGROUND: Salicylic acid is a chemical signal in plants infected by pathogens and it is responsible for the anti-inflammatory action of aspirin. Patients who take aspirin have a reduced risk of developing atherosclerosis and colorectal cancer, both of these pathologies having an inflammatory component. Dietary salicylic acid may help to prevent these conditions. We wondered if foods made from organically-reared plants might have a higher content of salicylic acid than those made from non-organic plants, since the latter are more likely to be protected from infection by the application of pesticides. OBJECTIVE: To determine if organic vegetable soups have a higher salicylic acid content than non-organic vegetable soups. METHODS: The contents of salicylic acid in organic and non-organic vegetable soups purchased from supermarkets were determined. Salicylic acid was identified by varying the chromatographic conditions and comparing the retention times of the unknown substance in the extracts with salicylic acid; by treating extracts of the soups with salicylate hydroxylase; and by using GCMS. Salicylic acid was determined by using HPLC with electrochemical detection. RESULTS: Salicylic acid was present in all of the organic and most of the non-organic vegetable soups. The median contents of salicylic acid in the organic and non-organic vegetable soups were 117 (range, 8-1040) ng x g(-1) and 20 (range, 0-248) ng x g(-1) respectively. The organic soups had a significantly higher content of salicylic acid (p=0.0032 Mann Whitney U test), with a median difference of 59 ng g(-1) (95 % confidence interval, 18-117ng x g(-1)). CONCLUSIONS: Organic vegetable soups contained more salicylic acid than non-organic ones, suggesting that the vegetables and plants used to prepare them contained greater amounts of the phenolic acid than the corresponding non-organic ingredients. Consumption of organic foods may result in a greater intake of salicylic acid.

Agriculture↗
PubMed1995

Benzoic acid 2-hydroxylase, a soluble oxygenase from tobacco, catalyzes salicylic acid biosynthesis.

Benzoic acid 2-hydroxylase (BA2H) catalyzes the biosynthesis of salicylic acid from benzoic acid. The enzyme has been partially purified and characterized as a soluble protein of 160 kDa. High-efficiency in vivo labeling of salicylic acid with 18O2 suggested that BA2H is an oxygenase that specifically hydroxylates the ortho position of benzoic acid. The enzyme was strongly induced by either tobacco mosaic virus inoculation or benzoic acid infiltration of tobacco leaves and it was inhibited by CO and other inhibitors of cytochrome P450 hydroxylases. The BA2H activity was immunodepleted by antibodies raised against SU2, a soluble cytochrome P450 from Streptomyces griseolus. The anti-SU2 antibodies immunoprecipitated a radiolabeled polypeptide of around 160 kDa from the soluble protein extracts of L-[35S]-methionine-fed tobacco leaves. Purified BA2H showed CO-difference spectra with a maximum at 457 nm. These data suggest that BA2H belongs to a novel class of soluble, high molecular weight cytochrome P450 enzymes.

Antibodies↗
PubMed1988

Effect of salicylic acid on mitochondrial-peroxisomal fatty acid catabolism.

To understand the possible role of salicylic acid in the pathogenesis of Reye's syndrome, we examined its effect on the oxidative metabolism of fatty acids in the rat liver mitochondrial-peroxisomal fraction. Fatty acids of different chain lengths are oxidized in different organelles. Octanoic acid is oxidized in mitochondria, lignoceric acid in peroxisomes, and palmitic acid in both mitochondria and peroxisomes. Salicylic acid (up to 1 mM concentration) had no effect on the oxidation of [1-14C]lignoceric acid. However, at the same concentration it inhibited the oxidation of [1-14C]palmitic acid by 26% and [1-14C] octanoic acid by 42%. The apparent Ki for the oxidation of [1-14C] octanoic acid, [1-14C]palmitic acid and [1-14C]lignoceric acid were 0.27, 6.0, and 14.8 mM, respectively. This selective inhibition of mitochondrial oxidation of medium-chain (octanoic acid) and long-chain (palmitic acid) fatty acids by salicylic acid may potentiate the accumulation of fatty acids in plasma in Reye's syndrome patients.

Animals↗
PubMed1991

Inhibition by salicylic acid of the activation and thus oxidation of long chain fatty acids. Possible role in the development of Reye's syndrome.

Administration of either aspirin or salicylic acid (3 mmol.kg-1 b.wt. i.p.) decreased by 50 and 65%, respectively, the in vivo oxidation of [U-14C]palmitic acid to [14C]CO2 in mice; after salicylic acid administration, exhalation of [14C]CO2 from [1-14C]palmitic acid, [1-14C]octanoic acid or [1-14C]butyric acid was decreased by 87, 33 and 38%, respectively. Inhibition lasted 9 hr. It was associated with markedly decreased blood glucose concentrations and increased plasma ketone bodies. Repeated administration of salicylic acid (2 mmol.kg-1 i.p. every 8 hr) tripled hepatic triglycerides and produced mild microvesicular steatosis of the liver at 22 hr in fasted mice. In vitro, salicylic acid (1.5 mM) had no or little effect on the formation of beta-oxidation products from [1-14C]octanoic or [1-14C]palmitoyl-L-carnitine, in the presence of ATP, carnitine (40 microM) and coenzyme A (40 microM), but decreased by 51% that from [1-14C]palmitic acid. In the latter system, increasing the concentrations of coenzyme A and carnitine to 200 microM suppressed the inhibitory effect of salicylic acid. Salicylic acid (1.5 mM) decreased by 80% the in vitro mitochondrial formation of palmitoyl-coenzyme A from [1-14C]palmitic acid and 10 microM coenzyme A; again, increasing the concentration of coenzyme A prevented inhibition. We conclude that salicylic acid decreases the mitochondrial activation and thus beta-oxidation of long chain fatty acids, presumably by sequestering extramitochondrial coenzyme A and possibly carnitine.

Adenosine Triphosphate↗
PubMed1987

Presence of salicylic acid in standardbred horse urine and plasma after various feed and drug administrations.

Plasma and urinary levels of salicylic acid were examined in Standardbred mares after administration of various feeds, containing different compositions of hay. In addition, horses were administered acetylsalicylic acid orally and methyl salicylate topically. Elevated salicylic acid levels were observed in horse urine and plasma in animals fed lucerne hay. The plasma and urinary elimination of salicylic acid exhibited a diurnal pattern which was related to the type of feed and the feeding schedule. Within 24 h after oral administration of acetylsalicylic acid, plasma and urine salicylic acid levels were consistent with residual levels observed after feeding lucerne hay. Elimination of salicylic acid was rapid and complete, with a half-life between 5 and 7 h. Topical administration of methyl salicylate (8.4 g) produced elevated urinary salicylic acid levels for 6 h. A smaller dose of methyl salicylate (3.4 g) did not elevate plasma or urine salicylic acid levels above those observed following administration of lucerne hay.

Administration, Oral↗
PubMedDate not supplied

Salicylic acid protects the skin from UV damage.

Aspirin(acetyl salicylate) has long been used as an analgesic. Salicylic acid has been reported to have anti-inflammatory properties. These activities include inhibiting activity of cox-1, cox-2, and NF-kb. In addition, salicylic acid has also been shown in some systems to induce Hsp70. We have demonstrated that salicylic acid inhibits UVB-induced sunburn cell formation, as well as increase the removal of UVB induced TT dimer formation in living skin equivalents. Given these protective properties of salicylic acid, we propose the use of salicylic acid as a topical therapeutic to protect the skin from sun damage.

Adult↗
PubMed1988

Insulin receptors and glucose homeostasis in type 2 diabetics influenced by acetyl-salicylic acid treatment.

The effect of acetyl-salicylic acid administration on insulin receptors on the erythrocytes and the changes of glucose homeostasis examined by hyperglycaemic clamps were evaluated in 8 Type 2 diabetics. Significantly increased number of insulin receptors and decreased insulin affinity constants were found in diabetics after the acetyl-salicylic acid treatment (p less than 0.02). Significantly decreased tissue sensitivity to insulin and metabolic clearance rate of insulin (p less than 0.02) were observed in Type 2 diabetics after the acetyl-salicylic acid treatment. We conclude that acetyl-salicylic acid may impair glucose homeostasis due to interference with insulin action in peripheral tissues.

Aged↗
PubMed2002

Spectroscopic evidence in support of horseradish peroxidase compound II-catalyzed oxidation of salicylic acid but not of phenylethylamine.

Salicylic acid and phenylethylamine are putative substrates for naturally occurring reactions for generation of reactive oxygen species, which are catalyzed by plant peroxidases. Here, we used commercially available highly purified horseradish peroxidase-C (HRP-C) as a model enzyme for spectroscopic analysis, and obtained data suggesting that the Compound II form of HRP-C does not utilize phenylethylamine as substrate. In contrast, addition of salicylic acid to Compound II resulted in rapid conversion of Compound II to the native form.

Catalysis↗
PubMed1996

Comparative genotoxicity of six salicylic acid derivatives in bone marrow cells of mice.

In vivo sister chromatid exchange (SCE) and chromosome aberrations (CA) were carried out for six salicylic acid derivatives in bone marrow cells of mice. Six salicylic acid derivatives, namely acetyl salicylic acid (aspirin), salicylic acid, salicylamide, sodium salicylate, diflunisal and niclosamide, were used for these experiments. Drugs were administered both intraperitoneally (i.p.) and orally by gavage. Out of these six salicylic acid derivatives tested, only diflunisal and niclosamide showed genotoxicity as measured by both SCE and CA assays. Acetyl salicylic acid and sodium salicylate showed weak genotoxicity as measured by SCE and CA, respectively, only at the highest dose tested.

Administration, Oral↗
PubMed1994

Evaluation of hepatic metabolism of salicylic acid in perfused rat liver.

Hepatic metabolism of salicylic acid was studied using a single-pass liver perfusion technique. Livers obtained from male, Sprague-Dawley rats (200-300 g) were perfused with Krebs-Henseleit bicarbonate buffer containing the drug (50-100 micrograms/mL) and glycine (0.5 or 5 mM) or glucose (5.5 mM) or bovine serum albumin (0.33%). Effluent samples over a 30-50 min interval were analyzed for salicylic acid and its metabolites (gentisic acid, salicyluric acid, and salicyl acyl and salicyl phenolic glucuronides). Effluent concentrations of salicylic acid did not differ from those in the perfusate, indicating that the liver is not a site for the metabolism of this drug. Hepatic uptake studies are needed to confirm this finding.

Animals↗