Protective Effect Of Salicylic Acid Research Articles

Components of the Ascorbate-Glutathione Complex and Phenylpropanoid Pathway in the Implementation of the Protective Effect of Salicylic Acid on Wheat Plants under Salinity

Components of the Ascorbate-Glutathione Complex and Phenylpropanoid Pathway in the Implementation of the Protective Effect of Salicylic Acid on Wheat Plants under Salinity

Salicylic acid enhances the resistance of Neoporphyra haitanensis to pathogen Vibrio mediterranei 117-T6

The economically important seaweed Porphyra are often infected by various diseases during sea farming. As one of the most important phytohormones in disease resistance, the protective effect of salicylic acid (SA) on Neoporphyra haitanensis during Vibrio mediterranei 117-T6 infection was investigated by biochemical methods and transcriptomic profile analysis. The addition of exogenous SA at a moderate concentration alleviated disease caused by the pathogenic bacteria. SA enhanced the photosynthetic activity of thalli by upregulating genes of the photosynthetic system along with genes associated with carbon fixation. A moderate release of H2O2 stimulated by SA was observed, which may be due to the upregulation of the photorespiratory C2 cycle and the inhibition of catalase activity. SA treatment enhanced the activity and transcription of antioxidant enzymes in the glutathione-ascorbate (GSH-AsA) cycle involved in balancing the redox system. In addition, the levels of multiple carotenoids were increased in N. haitanensis thalli, and genes involved in their synthesis were upregulated. The results suggest that exogenous SA may enhance the defense of N. haitanensis against pathogen attack by the release of H2O2. However, to avoid oxidative stress, alga can establish redox balance by activating the GSH-AsA cycle and by regulating the generation of carotenoids. In summary, this study indicates that N. haitanensis may have evolved mechanisms to respond to SA stimulation and protect against invading pathogens. Our research can provide valuable information for the farming of healthy N. haitanensis.

Impact of Salicylic Acid on Phenolic Metabolism and Antioxidant Activity in Four Grape Cultivars during Cold Storage

Salicylic acid (SA) plays an important role in the regulation of plant ripening and responses to abiotic stresses. In this study, the protective effect of SA on cold stress-caused oxidative damage in grape (Vitis vinifera L.) bunches was investigated during cold storage. Grape bunches treated with 2 mM SA and stored at 0°C with 85-90% RH for 30 days. Samples were selected from each treatment for physical and chemical analysis before storage, midpoint of storage, end of storage and end of shelf life. The results showed that the cold storage induced lipid peroxidation, decay incidence and loss of fresh weight, while SA pretreatment mitigated these effects in “Bidaneh Sefid” and “Qzl uzum” cultivars. In these cultivars, SA-induced protection against cold damage was accompanied by decrease in malondialdehyde (MDA) content, and caused an increase in catalase (CAT) and superoxide dismutase (SOD) activity. Additionally, SA-induced protection against cold injury was mediated through promoting total phenolics concentration and phenylalanine ammonia-lyase (PAL) activity. The present findings suggest that although variability in the protective effect of SA against cold damage was observed between grape cultivars, SA could alleviate the cold-induced oxidative stress in grape bunches during cold storage.

Purification and properties of lipoxygenase from wheat seedlings infected by Fusarium graminearum and treated by salicylic acid.

Lipoxygenase from wheat seedlings in normal conditions, infected by Fusarium graminearum and treated by salicylic acid was isolated. The isolated enzyme was purified by the methods of salting-out (60% ammonium sulphate), dialysis, gel-filtration and ion-exchange chromatography. Specific activity of the purified enzyme was 8.0-12.5 ΔЕ234/mg of protein, degree of purification – 11.6-15.3 times. The enzyme yield was 18.3-27.9%. Molecular mass of lipoxygenase is 90 kDa, amino acid composition is distinguished by a high content of glutamic acid, proline, valine, isoleucine, leucine and low level of histidine, tyrosine, phenylalanine, threonine, tryptophan, cystein. Research of lipoxygenase substrate dependence indicated that the enzyme catalysed with the maximum velocity of the reaction of arachidonic acid oxidation at a substrate concentration of 4.5 mM at pH 7.2, the reaction of linoleic acid oxidation at a substrate concentration of 4.5 mM at pH 7.2 and the reaction of linolenic acid oxidation at a substrate concentration of 9.0 mM at pH 8.0. The change of wheat lipoxygenase activity depending on genotype resistance to Fusarium graminearum and millieu of germination was shown. One of the manifestations of the protective effect of salicylic acid is its ability to induce changes of lipoxygenase activity.

Salicylic acid-induced protection against cadmium toxicity in wheat plants

We have studied the influence of pretreatment of wheat seedlings (Triticum aestivum L.) with 50μM salicylic acid (SA) on plant resistance to subsequent action of 1mM cadmium acetate. SA pretreatment decreased the extent of detrimental effect of cadmium on wheat plants, as judged by the decline in the level of stress-induced accumulation of MDA and electrolyte leakage. Furthermore, SA-pretreatment contributed to maintenance of growth characteristics of wheat seedlings at the level close to the control under stress conditions and to acceleration of growth recovery during post-stress period. Detected defense effect of SA may be due to a decline in the amplitude of cadmium-induced accumulation of abscisic acid (ABA) and to reduced fall of indoleacetic acid (IAA) and cytokinins (CK) in stressed plants. In the course of one day treatment, SA activated phenylalanine ammonia-lyase (PAL), the key enzyme of lignin biosynthesis, in roots of seedlings under normal growth conditions contributing to the strengthening of carrier functions of cell walls. This assumption is supported by the data showing significant decline in cadmium accumulation in SA-pretreated plants, especially in the shoots. Cd-treatment was shown to result in accumulation of dehydrins with molecular mass 22, 28, 55 and 69kDa in wheat seedlings, although low molecular weight dehydrins (22 and 28kDa) showed greater stress sensitivity. It is noteworthy that SA-pretreatment by itself led to 1.5-fold increase in the content of low molecular weight dehydrins. Nevertheless, SA-pretreated seedlings were characterized by significantly lower Cd-induced accumulation of all of the four dehydrins, apparently due to inhibition of cadmium flow into the plants. The obtained data suggest involvement of dehydrins in the range of defense reactions induced by SA-treatment contributing significantly to development of plant resistance to subsequent action of stress. The use of fluridone allowed us to demonstrate the key role of endogenous ABA in SA-induced changes in the level of dehydrins as well as in the protective effect of SA on wheat plants under cadmium stress resulting from development of defense responses in the course of SA-treatment.

The in vitro protective effect of salicylic acid against paclitaxel and cisplatin-induced neurotoxicity.

Paclitaxel (PAC) and cisplatin (CIS) are two established chemotherapeutic drugs used in combination for the treatment of various solid tumors. However, the usage of PAC and CIS are limited because of the incidence of their moderate or severe neurotoxic side effects. In this study, we aimed to assess the protective role of salicylic acid (SA) against neurotoxicity caused by PAC and CIS. For this purpose, newborn Sprague Dawley rats were decapitated in sterile atmosphere and primary cortex neuron cultures were established. On the 10th day SA was added into culture plates. PAC and CIS were added on the 12th day. The cytotoxicity was determined by using the MTT [3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide] assay. Oxidative alterations were assessed using total antioxidant capacity and total oxidative stress assays in rat primary neuron cell cultures. It was shown that both concentrations of PAC and CIS treatments caused neurotoxicity. Although SA decreased the neurotoxicity by CIS and PAC, it was more effective against the toxicity caused by CIS rather than the toxicity caused by PAC. In conclusion it was clearly revealed that SA decreased the neurotoxic effect of CIS and PAC in vitro.

Effect of salicylic acid on the attenuation of aluminum toxicity in Coffea arabica L. suspension cells: A possible protein phosphorylation signaling pathway

The protective effect of salicylic acid (SA) on aluminum (Al) toxicity was studied in suspension cells of Coffea arabica L. The results showed that SA does not produce any effect on cell growth and that the growth inhibition produced by aluminum is restored during simultaneous treatment of the cells with Al and SA. In addition, the cells exposed to both compounds, Al and SA, showed evident morphological signals of recovery from the toxic state produced in the presence of Al. The cells treated with SA showed a lower accumulation of Al, which was linked to restoration from Al toxicity because the concentration of Al3+ outside the cells, measured as the Al3+–morin complex, was not modified by the presence of SA. Additionally, the inhibition of phospholipase C by Al treatment was restored during the exposure of the cells to SA and Al. The involvement of protein phosphorylation in the protective effect of SA on Al-toxicity was suggested because staurosporine, a protein kinase inhibitor, reverted the stimulatory effect of the combination of Al and SA on protein kinase activity. These results suggest that SA attenuates aluminum toxicity by affecting a signaling pathway linked to protein phosphorylation.

Protective effect of salicylic acid on Hg0 intoxication in mice

Elemental mercury (Hg0) is a hazardous metal with significant human exposure through diverse sources. In this study, the role of salicylic acid (SA) was assessed against Hg0-induced injury in mice, with the aim of screening alternative clinical drugs to prevent or treat Hg0 poisoning. An exposure to Hg0 (1.0 mg/m3 in a glass box) for 2 h per day for successive 15 d significantly increased Hg accumulation in mouse brain and lung, inhibited the animal growth and altered the neurobehavior such as impairing the spatial learning and memory in the Barnes maze test. However, although oral SA (5.5 mg/kg body weight) during the Hg0 exposure did not reduce the Hg levels in these organs, it effectively counteracted the Hg0-induced growth inhibition, and improved the behavioral performance, accompanied by a series of ameliorations in the antioxidative defense and anti-inflammatory response. For instance, when compared with control, Hg0-inhaled animals had significant decreases in the activities of superoxide dismutase and peroxidase, and in the levels of reduced form of glutathione and the ratio to its oxidized form, concomitantly with a high accumulation of hydrogen peroxide and malondialdehyde in the brain and lung. However, these values in Hg0 + SA-exposed animals were comparable with the basal levels in control. Likewise, interleukin-6 in the brain and lung of Hg0-exposed animals were dramatically elevated, whereas it was maintained to the basal level in Hg0 + SA-exposed animals. These data suggested that application of SA could protect mice against Hg0-induced injury.

Salicylic Acid Attenuates Gentamicin-Induced Nephrotoxicity in Rats

Gentamicin (GM) is a widely used antibiotic against serious and life-threatening infections, but its usefulness is limited by the development of nephrotoxicity. The present study was designed to determine the protective effect of salicylic acid (SA) in gentamicin-induced nephrotoxicity in rats. Quantitative evaluation of gentamicin-induced structural alterations and degree of functional alterations in the kidneys were performed by histopathological and biochemical analyses in order to determine potential beneficial effects of SA coadministration with gentamicin. Gentamicin was observed to cause a severe nephrotoxicity which was evidenced by an elevation of serum urea and creatinine levels. The significant increases in malondialdehyde (MDA) levels and protein carbonyl groups indicated that GM-induced tissue injury was mediated through oxidative reactions. On the other hand, simultaneous SA administration protected kidney tissue against the oxidative damage and the nephrotoxic effect caused by GM treatment. Exposure to GM caused necrosis of tubular epithelial cells. Necrosis of tubules was found to be prevented by SA pretreatment. The results from our study indicate that SA supplement attenuates oxidative-stress associated renal injury by reducing oxygen free radicals and lipid peroxidation in gentamicin-treated rats.

The protective effect of salicylic acid on lysozyme against riboflavin-mediated photooxidation

As a metabolite of aspirin in vivo, salicylic acid was proved to protect lysozyme from riboflavin-mediated photooxidation in this study. The antioxidative properties of salicylic acid were further studied by using time-resolved laser flash photolysis of 355 nm. It can quench the triplet state of riboflavin via electron transfer from salicylic acid to the triplet state of riboflavin with a reaction constant of 2.25 × 10 9 M −1 s −1. Mechanism of antioxidant activities of salicylic acid on lysozyme oxidation was discussed. Salicylic acid can serve as a potential antioxidant to quench the triplet state of riboflavin and reduce oxidative pressure.

Salicylic acid alleviates NaCl-induced changes in the metabolism of Matricaria chamomilla plants

Influence of 100 mM NaCl and 50 microM salicylic acid (SA) and their combination on the metabolism of chamomile (Matricaria chamomilla) during 7 days was studied. NaCl reduced growth and selected physiological parameters and SA in combined treatment (NaCl + SA) reversed majority of these symptoms. Application of SA reduced NaCl-induced increase of Na+ in the rosettes, but not in the roots. Accumulation of total amino acids was stimulated in NaCl-treated roots, especially due to exceptional increase of proline (4.4-fold). Among phenolic acids, accumulation of protocatechuic acid was the most enhanced in NaCl-exposed leaf rosettes (ca. 3-fold) while chlorogenic and caffeic acids in the roots (2.4- and 2.8-fold, respectively). Total soluble phenols increased after NaCl and SA treatments, but root lignin content was not affected. Activity of phenylalanine ammonia-lyase and shikimate dehydrogenase increased in response to NaCl, but cinnamyl alcohol dehydrogenase was not affected and polyphenol oxidase decreased. Stress parameters were elevated by NaCl treatment (superoxide radical and malondialdehyde content, activities of catalase, ascorbate- and guaiacol-peroxidase) and substantially prevented by SA, while accumulation of hydrogen peroxide decreased. Overall, SA showed strong beneficial properties against NaCl-induced negative symptoms. Protective effect of SA was the most visible at the level of guaiacol-peroxidase and through amelioration of stress parameters and mineral nutrient contents.

Concentration-dependent effect of salicylic acid application on wheat seedling resistance to take-all fungus, Gaeumannomyces graminis var. tritici

Application of 0.1 and 0.2 mM salicylic acid (SA) significantly reduced take-all disease caused by Gaeumannomyces graminis var. tritici (Ggt) and increased the root and shoot lengths and biomass, whereas 0.5 and 1 mM SA had no significant effect. The effective SA concentrations also increased the activities of soluble peroxidase (SPOX) and cell-wall-bound peroxidase (CWPOX) and the concentration of total phenolic compounds. SPOX activity was highest at days 4 and 3 in healthy roots and those inoculated with Ggt, respectively, and that of CWPOX at day 6 in both healthy and inoculated roots. The concentration of phenolic compound was also highest at day 3 in both healthy roots and those inoculated with Ggt. The results indicate that the protective effect of SA depends on certain concentrations which increase peroxidase activity and phenolic compounds accumulation in the wheat roots; higher SA concentrations did not differ from the controls.

Activity of Lectins of Winter Wheat Seedlings Infected with Mycoplasma and Treated with Salicylic Acid

Changes in activity of soluble and cell wall lectins have been revealed in seedlings of winter wheat Triticum aestivum L. cultivar Mironovskaya 808 after infection with mycoplasma Acholeplasma laidlawii 118. The protective effect of salicylic acid was manifested as negating the bursts of lectin activity induced by mycoplasma infection.

Prevention by parenteral aspirin of indomethacin-induced gastric lesions in rats: mediation by salicylic acid.

Nonsteroidal antiinflammatory drugs (NSAIDs) produce gastric damage in experimental animals, irrespective of the route of administration. However, aspirin (ASA) causes damage only when it is given orally. In the present study, we examined the gastric ulcerogenic effect of subcutaneously administered ASA in rats, in comparison with various NSAIDs, and investigated the reason why ASA does not cause damage in the stomach, in relation to its metabolite salicylic acid (SA). Since the antiinflammatory action of SA is known to be mediated, partly, by endogenous adenosine (AD), we also examined the possible involvement of AD in the protective action of SA. Various NSAIDs (indomethacin, flurbiprofen, naproxen, diclrofenac, ASA, SA) were administered subcutaneously, and the gastric mucosa was examined macroscopically 4 hr later. All NSAIDs tested, except ASA and SA, caused hemorrhagic lesions in the stomach, with a marked gastric hypermotility and a decrease of mucosal PGE2 contents. These ulcerogenic and motility responses caused by NSAIDs were blocked by pretreatment with atropine or PGE2. ASA, although inhibiting PGE2 generation, caused neither hypermotility nor damage in the stomach. On the other hand, SA alone inhibited basal gastric motility without any effect on mucosal PGE2 contents, and this agent, when given together with indomethacin, prevented gastric hypermotility and lesion formation in response to indomethacin, without affecting the reduced PGE2 contents. Likewise, ASA inhibited these responses to indomethacin, yet the effects appeared later than those of SA. Following administration of ASA, the blood SA levels reached a peak within 30 min and remained elevated for 4 hr. In addition, the protective effect of SA was not significantly influenced by either the AD deaminase or the AD-receptor antagonists. These results suggest that the failure of parenteral ASA to induce gastric damage may be explained by a protective action of SA metabolized from ASA. SA has a cytoprotective action against NSAID-induced gastric lesions, and this action is not mediated by endogenous AD but may be functionally associated with inhibition of the gastric motility response.

Protection by aspirin of indomethacin-induced small intestinal damage in rats: mediation by salicylic acid

Most of non-steroidal anti-inflammatory drugs (NSAIDs) except aspirin (ASA) produce intestinal damage in rats. In the present study, we re-examined the intestinal toxic effect of ASA in rats, in comparison with various NSAIDs, and investigated why ASA does not cause damage in the small intestine, in relation to its metabolite salicylic acid (SA). Various NSAIDs (indomethacin; 10 mg/kg; flurbiprofen; 20 mg/kg; naproxen; 40 mg/kg; dicrofenac; 40 mg/kg; ASA; 20–200 mg/kg) were administered s.c., and the small intestinal mucosa was examined macroscopically 24 h later. All NSAIDs tested, except ASA, caused hemorrhagic lesions in the small intestine, with a decrease of mucosal PGE 2 contents. ASA did not provoke any damage, despite inhibiting (prostaglandin) PG production, and prevented the occurrence of intestinal lesions induced by indomethacin, in a dose-related manner. This protective action of ASA was mimicked by the equimolar doses of SA (17.8–178 mg/kg). Indomethacin caused intestinal hypermotility, in preceding to the ocurrence of lesion, and this event was followed by increases of enterobacterial translocation in the mucosa. Both ASA and SA prevented both the intestinal hypermotility and the bacterial translocation seen after indomethacin treatment. In addition, the protective effect of SA was not significantly influenced by either the adenosine deaminase or the adenosine receptor antagonists. Following administration of ASA, the blood SA levels reached a peak within 30 min and remained elevated for more than 7 h. These results suggest that SA has a cytoprotective action against indomethacin-induced small intestinal lesions, and this action may be associated with inhibition of the intestinal hypermotility and the bacterial translocation, but not mediated by endogenous adenosine. Failure of ASA to induce intestinal damage may be explained, at least partly, by a protective action of SA, the metabolite of ASA.

Salicylic Acid Blocks Indomethacin- and Aspirin-Induced Cyclo-Oxygenase Inhibition in Rat Gastric Mucosa

Salicylic acid reduces gastric mucosal lesions induced by aspirin and indomethacin. Aspirin and indomethacin reduce gastric mucosal cyclo-oxygenase activity. These studies were designed to determine whether or not salicylic acid interacts with gastric mucosal cyclo-oxygenase, decreasing the inhibitory effect of aspirin and indomethacin as has been observed in platelets and vascular tissue. The interaction between salicylic acid and two cyclo-oxygenase inhibitors, indomethacin and aspirin, was assessed on ex vivo prostaglandin generation in the rat gastric mucosa. Salicylic acid (100 mg/kg) was administered orally 30 min before the subcutaneous injection of either indomethacin (0.5-10 mg/kg) or aspirin (5.0-20 mg/kg). Pretreatment produced a shift of the mean 50% inhibitory dose for PGF2 alpha formation from 0.92 to 7.6 mg/kg for indomethacin and from 7.8 to 20 mg/kg for aspirin. Similar results were achieved with ex vivo prostacyclin synthesis as measured by the level of 6-keto-PGF 1 alpha. These data are consistent with competitive enzyme kinetics, and may, in part, explain the protective effect of salicylic acid against the ulcerogenicity of aspirin and indomethacin on the gastric mucosa.