Changes in the Growth, Chemical Composition, and Antioxidant Activity in the Aquatic Plant Wolffia arrhiza (L.) Wimm. (Lemnaceae) Exposed to Jasmonic Acid

The present study was undertaken to test the influence of exogenously applied jasmonic acid (JA) at concentrations of 0.01–100 μM upon the growth and metabolism of the aquatic plant Wolffia arrhiza (Lemnaceae). JA acted in a concentration-dependent manner. JA at 0.1 μM stimulated plant growth and accumulation of cellular components (proteins, monosaccharides, chlorophylls, phaeophytins, and carotenoids). Treatment with JA at 0.1 μM enhanced W. arrhiza viability by the induction of biomass production and increased the level of photosynthetic pigments, monosaccharides, and soluble proteins. Moreover, JA at 0.1 μM activated the enzymatic (catalase, ascorbate peroxidase, NADH peroxidase) and nonenzymatic antioxidant (ascorbate, glutathione) system in W. arrhiza and, therefore, suppressed lipid peroxidation. In contrast, decreases in fresh weight, major photosynthetic pigments, monosaccharides, and soluble protein content were observed in W. arrhiza exposed to 100 μM JA. JA applied at 100 μM also stimulated the formation of lipid peroxides which are responsible for membrane damage. In the presence of 100 μM JA, antioxidant enzyme (catalase, ascorbate peroxidase, NADH peroxidase) activity and ascorbate as well as glutathione content were inhibited. The data support the hypothesis that JA plays an important role in W. arrhiza growth and metabolism, regulating oxidative status by direct influence on the enzymatic as well as nonenzymatic antioxidant machinery.     

Cadmium-induced oxidative stress in two potato cultivars

A hydroponic experiment was carried out to characterize the oxidative stress responses of two potato cultivars (Solanum tuberosum L. cvs. Asterix and Macaca) to cadmium (Cd). Plantlets were exposed to four Cd levels (0, 50, 100, 150 and 200 μM) for 7 days. Cd concentration was increased in both roots and shoot. Number of sprouts and roots was not decreased, whereas Cd treatment affected the number of nodal segments. Chlorophyll content and ALA-D activity were decreased in both cultivars, whereas carotenoids content was decreased only in Macaca. Cd caused lipid peroxidation in roots and shoot of both cultivars. Protein oxidation was only verified at the highest Cd level. H₂O₂ content was increased in roots and shoot of Asterix, and apparently, a compensatory response between roots and shoot of Macaca was observed. SOD activity was inhibited in roots of Asterix at all Cd treatments, whereas in Macaca it was only increased at two highest Cd levels. Shoot SOD activity increased in Asterix and decreased in Macaca. Root CAT activity in Asterix decreased at 100 and 150 μM, whereas in Macaca it decreased only at 50 μM. Shoot CAT activity was decreased in Macaca. Root AsA content in Macaca was not affected, whereas in shoot it was reduced at 100 μM and increased at 200 μM. Cd caused increase in NPSH content in roots and shoot. Our results suggest that Cd induces oxidative stress in both potato cultivars and that of the two cultivars, Asterix showed greater sensitivity to Cd levels.     

Oxidative Stress Induced by Cadmium in the C6 Cell Line: Role of Copper and Zinc

In this report, we have investigated the role of copper (Cu) and zinc (Zn) in oxidative stress induced by cadmium (Cd) in C6 cells. Cells were exposed to 20 μM Cd, 500 μM Cu, and 450 μM Zn for 24 h. Then, toxic effects, cellular metals levels, oxidative stress parameters, cell death, as well as DNA damage were evaluated. Cd induced an increase in cellular Cd, Cu, and Zn levels. This results not only in the inhibition of GSH-Px, GRase, CAT, and SOD activities but also in ROS overproduction, oxidative damage, and apoptotic cell death not related to Cu and Zn mechanisms. The thiol groups and GSH levels decreased, whereas the lipid peroxidation and DNA damage increased. The toxicity of Zn results from the imbalance between the inhibition of antioxidant activities and the induction of MT synthesis. The increase in Cu and Zn levels could be explained by the disruption of specific transporter activities, Cd interference with signaling pathways, and metal displacement. Our results suggest that the alteration of Cu and Zn homeostasis is involved in the oxidative stress induced by Cd.     

Antioxidant effect of a phytoestrogen equol on cultured muscle cells of embryonic broilers

Previous studies have shown that the in ovo injection of equol can markedly improve the water-holding capacity of muscles of broilers chickens at 7 wk of age through promotion of the antioxidant status. We aimed to investigate directly the antioxidant effects of equol on muscle cells in broilers. Muscle cells were separated from leg muscle of embryos on the 11th day of incubation and treated with equol and H₂O₂, either alone or together. Cells were pretreated with medium containing 1, 10, or 100 μM equol for 1 h prior to the addition of 1 mM H₂O₂ for a further 1 h. Photomicrographs of cells were obtained. Cell viability, malondialdehyde (MDA) content, and L-lactate dehydrogenase (LDH) activity in the cell supernatant, as well as intracellular total superoxide dismutase (T-SOD) and glutathione peroxidase (GSH-Px) activities were determined. Treatment with 1 mM H₂O₂ caused serious damage to cells, indicated by comets with no clear head region but a very apparent tail of DNA fragments. Pretreatment with low (1 μM) but not high concentrations of equol (10 μM) inhibited cell damage, while 100 μM equol caused more serious damage than H₂O₂ alone. Pretreatment with 1 μM equol had no effect on cell viability, while pretreatment with 10 and 100 μM equol significantly decreased cell viability in a dose-dependent manner. Compared with H₂O₂ alone, pretreatment with low-dosage equol markedly decreased LDH activity and MDA production in the supernatant, significantly increased intracellular T-SOD activity (P < 0.05) and tended to increase intracellular GSH-Px activity (0.05 < P < 0.1). Pretreatment with high-dosage equol (10 and 100 μM) significantly enhanced LDH activity, but had no effect on MDA content, T-SOD or GSH-Px activity induced by H₂O_2, except for an obvious increase in GSH-Px activity caused by 10 μM equol. These results indicate that equol at low dosage can prevent skeletal muscle cell damage induced by H₂O₂, while pretreatment with high-dosage equol shows a synergistic effect with H₂O₂ in inducing cell damage.     

Paraquat pre-treatment increases activities of antioxidant enzymes and reduces lipid peroxidation in salt-stressed cucumber leaves

To investigate whether paraquat (PQ) is involved in regulation of antioxidant enzymes and lipid peroxidation under short-term salt stress, and to elucidate the physiological mechanism of salt stress mitigated by PQ, a cucumber cultivar (cv. Chunguang no. 2) was exposed to 100 mM NaCl for 48 h after pre-treatment with 10 μM PQ for 1 h. When compared to the control, salt stress increased the levels of malonaldehyde (MDA), superoxide radical (O₂^·−) and hydrogen peroxide (H₂O₂) and the activities of antioxidant enzymes, such as superoxide dismutase (EC 1.15.1.1), ascorbate peroxidase (EC 1.11.1.11) and glutathione reductase (EC 1.6.4.2) in the cucumber leaves. Under salt conditions, PQ pre-treatment prevented oxidative stress as observed by the decreases in MDA, H₂O₂ and O₂^·− that correlated with the increase in antioxidant defenses. We propose that, at low concentrations, the PQ pre-treatment can reduce the salt-induced oxidative damage by increasing the antioxidative mechanisms in cucumber plants.     

Exogenous application of salicylic acid alleviates cadmium toxicity and reduces hydrogen peroxide accumulation in root apoplasts of Phaseolus aureus and Vicia sativa

We examined ameliorative effects of salicylic acid (SA) on two cadmium (Cd)-stressed legume crops with different Cd tolerances, viz. Phaseolus aureus (Cd sensitive) and Vicia sativa (Cd tolerant). Cd at 50 μM significantly increased the production of hydrogen peroxide (H₂O₂) and superoxide anion (O₂^·−) in root apoplasts of P. aureus and V. sativa. When comparing the two species, we determined that Cd-induced production of H₂O₂ and O₂^·− was more pronounced in P. aureus root apoplasts than in V. sativa root apoplasts. V. sativa had higher activities of superoxide dismutase (SOD), catalase (CAT), and ascorbate peroxidase (APX) than P. aureus in root symplasts and apoplasts. Seed-soaking pretreatment with 100 μM SA decreased Cd-induced production of H₂O₂ and O₂^·− in apoplasts of both species, and increased activities of symplastic and apoplastic SOD, symplastic APX, and apoplastic CAT under Cd stress. Hence, SA-induced Cd tolerances in P. aureus and V. sativa are likely associated with increases in symplastic and apoplastic antioxidant enzyme activities.     

Cadmium-induced early changes in O2 •−, H2O2 and antioxidative enzymes in soybean (Glycine max L.) leaves

Cadmium-induced initial changes in the production of reactive oxygen species (ROS) and antioxidant mechanism were investigated in soybean (Glycine max L. cv. Don Mario 4800 RR) leaves. Whole plants (WP) and plants without roots (PWR) were exposed to 0.0, 10.0 and 40.0 μM Cd for 0, 4, 6 and 24 h. Compared to PWR, a higher level of endogenous Cd in WP was associated with a lower oxidative stress measured in terms of lipid peroxidation. Furthermore, O₂ ^•− content decreased in the leaves of Cd-treated WP, whereas it increased in those of Cd-treated PWR. Although O₂ ^•− accumulation in PWR was associated with a decrease in superoxide dismutase (SOD) activity, O₂ ^•− diminution in WP leaves was not related to any increase in SOD activity. H₂O₂ content increased in the leaves of both Cd-treated WP and PWR, and it was concomitant with a corresponding decline in catalase (CAT) and ascorbate peroxidase (APX) activities. When diphenyl iodonium (DPI), an inhibitor of NADPH oxidase, was added, H₂O₂ content remained unchanged in Cd-treated WP, suggesting that NADPH oxidase does not participate in the early hours of Cd toxicity. Taken together, our results showed that early ROS evolution and oxidative damage were different in WP and PWR. This suggests that the response in soybean leaves during the early hours of Cd toxicity is probably modulated by the root.     

Genotype-Dependent Effect of Exogenous Nitric Oxide on Cd-induced Changes in Antioxidative Metabolism, Ultrastructure, and Photosynthetic Performance in Barley Seedlings (Hordeum vulgare)

A greenhouse hydroponic experiment was performed using Cd-sensitive (cv. Dong 17) and Cd-tolerant (Weisuobuzhi) barley seedlings to evaluate how different genotypes responded to cadmium (Cd) toxicity in the presence of sodium nitroprusside (SNP), a nitric oxide (NO) donor. Results showed that 5 μM Cd increased the accumulation of O₂^•−, H₂O₂, and malondialdehyde (MDA) but reduced plant height, chlorophyll content, net photosynthetic rate (P _n), and biomass, with a much more severe response in the Cd-sensitive genotype. Antioxidant enzyme activities increased significantly under Cd stress in the roots of the tolerant genotype, whereas in leaves of the sensitive genotype, superoxide dismutase (SOD) and ascorbate peroxide (APX), especially cytosol ascorbate peroxidase (cAPX), decreased after 5–15 days Cd exposure. Moreover, Cd induces NO synthesis by stimulating nitrate reductase and nitric oxide synthetase-like enzymes in roots/leaves. A Cd-induced NO transient increase in roots of the Cd-tolerant genotype might partly contribute to its Cd tolerance. Exogenous NO dramatically alleviated Cd toxicity, markedly diminished Cd-induced reactive oxygen species (ROS) and MDA accumulation, ameliorated Cd-induced damage to leaf/root ultrastructure, and increased chlorophyll content and P _n. External NO counteracted the pattern of alterations in certain antioxidant enzymes induced by Cd; for example, it significantly elevated the depressed SOD, APX, and catalase (CAT) activities in the Cd-sensitive genotype after 10- and 15-day treatments. Furthermore, NO significantly increased stromal APX and Mn-SOD activities in both genotypes and upregulated Cd-induced decrease in cAPX activity and gene expression of root/leaf cAPX and leaf CAT1 in the Cd-sensitive genotype. These data suggest that under Cd stress, NO, as a potent antioxidant, protects barley seedlings against oxidative damage by directly and indirectly scavenging ROS and helps to maintain stability and integrity of the subcellular structure.     

Glutamate induces oxidative stress and apoptosis in cerebral vascular endothelial cells: contributions of HO-1 and HO-2 to cytoprotection

In cerebral circulation, epileptic seizures associated with excessive release of the excitatory neurotransmitter glutamate cause endothelial injury. Heme oxygenase (HO), which metabolizes heme to a vasodilator, carbon monoxide (CO), and antioxidants, biliverdin/bilirubin, is highly expressed in cerebral microvessels as a constitutive isoform, HO-2, whereas the inducible form, HO-1, is not detectable. Using cerebral vascular endothelial cells from newborn pigs and HO-2-knockout mice, we addressed the hypotheses that 1) glutamate induces oxidative stress-related endothelial death by apoptosis, and 2) HO-1 and HO-2 are protective against glutamate cytotoxicity. In cerebral endothelial cells, glutamate (0.1–2.0 mM) increased formation of reactive oxygen species, including superoxide radicals, and induced major keystone events of apoptosis, such as NF-B nuclear translocation, caspase-3 activation, DNA fragmentation, and cell detachment. Glutamate-induced apoptosis was greatly exacerbated in HO-2 gene-deleted murine cerebrovascular endothelial cells and in porcine cells with pharmacologically inhibited HO-2 activity. Glutamate toxicity was prevented by superoxide dismutase, suggesting apoptotic changes are oxidative stress related. When HO-1 was pharmacologically upregulated by cobalt protoporphyrin, apoptotic effects of glutamate in cerebral endothelial cells were completely prevented. Glutamate-induced reactive oxygen species production and apoptosis were blocked by a CO-releasing compound, CORM-A1 (50 µM), and by bilirubin (1 µM), consistent with the antioxidant and cytoprotective roles of the end products of HO activity. We conclude that both HO-1 and HO-2 have anti-apoptotic effects against oxidative stress-related glutamate toxicity in cerebral vascular endothelium. Although HO-1, when induced, provides powerful protection, HO-2 is an essential endogenous anti-apoptotic factor against glutamate toxicity in the cerebral vascular endothelium. endothelium; carbon monoxide; bilirubin; injury; reactive oxygen species; heme oxygenase     

Cadmium-induced oxidative damage and antioxidative defense mechanisms in <Emphasis Type="Italic">Vigna mungo</Emphasis> L.

Cadmium (Cd)-induced oxidative stress and antioxidant defense mechanisms were analyzed in roots and leaves of Vigna mungo L. Seeds were germinated in perlite-vermiculite and irrigated with Hoagland nutrient solution. At day 6, seedlings were exposed to 40 μM Cd under semi-hydroponic conditions for a period of 12 days. Growth anomalies and abnormal chromatin condensation were observed in Cd-treated plants, in comparison with control ones. Cd accumulation was observed in roots of treated plants. The analyses of antioxidative defense and oxidative parameters in roots, stems and leaves showed different tissue-specific responses. Superoxide dismutase (SOD) and guaiacol peroxidase (GPx) activities and the level of lipid peroxidation (MDA content) decreased in roots. However, they increased in leaves. Catalase activity and chlorophyll content, on the other hand, decreased over exposure to Cd stress. Total glutathione, non-protein thiols, reduced glutathione (GSH) and phytochelatins increased significantly, while oxidized glutathione (GSSG) decreased, as compared with control plants. The present data suggest that the presence of Cd in soil and water can cause oxidative damage that may be detrimental for optimum production of nutritional mung.     

Cross-Talk Between Body Iron Stores and Diabetes: Iron Stores are Associated with Activity and Microsatellite Polymorphism of the Heme Oxygenase and Type 2 Diabetes

To assess the relationship between the length of (GT) _n repeats in HO-1 gene promoter and heme oxygenase (HO) enzymatic activity in mononuclear cells with iron (Fe) stores in type 2 diabetic mellitus (DM2) patients and metabolic syndrome (MS) subjects, we studied 163 patients with DM2, 185 with MS, and 120 controls subjects. We evaluated iron status (hemoglobin and serum Fe, ferritin, and transferrin receptor), and we determined the length of (GT) _n repeats in HO-1 gene promoter by capillary electrophoresis and HO enzymatic activity in mononuclear cells and assessed the relationship between these results and Fe stores. Only 1/163, 6/185, and 7/120 had iron deficiency anemia in DM2 patients, MS subjects, and controls, respectively. No iron overload (ferritin >200 μg/L) was detected in all the subjects studied. DM2 patients had higher iron deposits, total body iron, and heme oxygenase activity (a suggestion of high oxidative stress condition) than MS subjects and controls. In DM2, we found a positive association between serum iron and HO activity. There were no difference in allelic frequency between the three groups; however, among DM2 and MS patients, the frequency of short/medium (SM) genotype of (GT) _n repetition was increased and medium/medium (MM) genotype of (GT) _n repetition was lower than controls. These results imply that DM2 patients and individuals with MS carrying SM repeats might have higher susceptibility to develop diabetes consequences. This increased susceptibility could be Fe-mediated oxidative stress.     

Copper-induced changes in the growth, oxidative metabolism, and saponin production in suspension culture roots of Panax ginseng in bioreactors

Roots of Panax ginseng exposed to various concentrations of Cu (0.0, 5, 10.0, 25.0, and 50.0 μM) accumulated high amounts of Cu in a concentration-dependent and duration-dependent manner. Roots treated with 50 μM Cu resulted in 52% and 89% growth inhibition after 20 and 40 days, respectively. Saponin synthesis was stimulated at a Cu concentration between 5 and 25 μM but decreased at 50 μM Cu. Malondialdehyde content (MDA), lipoxygenase activity (LOX), superoxide ion (O₂ ^•−) accumulation, and H₂O₂ content at 5 and 10 μM Cu-treated roots were not increased but strongly increased at 50 μM Cu resulting in the oxidation of ascorbate (ASC) and glutathione (GSH) to dehydroascorbate (DHA) and glutathione disulfide (GSSG), respectively indicating a clear oxidative stress. Seven well-resolved bands of superoxide dismutase (SOD) were detected in the gel and an increase in SOD activity seemed to be mainly due to the induction of Fe-SOD 3. Five to 10 μM Cu slightly induced activity of ascorbate peroxidase (APX) and dehydroascorbate reductase (DHAR), guaiacol peroxidase (G-POD) but inhibited monodehydroascorbate reductase (MDHAR) and glutathione reductase (GR) enzyme activities. No changes in catalase (CAT) activity and in activity gel were found up to 25 μM Cu, but both G-POD and CAT activities were inhibited at 50 μM Cu. Glutathione metabolism enzymes such as γ-glutamylcysteine synthetase (γ-GCS), glutathione-S-transferase (GST), and glutathione peroxidase activities (GPx) were activated at 5 and 10 μM Cu but were strongly inhibited at 50 μM Cu due to the Cu accumulation in root tissues. The strong depletion of GSH at 50 μM Cu was associated to the strong induction of γ-glutamyltranspeptidase (γ-GGT) activity. These results indicate that plant could grow under Cu stress (5–25 μM) by modulating the antioxidant defense mechanism for combating Cu induced oxidative stress.     

Methylprednisolone and Indomethacin Inhibit Oxidative Stress Mediated Apoptosis in Rat C6 Glioblastoma Cells

Glioblastoma patients receive anti-inflammatory agent for alleviation of vasogenic edema and pain prior to surgery, radiotherapy, and chemotherapy. Oxidative stress is an important mechanism of action of some chemotherapeutic agents in the treatment of glioblastoma. So, we examined the modulatory effects of methylprednisolone (MP, a steroidal anti-inflammatory agent) and indomethacin (IM, a non-steroidal anti-inflammatory agent) on apoptosis in rat C6 glioblastoma cells following oxidative stress with hydrogen peroxide (H₂O₂). Exposure of C6 cells to 1 mM H₂O₂ for 24 h caused significant amounts of morphological and biochemical features of apoptosis. Expressions of Bax and Bcl-2 at mRNA and protein levels were altered resulting in an increase in Bax : Bcl-2 ratio in apoptotic cells, which also exhibited overexpression of 80 kDa calpain and an increase in calpain-cleaved 145 kDa α-spectrin breakdown product. Immunofluorescent and propidium iodide labeling detected caspase-3-p20 fragment in apoptotic cells, indicating activation of caspase-3 as well. Treatment of cells with 1 μM MP or 10 μM IM alone did not induce apoptosis. Pretreatment (1 h) with either 1 μM MP or 10 μM IM significantly inhibited H₂O₂ mediated apoptosis in C6 cells. Thus, pretreatment of glioblastoma with an anti-inflammatory agent, either steroidal or non-steroidal, may compromise the action of a chemotherapeutic agent that mediates therapeutic action via oxidative stress.     

Low concentration of GA activates a preconditioning response in HepG2 cells during oxidative stress—roles of Hsp90 and vimentin

Oxidative stress can be a significant cause of cell death and apoptosis. We performed studies in HepG2 cells to explore whether prior exposure to oxidative stress (“oxidative preconditioning”) and geldanamycin (GA) treatment can protect the cell from damage caused by subsequent oxidative insults. The cells were treated with 10 nM GA for 24 h before oxidative stress. Oxidative preconditioning was achieved by 2 h exposures to H₂O₂ (50 μM) separated by a 10-h recovery period in normal culture medium. Oxidative stress was induced by exposure to 500 μM H₂O₂ for 24 h. The effects of GA and oxidative preconditioning were investigated on the formation of Hsp90, vimentin, insoluble vimentin aggregates, and cleavage of vimentin in a cell culture model of oxidative stress. GA treatment leads to enhanced expression of Hsp90 and vimentin and to inhibition of vimentin protein aggregation. Similar results were obtained by oxidative preconditioning. It is confirmed that low concentrations of GA protected HepG2 cells from subsequent oxidative stress by increasing the levels of Hsp90 and by alleviating the extent of cell apoptosis induced by oxidative stress, which is similar to oxidative preconditioning. However, in contrast to preconditioning, GA treatment obviously changed binding activity of Hsp90 to vimentin cleavages. All the above indicated that low concentrations of GA treatment triggered cell protection from oxidative stress. Both the level of Hsp90 and its ability to bind with vimentin were changed by low concentrations of GA and might contribute to oxidative stress protection.     

Cadmium stress induces changes in the lipid composition and biosynthesis in tomato (<Emphasis Type="Italic">Lycopersicon esculentum</Emphasis> Mill.) leaves

The effects of cadmium (Cd) stress on lipid composition and biosynthesis were investigated in young leaves of ten-day-old tomato seedlings (Lycopersicon esculentum Mill. cv. Ibiza F1). Cd was found to be mainly accumulated in roots, but a severe inhibition of biomass production occurred in leaves, even at its low concentration (1.0 μM). Seven days after Cd treatment, the membrane lipids were extracted and separated on silica-gel thin layer chromatography (TLC). Fatty acid methyl esters were analyzed by FID-GC on a capillary column. Our results showed that Cd stress decreased the quantities of all lipids classes (phospholipids, galactolipids and neutral lipids). Likewise, there was also a decline in the levels of tri-unsaturated fatty acids, such as linolenic (C18:3) and hexadecatrienoic (C16:3) acids. The linolenic acid (C18:3) decreased in monogalactosyldiacylglycerol (MGDG) and all phospholipids, while hexadecatrienoinic acid (C16:3) declined mainly in MGDG. Moreover, Cd at high concentrations (25.0 and 50.0 μM) significantly enhanced the levels of lipid peroxides. Radiolabelling experiments were carried out by laying down microdroplets of [1-¹⁴C]acetate–a major precursor of lipid biosynthesis–on attached leaves of the control and Cd-treated plants. After incubation for 1, 2, 12 and 24 h, the leaves were harvested and lipids extracted and analysed. Cd stress was found to decrease the incorporation of [1-¹⁴C]acetate in total lipids. The biosynthesis of total lipids was altered with 25.0 and 50.0 μM Cd. The decline in the incorporation of [1-¹⁴C]acetate due to Cd stress was observed in all lipid classes. There was also a substantial decline in the incorporation of [1-¹⁴C]acetate in tri-unsaturated fatty acids. The results indicate that Cd treatment induces an oxidative stress by inhibiting the chloroplastic and extrachloroplastic lipid-biosynthesis pathways as well as lipid peroxidation.     

Effect of salicylic acid and methyl jasmonate on antioxidant systems of <Emphasis Type="Italic">Haematococcus pluvialis</Emphasis>

The influence of phytohormones, salicylic acid (SA) and methyl jasmonate (MJ) on the antioxidant systems in Haematococcus pluvialis was investigated. Both SA and MJ at 500 μM concentration reduced the growth of alga with salicylic acid, having more pronounced effect. Carotenoid and chlorophyll contents were decreased by SA and increased by MJ. Salicylic acid (100 μM) increased astaxanthin content to 6.8-fold under low light (30 μmol m⁻² s⁻¹), while MJ (10 μM) showed marginal increase in astaxanthin. Salicylic acid (500 μM) increased superoxide dismutase activity to 4.5- and 3.3-fold and ascorbate peroxidase (APX) activity to 15.5- and 7.1-fold under low and high light, respectively. Methyl jasmonate increased catalase activity (1.4-fold) under high light and APX activity (5.4-fold) under low light. Different mechanism of oxidative stress induced antioxidant production may be the plausible reason for this varied response for salicylic acid and methyl jasmonate. Higher concentrations of SA and MJ inhibited astaxanthin accumulation by different mechanisms either by scavenging the free radicals or by increasing primary carotenoids production. At lower concentrations, these phytohormones could be used for elicitation of secondary carotenoid production.