Estimating the accumulation and transfer of Nodularia spumigena toxins by the blue mussel Mytilus edulis: an appraisal from culture and mesocosm experiments.

Accumulation of Nodularia spumigena toxins by Mytilus edulis was studied during laboratory and mesocosm experiments in order to investigate the possible pathways of nodularin in mussels and calculate toxin budgets. Mussels were exposed to 0.2-15.6 microg nodularin l(-1), fed for up to 5 days with Nodularia cells from culture, or blooming in different nutrient-treated seawater. Toxin concentration was monitored with LC-ESI-MS. During different exposures, the amount of nodularin detected in mussels increased linearly with increasing toxin concentration in food and attained 0.28-13.8 microg of nodularin g dw(-1) of the mussel whole body tissue after 12 h. The digestive gland was found to be the tissue with the highest toxin concentration. Nodularin concentration in faeces was not proportional to faeces production or to toxin concentration in food; however, it seemed to be mostly related to food quality as well as to food availability. The percentage of nodularin taken up by the mussels, relative to the amount contained in the offered food, varied from 10% to 20%, depending on food quality. During a 5-day toxin accumulation experiment, the acute reduction of the toxin in mussel tissues the second day and the following stabilization, showed that probably mussels maintain low toxin levels via efficient elimination and/or toxin metabolism. After a 72 h depuration period, mussels showed 75% reduction in their toxin content.     

Comparison of ELISA and LC-MS analyses for yessotoxins in blue mussels (Mytilus edulis).

Blue mussels (Mytilus edulis) collected from Fl?devigen Bay, Norway, in 2001 and 2002 were analysed for yessotoxins (YTXs) by ELISA and yessotoxin (YTX), 45-hydroxyYTX, and carboxyYTX by LC-MS. Results from the two methods were compared to evaluate the ELISA. The response in the ELISA was 3-13 times higher than LC-MS, probably due to the antibodies binding to other YTX analogues not included in the LC-MS analysis. Nevertheless, the correlation between ELISA and LC-MS was good, with r2 values> or =0.8. The results indicate that the ELISA is a reliable method for estimating the total level of YTXs in mussels, and are consistent with extensive metabolism of algal YTXs in mussels. YTX was a minor component in the blue mussels at all times compared to 45-hydroxyYTX and especially carboxyYTX, except when the P. reticulatum bloom occurred. The results also indicate the presence of significant amounts of YTX analogues in addition to those measured by LC-MS. All samples below 4 mg/kg by ELISA were below the current EU regulatory limit of 1 mg/kg by LC-MS. Therefore, we propose using ELISA as a screening tool with a cut-off limit at 4 mg/kg for negative samples, whereas samples above this limit would be reanalyzed by LC-MS.     

Effects of Selol 5% supplementation on tissue antioxidant enzyme levels and peroxidation marker in healthy mice

Background

Selenium (Se) is an essential micronutrient for animals and humans used in the prevention or treatment of cancer. Selol is a mixture of selenitetriglycerides, containing Se(IV). It does not exhibit mutagenic activity and is less toxic than inorganic sodium selenite containing Se(IV). The antioxidant properties of the Selol were demonstrated using the blood of healthy animals. The aim of the study was to evaluate Selol as a Se supplement by determining the effect of its administration on the Se level and the antioxidant status in the tissues.

Yessotoxins in Norwegian blue mussels (Mytilus edulis): uptake from Protoceratium reticulatum, metabolism and depuration.

The Protoceratium reticulatum cell density at Flodevigen reached a maximum of 2200 cells/L on 16 May 2001. The levels of yessotoxins (YTXs) in blue mussels (Mytilus edulis) at the same site increased sharply by 14 May and peaked on 28 May, after which they steadily declined. No other algal species present showed a similar pattern of correspondence. Together with the recent finding that Norwegian strains of P. reticulatum produce YTXs, these results indicate that P. reticulatum causes yessotoxin (YTX) contamination of shellfish in Norway, and that only relatively low cell densities are necessary for this to occur. The mussels from Flodevigen were analyzed by LC-MS for YTX, 45-hydroxyYTX, carboxyYTX, and a new yessotoxin believed to be 45-hydroxycarboxyYTX, and by ELISA for YTXs. The seasonal variations in toxin content versus time measured by the two methods were qualitatively very similar, although the response in the ELISA was 3-9 times higher due to the antibodies detecting other YTXs that were not detected by the LC-MS method. Changes in the LC-MS profile for YTXs, and in the ratio of YTXs by LC-MS to YTXs by ELISA with time, were consistent with extensive metabolism of YTX in the mussels. Kinetic analysis of the LC-MS data showed an initial half-life of 20 days for YTX, and for YTX+45-hydroxyYTX, in the mussels. Similar analysis of the ELISA data gave a half-life of 24 days for YTXs. The depuration rate remained consistent over a 3-month period during which the temperature remained at 13-16 degrees C.     

Gentiana asclepiadea exerts antioxidant activity and enhances DNA repair of hydrogen peroxide- and silver nanoparticles-induced DNA damage

Exposure to high levels of different environmental pollutants is known to be associated with induction of DNA damage in humans. Thus DNA repair is of great importance in preventing mutations and contributes crucially to the prevention of cancer. In our study we have focused on quantitative analysis of Gentiana asclepiadea aqueous or methanolic extracts obtained from flower and haulm, their antioxidant potency in ABTS post-column derivatisation, and their potential ability to enhance DNA repair in human lymphocytes after hydrogen peroxide (H₂O₂) treatment (250 μM, 5 min). We also studied DNA repair in human kidney HEK 293 cells after exposure to 20 nm silver nanoparticles (AgNPs) (100 μg/ml, 30 min) in the presence and absence of the plant extract. We have found that mangiferin along with unidentified polar compounds are the most pronounced antioxidants in the studied extracts. Extract from haulm exhibited slightly stronger antioxidant properties compared to flower extracts. However, all four extracts showed significant ability to enhance DNA repair in both cell types after H₂O₂ and AgNP treatments.     

Accumulation of gliotoxin, a cytotoxic mycotoxin from Aspergillus fumigatus, in blue mussel (Mytilus edulis).

A strain of Aspergillus fumigatus has been isolated from sediments of a mussel bed. When cultured in hyper saline conditions (with sea-water), it produces a cytotoxic and immunosuppressive toxin, gliotoxin, which is excreted in an exudate. In order to know if this toxin could represent a risk for shellfish consumers, an experiment of bioaccumulation of gliotoxin in mussel has been carried out. After 6 days of contamination, toxin was accumulated in the meat of the mussels, at a level up to 2.9 microg/mg of extract weight, with a mode of contamination different to the classical digestive process described for a majority of marine toxins, but similar to the contamination mode of domoic acid.     

Effects of Selol 5% supplementation on the activity or concentration of antioxidants and malondialdehyde level in the blood of healthy mice

BackgroundSelol is a novel organoselenium Se(IV) compound. It reveals lower potential of toxicity than sodium selenite and does not exhibit mutagenic activity. Its antioxidant and anticancer properties including overcoming cancer cell resistance to standard therapy of the drug were proven. This is the first publication describing the influence of Selol 5% on the activity of blood antioxidant status in vivo.Materials and methodsWe investigated the influence of Selol 5% short-term (24 h) and long-term (28 days) administration on the activity of antioxidant enzymes, including the main selenoenzymes, in healthy mice plasma and erythrocytes. Plasma oxygen radical absorbance capacity value (ORAC) and the concentration of malonyldialdehyde (MDA) in plasma as a biomarker of oxidative stress as well as the value of selenium (Se) concentration in erythrocytes were shown.ResultsA significant increase of the selenium dependent glutathione peroxidase (Se-GSHPx) activity in plasma and erythrocytes, plasma selenoprotein P concentration, ORAC values, and Se concentration were observed during long-term supplementation as well as after Selol 5% single-dose administration, with two distinct increases of activity a few hours after the beginning of the experiment and before its end. We found a decreased thioredoxin reductase (THRR) activity and an increased MDA level during Selol 5% long-term supplementation. Glutathione S-transferase activity (GST) remained unchanged.ConclusionSelol 5% supplementation in vivo affects the selenoenzymes activities as well as the antioxidant status of plasma and erythrocytes. Selol 5% is an inhibitor of thioredoxin reductase activity, which can be important in anticancer therapy.     

Further insight into the impact of sodium selenite on selenoenzymes: high-dose selenite enhances hepatic thioredoxin reductase 1 activity as a consequence of liver injury

Selenium (Se) at supranutritional levels can enhance the activity of glutathione S-transferase (GST), whose gene is a target of nuclear factor erythroid-2 related factor 2 (Nrf2). Recent studies indicated that the thioredoxin reductase 1 (TrxR1) gene could also be targeted by Nrf2. Thus, high-dose Se may stimulate TrxR1 provided it enhances GST activity. Indeed, one study found that Se at supranutritional levels transiently increased hepatic TrxR1 activity. However, another study reported that supranutritional Se had no such effect on hepatic TrxR1 activity. In view of this discrepancy, the present research investigated whether high-dose Se has any impact on hepatic TrxR1. Moreover, we investigated whether Se preferentially activates GST over TrxR1. We observed that when sodium selenite (SS) caused liver injury, both hepatic TrxR1 activity and hepatic GST activity increased. Further experiments indicated that SS increased hepatic GST activity at either toxic or high but non-toxic dose levels; however, increase in hepatic TrxR1 activity occurred only at toxic levels, suggesting that enhanced TrxR1 activity correlates with liver injury. To corroborate this, we showed that hepatotoxic agents, thioacetamide or carbon tetrachloride, caused marked increases in hepatic TrxR1 activity. In conclusion, high-dose SS indeed can enhance hepatic TrxR1 activity, but only on the condition that it causes liver injury. High-dose SS affects hepatic GST more readily than hepatic TrxR1. Thus, the cancer-preventive mechanism of Se at non-toxic supranutritional levels relies more on its modulation of GST rather than TrxR1, at least in liver tissue.     

Comparative assessment of cardiac activity and DNA damage in haemocytes of the Mediterranean mussel Mytilus galloprovincialis in exposure to tributyltin chloride

This study gives an insight in sensitivity of heart rate (Hr) of Mytilus galloprovincialis as a physiological biomarker. Impact of tributyltin chloride (TBT-Cl) on Hr was studied in parallel with evaluation of mutagenic, genotoxic and cytotoxic potential of TBT-Cl (10, 100 and 1000 μg/L) within 96 h treatment in static conditions. Mutagenic potential was assessed by SOS/umuC assay while genotoxicity was assessed in haemocytes of M. galloprovincialis by using the comet assay and the micronucleus test. Benzo(a)pyrene (B(a)P) was used as a positive control. Hr variations detected in TBT-Cl treatments can be linked to data obtained in the genotoxicological assays indicating that Hr can be considered and used as a reliable physiological biomarker for detecting the presence of organotin compounds. However despite the observed genotoxic potential of B(a)P, a noteworthy Hr response was not observed which further questions the potential of Hr in the detection of different types of pollutants.     

Protective effect of N-acetylcysteine against radiation induced DNA damage and hepatic toxicity in rats

The present study was designed to evaluate the radioprotective effect of N- acetylcysteine (NAC) on gamma-radiation induced toxicity in hepatic tissue in rat. The cellular changes were estimated using malondialdehyde (MDA, an index of lipid peroxidation), superoxide dismutase (SOD), glutathione peroxidase (GSHPx), reduced glutathione (GSH), and total nitrate/nitrite (NO(x)) as markers of hepatic oxidative stress in rats following gamma-irradiation. The DNA damage was determined by agarose gel electrophoresis. To achieve the ultimate goal of this study, 40 adult rats were randomly divided into 4 groups of 10 animals each. Group I was injected intraperitoneally with saline solution for 7 consecutive days and served as control group. Group II was irradiated with a single dose of 6Gy gamma-radiation. Group III was daily injected with NAC (1g/kg, i.p.) for 7 consecutive days. Group IV received a daily i.p. injection of NAC (1g/kg, i.p.) for 7 consecutive days and 1h after the last dose, rats were irradiated with a single dose (6Gy) gamma-radiation. The animals were sacrificed after 24h. DNA damage was observed in tissue after total body irradiation with a single dose of 6Gy. Malondialdehyde and total nitrate/nitrite were increased significantly whereas the levels of GSH and antioxidant enzymes were significantly decreased in gamma-irradiated group. Pretreatment with NAC showed a significant decrease in the levels of MDA, NO(x) and DNA damage. The antioxidant enzymes increased significantly along with the levels of GSH. Moreover, histopathological examination of liver tissues confirmed the biochemical data. Thus, our results show that pretreatment with N-acetylcysteine offers protection against gamma-radiation induced cellular damage.     

Single contaminant and combined exposures of polyethylene microplastics and fluoranthene: accumulation and oxidative stress response in the blue mussel,Mytilus edulis

The microplastic “vector effect” has received increasing attention. The aim of this study was to investigate the influence of polyethylene microplastic beads (PE MP) on accumulation and associated oxidative stress responses attributed to fluoranthene (Flu) in blue mussels, Mytilus edulis. Blue mussels were exposed for 96 h to four treatment groups: Flu-only, MP-only, Flu and MP coexposure, and Flu-incubated MP. Treatments were conducted at a low and high concentration (50 μg/L and 100 Flu μg/L and 100, and 1000 MP/mL). Results demonstrated that in both the gill and digestive gland, coexposure did not markedly affect Flu uptake, but this treatment significantly decreased tissue Flu concentrations. Antioxidant responses including activities of superoxide dismutase (SOD), catalase (CAT), glutathione peroxidases (GPx), and levels of total glutathione (GSH) in both gills and digestive glands were significantly altered suggesting a perturbation of redox state induced by the exposure conditions. Although individual biomarkers varied, the biomarker profile enabled certain generalizations to be made. Antioxidant responses occurred more likely in gill tissue than in digestive gland. Individual contaminant exposures to Flu or MP led to varying responses, but coexposures and incubated exposures did not result in additive or synergistic effects. Exposure concentrations (i.e., low or high treatments) were not a consistent a predictor of response; and the internal Flu dose did not consistently predict outcome of various biomarkers. Importantly, MP-only exposure appeared to be capable of eliciting direct effects on the oxidative stress system as demonstrated by the activities of CAT and GPx. These findings warrant further investigation.     

Azaspiracid poisoning (AZP) toxins in shellfish: Toxicological and health considerations

It has been almost a decade since a previously unknown human toxic syndrome, azaspiracid poisoning (AZP), emerged as the cause of severe gastrointestinal illness in humans after the consumption of mussels (Mytilus edulis). Structural studies indicated that these toxins, azaspiracids, were of a new unprecedented class containing novel structural features. It is now known that the prevalent azaspiracids in mussels are AZA1, AZA2 and AZA3, which differ from each other in their degree of methylation. Several hydroxylated and carboxylated analogues of the main azaspiracids have also been identified, presumed to be metabolites of the main toxins. Since its first discovery in Irish mussels, the development of facile sensitive and selective LC-MS/MS methods has resulted in the discovery of AZA in other countries and in other species. Mice studies indicate that this toxin class can cause serious tissue injury, especially to the small intestine, and chronic exposure may increase the likelihood of the development of lung tumours. Studies also show that tissue recovery is very slow following exposure. These observations suggest that AZA is more dangerous than the other known classes of shellfish toxins. Consequently, in order to protect human consumers, proper risk assessment and regulatory control of shellfish and other affected species is of the utmost importance.     

Ginkgo biloba extract protects against mercury(II)-induced oxidative tissue damage in rats.

Mercury(II) is a highly toxic metal which induces oxidative stress in the body. In this study we aimed to investigate the possible protective effect of Ginkgo biloba (EGb), an antioxidant agent, against experimental mercury toxicity in rat model. Following a single dose of 5mg/kg mercuric chloride (HgCl(2); Hg group) either saline or EGb (150mg/kg) was administered for 5days. After decapitation of the rats trunk blood was obtained and the tissue samples from the brain, lung, liver, and kidney were taken for the determination of malondialdehyde (MDA) and glutathione (GSH) levels, myeloperoxidase (MPO) activity and collagen contents. Formation of reactive oxygen species in the tissue samples was monitored by chemiluminescence (CL) technique. BUN, creatinin, ALT, and AST levels and tumor necrosis factor-alpha (TNF-alpha) and lactate dehydrogenase (LDH) activity were assayed in serum samples. The results revealed that HgCl(2) induced oxidative damage caused significant decrease in GSH level, significant increase in MDA level, MPO activity and collagen content of the tissues. Treatment of rats with EGb significantly increased the GSH level and decreased the MDA level, MPO activity, and collagen contents. Similarly, serum ALT, AST and BUN levels, as well as LDH and TNF-alpha, were elevated in the Hg group as compared to control group. On the other hand, EGb treatment reversed all these biochemical indices. Our results implicate that mercury-induced oxidative damage in brain, lung, liver, and kidney tissues protected by G. biloba extract, with its antioxidant effects.     

Inula crithmoides extract protects against ochratoxin A-induced oxidative stress, clastogenic and mutagenic alterations in male rats

Ochratoxin A (OTA) is a mycotoxin often found in cereals and agricultural products. There is unequivocal evidence of renal carcinogenicity of OTA in male rats, although the mechanism of action is unknown. Several reports suggest that exposure to OTA resulted in oxidative stress, genotoxicity and DNA damage. Therefore, the aim of the current study was to evaluate the protective effects of aqueous extract of Inula crithmoides growing in Egypt against OTA-induced mutagenicity and oxidative stress. Forty male Sprague-Dawley rats were divided into four groups and treated for 15 days as follows: control group and the groups treated with OTA (3mg/kg b.w), I. crithmoides extract alone (370mg/kg b.w) and OTA+I. crithmoides extract. Blood and tissue samples were collected for different biochemical analyses. Bone marrow micronucleus test and blood for random amplified polymorphism DNA-PCR (RAPD-PCR) method were performed to assess the antigenotoxic effect of the extract. The results indicated that OTA induced toxicological effects typical to those reported in the literature and increased the frequencies of MnPCEs in bone marrow. The RAPD-PCR analysis revealed the appearance of new bands in DNA resulting from genetic alteration. The extract alone was safe and succeeded in counteracting the oxidative stress and protect against the cytotoxicity resulting from OTA.     

OGG1 Ser326Cys polymorphism interacts with cigarette smoking to increase oxidative DNA damage in human sperm and the risk of male infertility

8-Oxoguanine DNA glycosylase 1 (OGG1) plays an important role in repairing oxidative DNA damage induced by chemical agents, such as tobacco. This study examined the effects of OGG1 Ser326Cys polymorphism and cigarette smoking, alone or combined, on sperm oxidative DNA damage and the risk of male infertility. A total of 620 idiopathic infertile subjects and 480 fertile controls were recruited in this study. Sperm 8-hydroxydeoxyguanine (8-OHdG) was measured by immunofluorescent assay using flow cytometry and genotypes were determined by OpenArray platform with a chip-based Taq-Man genotyping technology. Our results demonstrated that both cigarette smoking and OGG1 polymorphism can affect the sperm 8-OHdG levels. Individuals with variant Cys/Cys homozygote showed higher levels of sperm 8-OHdG than wide-type homozygote carriers (Ser/Ser). Stratified analysis found that the association between OGG1 polymorphism and sperm 8-OHdG levels was only observed among smokers with pack-years ≥5 but not among those subjects with pack-years < 5 (pack-years = packs smoked per day × years as a smoker). Further analysis based on the case–control study revealed that variant allele (Cys) of OGG1 was significantly associated with male infertility risk in a dominant model (OR = 1.35, 95% CI: 1.01–1.82; trend P < 0.001). Furthermore, we found a significant gene–environment interaction between OGG1 Ser326Cys polymorphism and cigarette smoking in relation to male infertility risk (P_interation = 0.0003). These findings provided the first evidence about potential interactive effects of OGG1 polymorphism and cigarette smoking on male infertility risk.     

Diphlorethohydroxycarmalol, isolated from the brown algae Ishige okamurae, protects against radiation-induced cell damage in mice

The aim of this study was to evaluate the radioprotective effects of diphlorethohydroxycarmalol (DPHC), isolated from the brown algae Ishige okamurae, in mice subjected to gamma irradiation.DPHC significantly decreased the level of radiation-induced intracellular reactive oxygen species in cultured Chinese hamster lung fibroblast (V79-4) cells (p < 0.05), enhanced cell viability that decreased after exposure to γ-rays, and reduced radiation-induced apoptosis in the V79-4 cells.Pretreatment with DPHC (100 mg/kg) in mice prior to irradiation significantly protected the intestinal crypt cells in the jejunum (p < 0.01) and maintained villi height (p < 0.01), compared with those of the vehicle-treated irradiated group. Mice pretreated with DPHC also exhibited dose-dependent increases in the bone marrow cell viability. The dose-reduction factor for gamma irradiation in the DPHC-pretreated mice was 2.05 at 3.5 days after irradiation.These results suggest that DHPC plays a role in protecting cells from irradiation-induced apoptosis, through the scavenging of reactive oxygen species in vitro, and that DPHC significantly protected intestinal progenitor cells and bone marrows cells that were decreased by gamma irradiation in vivo.     

Antioxidant activity and protective effect of Turnera ulmifolia Linn. var. elegans against carbon tetrachloride-induced oxidative damage in rats

The present study aimed to determine whether the leaves of Turnera ulmifolia Linn. var. elegans extract exert significant antioxidant activity. The antioxidant activity of its hydroethanolic extract (HEETU) was evaluated by assessing (a) its radical scavenging ability in vitro, and (b) its in vivo effect on lipid peroxidation and antioxidant enzyme activities. The in vitro antioxidant assay (DPPH) clearly supported HEETU free radical scavenging potential. Moreover, glutathione content and antioxidant enzyme activities (glutathione peroxidase, superoxide dismutase and catalase) were significantly enhanced in CCl₄-treated rats due to oral HEETU-treatment (500 mg/kg b.w.) over 7 and 21 days. In addition, an improvement was observed in lipid peroxidation and serum biochemical parameters (aspartate aminotransferase and alanine aminotransferase), indicating a protective effect against CCl₄-induced liver injuries, confirmed by histopathological studies. The HEETU effect was comparable to the standard drug Legalon® (50 mg/kg b.w.) under the same experimental condition. Quantitative analysis of the HPLC extract revealed the presence of flavonoids, wich mediate the effects of antioxidant and oxidative stress. In conclusion, extract components exhibit antioxidant and hepatoprotective activities in vitro and in vivo.     

Genotoxicity study with special reference to DNA damage by comet assay in fission yeast, Schizosaccharomyces pombe exposed to drinking water.

The objective of this study was to investigate genotoxicity, especially DNA damage, in drinking water samples collected from tap by using fission yeast Schizosaccharomyces pombe as a model organism. Generally raw water potabolization is done by treatment with polymeric coagulant, alum, chlorine, etc. In the comet test, highly significant (P<0.001) effects of DNA damage were detected in treated water (tap water) when compared to negative control (raw water) as well as laboratory control (distilled water) samples for both 1 h and 2 h exposure. In the water treatment plant, raw water treatment is done by the process of prechlorination, alum and polymeric coagulant (CatflocT) dosing, postchlorination, filtration and final discharge for consumption. In conclusion it can be stated from the results that chlorinated disinfectant, alum and polymeric coagulant (CatflocT) mixture used in drinking water has a potent cumulative genotoxic effect in the eukaryotic cells and may pose potential genotoxic risk for human health following long-term consumption.     

DNA damage in male gonad cells of Green mussel (Perna viridis) upon exposure to tobacco products

DNA damage (determined by the Comet Assay) and the occurrence of deformed nuclei were measured as endpoints of genotoxicity in male gonad cells of the marine mussel (Perna viridis). Upon exposure of the organism to varying concentrations of extracts of smoked and non-smoked cigar tobacco over a period of 16 days, DNA damage was found to be highest in marine mussels exposed to extracts of smoked cigar tobacco. Conversely, more deformed nuclei were detected in marine mussels exposed to extracts of non-smoked cigar tobacco. The level of DNA damage and the number of deformed nuclei reach a maximum at day 12 of exposure to both extracts but decrease thereafter. This phenomenon is attributed to the organism’s capacity to maintain the integrity of its genetic material upon exposure to potential genotoxicants present in the tobacco extracts. A dose response in DNA damage and deformed nuclei was also detected in isolated gonad cells upon in vitro exposure to hydrogen peroxide a known DNA strand breaking agent. The results of this study indicate that the DNA in male gonad cells of the marine mussel is damaged upon exposure to genotoxicants, and suggests the suitability of the organism for future investigations into the effect of such agents on its reproductive capacities.Special Issue on Biomarkers of Marine Pollution and Bioremediation     

Taxifolin mitigates oxidative DNA damage in vitro and protects zebrafish (Danio rerio) embryos against cadmium toxicity

Taxifolin (TAX) is a natural source of bioflavonoid found in various conifers. In this study, initially we investigated the antioxidant potential of TAX under in vitro assays such as 2,2-diphenyl-1-picrylhydrazyl (DPPH), 2,2-azino-bis (3-ethylbenzthiazoline-6-sulfonic acid) (ABTS), ferric-ion reducing power (FRAP) and hydroxyl radical (OH). The activities of DPPH, ABTS, FRAP and OH radical levels were significantly inhibited by TAX with an IC₅₀ values of 16.48, 66.34, 18.17 and 11.42 μg/ml, respectively. Secondly, TAX exhibited a strong protection against OH mediated DNA damage on pUC19 plasmid DNA at 1.0 μg/ml. Finally, we evaluated the protective mechanism of TAX against cadmium intoxicated zebrafish embryos (Danio rerio). We found that embryos exposed to 100 μM Cd exhibited significantly reduced survival, delayed hatching and phenotypic abnormalities at 24, 48, 72 and 96 hours post fertilization (hpf). Similarly, Cd intoxicated embryos showed significantly increased cardiac function (131 beats/min) at 60 hpf. Conversely, treatment with TAX (0.1, 1.0 and 10 μM) significantly enhanced the antioxidant enzyme levels (SOD, CAT, GPx and GR) by reducing the lipid peroxidation (MDA) in zebrafish embryos. Collectively, our results concluded that TAX could act as a potent redox scavenger against oxidative DNA damage and also functions as a crucial suppressor of Cd toxicity in zebrafish embryos.