Protective Role Of Antioxidants Research Articles

Compounds from Ilex paraguariensis extracts have antioxidant effects in the brains of rats subjected to chronic immobilization stress.

Immobilization induces oxidative damage to the brain. Ilex paraguariensis extracts (Mate) and their major natural compound, chlorogenic acid (CGA), exert protective effects against reactive oxygen species formation. Here, the effects of Mate and CGA on oxidative damage induced by chronic immobilization stress (CIS) in the cortex, hippocampus, and striatum were investigated. For CIS, animals were immobilized for 6 h every day for 21 consecutive days. Rats received Mate or CGA by intragastric gavage 30 min before every restraint session. Endpoints of oxidative stress (levels of lipid peroxidation, protein carbonylation, and reduced (GSH) and oxidized (GSSG) forms of glutathione) were evaluated following CIS. While CIS increased oxidized lipid and carbonyl levels in all brain regions, CGA (and Mate to a lesser extent) attenuated lipid and protein oxidation as compared with control groups. GSH/GSSG balance showed a tendency to increase in all regions in response to stress and antioxidants. Taken together, our results support a protective role of dietary antioxidants against the neuronal consequences of stress.

Protective Role for Antioxidants in Acute Kidney Disease.

Acute kidney injury causes significant morbidity and mortality in the community and clinic. Various pathologies, including renal and cardiovascular disease, traumatic injury/rhabdomyolysis, sepsis, and nephrotoxicity, that cause acute kidney injury (AKI), induce general or regional decreases in renal blood flow. The ensuing renal hypoxia and ischemia promotes the formation of reactive oxygen species (ROS) such as superoxide radical anions, peroxides, and hydroxyl radicals, that can oxidatively damage biomolecules and membranes, and affect organelle function and induce renal tubule cell injury, inflammation, and vascular dysfunction. Acute kidney injury is associated with increased oxidative damage, and various endogenous and synthetic antioxidants that mitigate source and derived oxidants are beneficial in cell-based and animal studies. However, the benefit of synthetic antioxidant supplementation in human acute kidney injury and renal disease remains to be realized. The endogenous low-molecular weight, non-proteinaceous antioxidant, ascorbate (vitamin C), is a promising therapeutic in human renal injury in critical illness and nephrotoxicity. Ascorbate may exert significant protection by reducing reactive oxygen species and renal oxidative damage via its antioxidant activity, and/or by its non-antioxidant functions in maintaining hydroxylase and monooxygenase enzymes, and endothelium and vascular function. Ascorbate supplementation may be particularly important in renal injury patients with low vitamin C status.

Argininic acid alters markers of cellular oxidative damage in vitro: Protective role of antioxidants

We, herein, investigated the in vitro effects of argininic acid on thiobarbituric acid-reactive substances (TBA-RS), total sulfhydryl content and on the activities of antioxidant enzymes such as catalase (CAT), superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) in the blood, kidney and liver of 60-day-old rats. We also verified the influence of the antioxidants (each at 1.0mM) trolox and ascorbic acid, as well as of NG-nitro-l-arginine methyl ester (L-NAME) at 1.0mM, a nitric oxide synthase inhibitor, on the effects elicited by argininic acid on the parameters tested. The liver, renal cortex and renal medulla were homogenized in 10vol (1:10w/v) of 20mM sodium phosphate buffer, pH 7.4, containing 140mM KCl; and erythrocytes and plasma were prepared from whole blood samples obtained from rats. For in vitro experiments, the samples were pre-incubated for 1h at 37°C in the presence of argininic acid at final concentrations of 0.1, 1.0 and 5.0μM. Control experiments were performed without the addition of argininic acid. Results showed that argininic acid (5.0μM) enhanced CAT and SOD activities and decreased GSH-Px activity in the erythrocytes, increased CAT and decreased GSH-Px activities in the renal cortex and decreased CAT and SOD activities in the renal medulla of 60-day-old rats, as compared to the control group. Antioxidants and/or L-NAME prevented most of the alterations caused by argininic acid on the oxidative stress parameters evaluated. Data suggest that argininic acid alters antioxidant defenses in the blood and kidney of rats; however, in the presence of antioxidants and L-NAME, most of these alterations in oxidative stress were prevented. These findings suggest that oxidative stress may be make an important contribution to the damage caused by argininic acid in hyperargininemic patients and that treatment with antioxidants may be beneficial in this pathology.

Mitochondrion-associated protein peroxiredoxin 3 promotes benign prostatic hyperplasia through autophagy suppression and pyroptosis activation.

Benign prostatic hyperplasia (BPH) is one of the most common diseases in the senior men and age plays an important role in the initiation and development of BPH. Mammalian cells primarily use the autophagy-lysosome system to degrade misfolded/aggregated proteins and dysfunctional organelles such as mitochondria and suppress pyroptosis, a type of cell death that stimulates inflammatory responses and growth of other cells around. Peroxiredoxin 3 (PRDX3) is the only mitochondrion-associated member of peroxiredoxin family enzymes that exert their protective antioxidant role in cells through their peroxidase activity. We hypothesized that PRDX3 may inhibit autophagy to activate pyroptosis to induce growth of prostatic epithelial cells. Here we show that PRDX3 maintained the integrity of mitochondria and its depletion led to an enhancement of oxidative stresses. PRDX3-associated and PRDX3-free mitochondria co-existed in the same cells. PRDX3 expressed at higher levels in prostatic epithelial cells in prostate tissues from BPH patients and BPH-representative cell line than in prostate tissues from healthy donors and a cell line representing normal epithelial cells. PRDX3 suppressed autophagy flux and activated pyroptosis to induce inflammatory responses and stimulate the over-growth of prostate tissues. Therefore, higher levels of PDRX3 in prostatic epithelial cells may promote the initiation and development of BPH through autophagy inhibition and pyroptosis activation.

Nephroprotective Hepatoprotective Potential and Antioxidant Role of Carob Pods (Cerotonia siliqua L.) against Carbon Tetrachloride-induced Toxicity in Rats

Abstract: Objective: The aims of current study are the evaluation of the protective effect and antioxidant role of carob pods against carbon tetrachloride (CCl4)-induced oxidative stress, hepatotoxicity and nephropathy. Material and Methods: The present experiment was designed as I (control), II (0.5 ml/kg CCl4), III (%10 CP), IV (CCl4 0.5 ml/kg+%10 CP) groups. While rats in group I and III were fed with a diet without CCl4, II, and IV groups received twice 0.5 ml/kg/week, where IV group additionally received %10 CP supplementation for 50 days. The protective roles and antioxidant activity of the CP supplementation feed against CCl4-induced oxidative stress and toxicity were evaluated by histopathological changes, measuring hepatic and renal damage biomarkers (HRDB), antioxidant defence system constituents (ADSC) and malondialdehyde (MDA) parameters in the erythrocyte, liver, brain, kidney and spleen tissues of rats. Results: According to the results, the biochemical analysis showed a considerable increase in the serum AST (aspartate aminotransferase), ALT (alanin aminotransferase), GGT (gamma glutamyl transpeptidase) and LDH (lactate dehydrogenase) enzymes, creatinine and urea, and decrease in the group II as compared to that of I group. On contrary, such parameters were decreased in IV group as compared to that of group II. In addition, the results showed that CP supplementation diet restored the CCl4 induced MDA (malondialdehyde) and ADSC towards to control. The hepatoprotection of CP is further substantiated by the almost normal histological findings in IV group against degenerative changes in II group. Protective effects by CP are further substantiated by the almost normal HRDB for kidney and liver in IV treated group as against degenerative changes in the II treated rats. Conclusion: The results indicated that CP could be as an important as diet-derived antioxidants in preventing oxidative damage in the tissues by reducing the MDA or inhibiting the production of CCl4-induced free radicals and liver and kidney destruction. Key words: Carbon tetrachloride, Carob pods, Protective potential, Antioxidant role.

Supplementation of sperm media with zinc, D-aspartate and co-enzyme Q10 protects bull sperm against exogenous oxidative stress and improves their ability to support embryo development.

High levels of reactive oxygen species in the semen of infertile patients or spontaneously generated during in vitro sperm handling may impair sperm quality, fertilization and embryo developmental competence. We recently reported that zinc, d-aspartate and co-enzyme Q10, contained in the dietary supplement Genadis® (Merck Serono), have protective effects on human and bull sperm motility, lipid peroxidation and DNA fragmentation in vitro; furthermore, in bovine, treated spermatozoa had an improved ability to support embryo development. However, only a few studies have investigated the protective role of antioxidants during in vitro sperm handling in the presence of an exogenous oxidative stress. Herein, to simulate such conditions in an animal model, we induced exogenous oxidative stress on spermatozoa through the xanthine-xanthine oxidase system and investigated its effects on sperm function and subsequent embryo developmental competence in the presence of zinc, d-Asp and CoQ10 protection. The main results showed that exogenous oxidative stress decreased sperm motility, increased sperm DNA fragmentation, and reduced fertilization and blastocyst rates and quality. Pre-treatment with zinc, d-aspartate and co-enzyme Q10 before exogenous oxidative stress was able to prevent these effects. Supplementation of sperm culture media with zinc, d-aspartate and co-enzyme Q10 could protect sperm from oxidative stress damage during in vitro handling in assisted reproductive technologies.

Microcirculatory Disorders and Protective Role of Antioxidant in Severe Heat Stroke: A Rat Study.

This study aims to examine microcirculation and systemic hemodynamic disturbances in severe heat stroke (HS). A total of 147 rats were divided into HS group (HS), pretreated with superoxide dismutase (SOD+HS) group, and pretreated with normal saline (NS+HS) group. Heat stress was induced by incubating the animals in certain temperatures. Blood flow and vascular reactivity were monitored dynamically with intravital microscopy. Pulmonary permeability was reflected by wet-to-dry weight ratio, the concentration of Evans Blue (EB), and histopathology of lung. The results showed that heat stress could induce blood flow rate reduced, and SOD exhibited better protective role in blood flow rate. The arteriolar reactivity threshold to norepinephrine was markedly reduced at core temperature of 41°C, but no significant decrease occurred in SOD+HS group. Water content and EB concentration in lung tissue in HS group were increased along with temperature rise. SOD treatment could attenuate those changes. The pathological lung injury caused by heat stress was also milder in SOD+HS group than that in other two groups. Mean arterial pressure decreased at early stages of heat stress, but there was no decrease in SOD+HS group. There was a significant body weight loss during heat stress in all groups. Survival time in SOD+HS group was longer than that in other two groups. These results suggest that microcirculation disturbance occurs not only at the early stage but also before systemic hemodynamic disorder, monitoring microcirculation following HS is of prognostic value, and intervention with antioxidative agents may have certain protecting effects in severe HS.

ChemInform Abstract: The Rise of Radicals in Bioinorganic Chemistry

AbstractReview: [82 refs.

Galactose alters markers of oxidative stress and acetylcholinesterase activity in the cerebrum of rats: protective role of antioxidants.

We evaluated the in vitro effects of galactose at 0.1, 3.0, 5.0 and 10.0mM on thiobarbituric acid-reactive substances (TBA-RS), total sulfhydryl content, protein carbonyl content, on the activities of the antioxidant enzymes catalase (CAT), superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) and on acetylcholinesterase (AChE) activity in the cerebral cortex, cerebellum and hippocampus of rats. We also investigated the influence of the antioxidants (each at 1mM), α-tocopherol, ascorbic acid and glutathione, on the effects elicited by galactose on the parameters tested. Results showed that galactose, at a concentration of 3.0mM, enhanced TBA-RS levels in the hippocampus, cerebral cortex and cerebellum of rats. In the cerebral cortex, galactose at concentrations of 5.0 and 10.0mM increased TBA-RS and protein carbonyl content, and at 10.0mM increased CAT activity and decreased AChE activity. In the cerebellum, galactose at concentrations of 5.0 and 10.0mM increased TBA-RS, SOD and GSH-Px activities. In the hippocampus, galactose at concentrations of 5.0 and 10.0mM increased TBA-RS and CAT activity and at 10.0mM decreased GSH-Px. Data showed that at the pathologically high concentration (greater than 5.0mM), galactose induces lipid peroxidation, protein carbonylation, alters antioxidant defenses in the cerebrum, and also alters cholinesterase activity. Trolox, ascorbic acid and glutathione addition prevented the majority of alterations in oxidative stress parameters and the decrease in AChE activity that were caused by galactose. Our findings lend support to a potential therapeutic strategy for this condition, which may include the use of appropriate antioxidants for ameliorating the damage caused by galactose.

Influence of Different Levels of Lipoic Acid Synthase Gene Expression on Diabetic Nephropathy.

Oxidative stress is implicated in the pathogenesis of diabetic nephropathy (DN) but outcomes of many clinical trials are controversial. To define the role of antioxidants in kidney protection during the development of diabetic nephropathy, we have generated a novel genetic antioxidant mouse model with over- or under-expression of lipoic acid synthase gene (Lias). These models have been mated with Ins2Akita/+ mice, a type I diabetic mouse model. We compare the major pathologic changes and oxidative stress status in two new strains of the mice with controls. Our results show that Ins2Akita/+ mice with under-expressed Lias gene, exhibit higher oxidative stress and more severe DN features (albuminuria, glomerular basement membrane thickening and mesangial matrix expansion). In contrast, Ins2Akita/+ mice with highly-expressed Lias gene display lower oxidative stress and less DN pathologic changes. Our study demonstrates that strengthening endogenous antioxidant capacity could be an effective strategy for prevention and treatment of DN.

Identification of three selenoprotein T paralogs in goldfish (Carassius auratus) and expression analysis in response to environmental stressors.

Selenoproteins, which contain the selenocysteine (Sec), play crucial roles in antioxidant protection. In the present study, we have identified and characterized three selenoprotein T paralogs (designated as gfSelT1a, gfSelT1b and gfSelT2) in goldfish, Carassius auratus. The SECIS element was found in the 3'-UTRs of gfSelT1a, gfSelT1b and gfSelT2 mRNA. Sequence analysis showed that they all possess the CxxU motif (where U represents Sec) in the N-terminal. Constitutive expressions of gfSelT1a, gfSelT1b and gfSelT2 were observed in all tissues studied. In liver, gfSelT1a, gfSelT1b and gfSelT2 mRNA expression levels significantly decreased when fasting and increased after re-feeding. The expressions of gfSelT1a, gfSelT1b and gfSelT2 were all inducible by cadmium exposure and H2O2-mediated oxidative stress, except the transcripts of gfSelT1b decreasing with H2O2 stimulation in brain. Furthermore, the expressions of gfSelT1a, gfSelT1b and gfSelT2 consistently increased in spleen but decreased in brain in response to heat stress. However, in liver only gfSelT1a mRNA expression significantly increased. In a word, this is the first report of the presence of three SelT genes in goldfish and their distinct expression patterns in response to environmental stressors. Our results suggest a potential involvement of gfSelT1a, gfSelT1b and gfSelT2 in host protection against environmental stressors including heavy mental, oxidative stress and heat stress in goldfish.

In vivo and in vitro effects of selected antioxidants on rabbit meat microbiota

The purpose of this study was to investigate the effect of dietary vitamin E or EconomasE™ supplementation on the growth of several background/pathogenic bacteria on rabbit carcasses and hamburgers during refrigerated storage. For 51days, 270 New Zealand rabbits received either a basal diet, or experimental diets enriched with 100 or 200mg/kg of vitamin E or EconomasE™. The bacteria studied were Salmonella, Listeria monocytogenes, Pseudomonas, Enterobacteriaceae, Escherichia coli, coagulase-positive staphylococci, plus both mesophilic and psychrotrophic aerobes. The growth of Listeria monocytogenes on contaminated patties was evaluated through a challenge test. The potential protective or antimicrobial effect of vitamin E or EconomasE™ on Listeria monocytogenes or Pseudomonas aeruginosa was assessed in vitro. Diet did not influence the concentrations of bacteria found on rabbit carcasses and developing on hamburgers. Vitamin E (in vivo and in vitro) and EconomasE™ in vivo had a protective antioxidant role, while EconomasE™ in vitro had strong antibacterial activity against Listeria monocytogenes, but not against Pseudomonas aeruginosa.

The Rise of Radicals in Bioinorganic Chemistry.

Prior to 1950, the consensus was that biological transformations occurred in two-electron steps, thereby avoiding the generation of free radicals. Dramatic advances in spectroscopy, biochemistry, and molecular biology have led to the realization that protein-based radicals participate in a vast array of vital biological mechanisms. Redox processes involving high-potential intermediates formed in reactions with O2 are particularly susceptible to radical formation. Clusters of tyrosine (Tyr) and tryptophan (Trp) residues have been found in many O2-reactive enzymes, raising the possibility that they play an antioxidant protective role. In blue copper proteins with plastocyanin-like domains, Tyr/Trp clusters are uncommon in the low-potential single-domain electron-transfer proteins and in the two-domain copper nitrite reductases. The two-domain muticopper oxidases, however, exhibit clusters of Tyr and Trp residues near the trinuclear copper active site where O2 is reduced. These clusters may play a protective role to ensure that reactive oxygen species are not liberated during O2 reduction.

Oxidative stress and antioxitant therapy of chronic periodontitis

Chronic periodontitis is a progressive, infectious inflammation disease, caused by the dysbiosis of oral resident flora, leading to the destruction of periodontium. The onset of pathogenic microorganisms is the etiological factor of periodontitis, while the immuno-inflammatory response affects the progression of the disease. Under chronic periodontitis, oxidative stress occurs when excessive reactive oxygen species are produced and exceed the compensative capacity of the organism. Oxidative stress leads to the destruction of periodontium, in a direct way(damaging the biomolecule) or an indirect way(enhancing the produce of inflammatory cytokine and destructive enzymes). Therefore, as the antagonist of the reactive oxygen species, antioxidants may be helpful to treat the chronic periodontitis. This paper reviewed relevant literatures about the destructive role of excessive reactive oxygen species and protective role of antioxidants in chronic periodontitis.

The antioxidant effects of pomegranate extract on local and remote organs in a mesenteric ischemia and reperfusion model

Objectives: We investigated whether pomegranate extract plays a protective antioxidant role against mesenteric ischemia–reperfusion injury (IR), which can lead to a systemic response and damage distant organs, such as the lung, liver, and kidney.Methods: Forty female Wistar–Albino rats were separated into four groups: laparotomy, laparotomy + PG, mesenteric IR, and mesenteric IR and pomegranate (IR + PG). In the laparotomy + PG and IR + PG groups, pomegranate (225 mg/kg) was given by oral gavage at the beginning of the study. Ischemia was induced for 30 minutes, and reperfusion was subsequently allowed for 60 minutes in the IR and IR + PG groups. The malondialdehyde (MDA) and total antioxidant activity (AOA) levels were evaluated in blood samples. Additionally, all tissues were removed for the measurement of AOA and total oxidant status as well as for subsequent histopathological evaluation. The oxidative stress index was calculated.Results: Histopathological changes in all organs were significantly higher in the IR group and significantly lower in the IR + PG group vs. the other groups. Serum MDA levels were significantly lower in the IR + PG group than in the IR group. No significant difference was found in AOA levels of the groups.Discussion: These data may explain the positive protective effects of pomegranate based on the histopathologic findings in ischemic conditions in an intestinal IR injury model.

CXCL12 protects pancreatic β-cells from oxidative stress by a Nrf2-induced increase in catalase expression and activity.

Due to intrinsically low levels of antioxidant enzyme expression and activity, insulin producing pancreatic β-cells are particularly susceptible to free radical attack. In diabetes mellitus, which is accompanied by high levels of oxidative stress, this feature of β-cells significantly contributes to their damage and dysfunction. In light of the documented pro-survival effect of chemokine C-X-C Ligand 12 (CXCL12) on pancreatic β-cells, we examined its potential role in antioxidant protection. We report that CXCL12 overexpression enhanced the resistance of rat insulinoma (Rin-5F) and primary pancreatic islet cells to hydrogen peroxide (H2O2). CXCL12 lowered the levels of DNA damage and lipid peroxidation and preserved insulin expression. This effect was mediated through an increase in catalase (CAT) activity. By activating downstream p38, Akt and ERK kinases, CXCL12 facilitated Nrf2 nuclear translocation and enhanced its binding to the CAT gene promoter, inducing constitutive CAT expression and activity that was essential for protecting β-cells from H2O2.

Antidiabetic properties of lyophilized extract of acorn (Quercus brantii Lindl.) on experimentally STZ-induced diabetic rats

Ethnopharmacological relevanceAcorn obtained from the Quercus brantii Lindl. (QB) tree has been used in Turkish folk medicine. Some studies have reported as an antioxidant, antimicrobial, anti-inflammatory, gastroprotective, antitumoural of QB properties previously. however, its effect on the management of type diabetic 2 and oxidative stress complications is still unexplored. The aims of our study were the evaluation of the protective effect and antioxidant role of acorn lyophilized seed plant extract against STZ-induced diabetic complications as oxidative stress, hepatotoxicity and nephropathy, lipidemia and serum biomarkers of diabetes (SBD). Materials and methodsIn-vivo studies were performed on STZ-induced diabetic rats Experiment was designed as I [Normal Control (NC)], II [Diabetes mellitus (DM)], III [DM+Acarbose (20mg/kg b.w) (DM+AC-20)], IV [DM+QB (100mg/kg b.w) (DM+QB-100)], V [DM+QB (250mg/kg b.w) (DM+QB-250)] and VI [DM+QB (500mg/kg b.w) (DM+QB-500)] groups. ResultsThis study showed that the biochemical analysis showed a considerable increase in the HRDB, DB, LP, MDA and fluctuated ADSC in the II group as compared to that of control group whereas, AC and the plant lyophilized seed plant extract supplementations diet restored the STZ-induced diabetic complications towards the control. α-glycosidase activity in DM group showed statistically significant increase with respect to control group in small intestine. Moreover, in accordance with the effects of seed extract; in diabetic rat groups to whom acorn seed extract and acarbose were given, the levels of almost all the concerned parameters were reached to the ones measured at control group. As a result, it was concluded that acorn seed extract had certain healing effects on many complications caused by diabetes.

Renoprotective effect of Mangifera indica polysaccharides and silymarin against cyclophosphamide toxicity in rats

The present study aims to evaluate the possible protective role of polysaccharides extracted from the Egyptian mango Mangifera indica L. (MPS) and silymarin against cyclophosphamide (CP) nephrotoxicity in male albino rats. Male rats were randomly divided into, control group (administered distilled water orally for 10days) and MPS (500, 1000mg/kg, p.o.) and/or silymarin (150mg/kg, p.o.) treated groups for 10days. In the last 5days of treatment rats were administered CP (150mg/kg, i.p). The MPS revealed significant prophylactic effect against kidney injury induced by CP as demonstrated by enhancement of the kidney function via decreasing serum creatinine, urea and uric acid. Treatment of rats with MPS extract and/or silymarin significantly increased the level of reduced glutathione (GSH) and superoxide dismutase (SOD) activity while decreased the level of total malondialdehyde (MDA) and glutathione-S-transferase (GST). Also, histopathological examinations confirmed the protective efficacy of MPS and/or silymarin against CP nephrotoxicity. In conclusion, the obtained results of the present study support the protective antioxidant role of MPS and/or silymarin against CP-induced kidney disorder in rats.

The association of serum thiol disulphide homeostasis with cardiovascular risk in obese adolescent polycystic ovary syndrome patients

Serum thiol disulphide homeostasis plays an important role in antioxidant protection and has been shown to be involved in the pathogenesis of cardiovascular diseases. We aimed to investigate the association of serum thiol disulphide homeostasis with cardiovascular risk factors in obese adolescent PCOS patients.

Enhanced tocopherol levels during early germination events in Chamaerops humilis var. humilis seeds

Most angiosperms accumulate vitamin E in the form of tocopherols in seeds, exerting a protective antioxidant role. However, several palm trees principally accumulate tocotrienols, rather than tocopherols, in seeds, as it occurs in other monocots. To unravel the protective role of either tocopherols or tocotrienols against lipid peroxidation during seed germination in Chamaerops humilis var. humilis; seed viability, natural and induced germination capacity, seed water content, malondialdehyde levels (as an indicator of the extent of lipid peroxidation) and vitamin E levels (including both tocopherols and tocotrienols) were examined at various germination phases in a simulated, natural seed bank. At the very early stages of germination (operculum removal), malondialdehyde levels increased 2.8-fold, to decrease later up to 74%, thus indicating a transient lipid peroxidation at early stages of germination. Tocopherol levels were absent in quiescent seeds and did not increase during operculum removal, but increased later presumably dampening malondialdehyde accumulation. Thereafter, tocopherols continued increasing, while lipid peroxidation levels decreased. By contrast, tocotrienols levels remained constant or even decreased as germination progressed, showing no correlation with lipid peroxidation levels. We hypothesize that despite their high tocotrienol content, seeds synthesize tocopherols during germination to protect lipids from peroxidation events.