Alleviated Lipid Peroxidation Research Articles

Estrogen inhibits lipid peroxidation after hypoxic-ischemic brain damage in neonatal rats.

Sprague-Dawley neonatal rats within 7 days after birth were used in this study. The left common carotid artery was occluded and rats were housed in an 8% O2 environment for 2 hours to establish a hypoxic-ischemic brain damage model. 17β-estradiol (1 × 10-5 M) was injected into the rat abdominal cavity after the model was successfully established. The left hemisphere was obtained at 12, 24, 48, 72 hours after operation. Results showed that malondialdehyde content in the left brain of neonatal rats gradually increased as modeling time prolonged, while malondialdehyde content of 17β-estrodial-treated rats significantly declined by 24 hours, reached lowest levels at 48 hours, and then peaked at 72 hours after injury. Nicotinamide-adenine dinucleotide phosphate histochemical staining showed the nitric oxide synthase-positive cells and fibers dyed blue/violet and were mainly distributed in the cortex, hippocampus and medial septal nuclei. The number of nitric oxide synthase-positive cells peaked at 48 hours and significantly decreased after 17β-estrodial treatment. Our experimental findings indicate that estrogen plays a protective role following hypoxic-ischemic brain damage by alleviating lipid peroxidation through reducing the expression of nitric oxide synthase and the content of malondialdehyde.

Effects of pyrene on antioxidant systems and lipid peroxidation level in mangrove plants, Bruguiera gymnorrhiza

The effects of polycyclic aromatic hydrocarbon (PAH) (pyrene) on superoxide dismutase (SOD), ascorbate peroxidase (APX), catalase, peroxidase, malondialdehyde (MDA) and proline were studied in leaves, stems and roots of Bruguiera gymnorrhiza. The results showed that the responses of enzymatic and non-enzymatic antioxidants varied significantly among the three tissues studied. The activities of antioxidant enzymes in PAH-treated stems and roots fluctuated in different stress levels compared to the controls, while the antioxidant enzymes such as SOD, APX in leaves increased when stressed by PAH with a significant positive relation between PAH and leaf SOD or APX activity. Low PAH treatments could also stimulate proline in leaves and stems. MDA content was obviously accumulated in stems and roots under PAH stress while decreased in leaves, indicating that the increased antioxidant enzymes in leaves may partly alleviate lipid peroxidation. For pollution monitoring purpose, SOD and APX in leaves may be potential biomarkers of PAH pollution in intertidal estuaries.

Diammonium Glycyrrhizinate Upregulates PGC-1α and Protects against Aβ1–42-Induced Neurotoxicity

Mitochondrial dysfunction is a hallmark of beta-amyloid (Aβ)-induced neurotoxicity in Alzheimer's disease (AD), and is considered an early event in AD pathology. Diammonium glycyrrhizinate (DG), the salt form of Glycyrrhizin, is known for its anti-inflammatory effects, resistance to biologic oxidation and membranous protection. In the present study, the neuroprotective effects of DG on Aβ1–42-induced toxicity and its potential mechanisms in primary cortical neurons were investigated. Exposure of neurons to 2 µM Aβ1–42 resulted in significant viability loss and cell apoptosis. Accumulation of reactive oxygen species (ROS), decreased mitochondrial membrane potential, and activation of caspase-9 and caspase-3 were also observed after Aβ1–42 exposure. All these effects induced by Aβ1–42 were markedly reversed by DG treatment. In addition, DG could alleviate lipid peroxidation and partially restore the mitochondrial function in Aβ1–42-induced AD mice. DG also significantly increased the PGC-1α expression in vivo and in vitro, while knocking down PGC-1α partially blocked the protective effects, which indicated that PGC-1α contributed to the neuroprotective effects of DG. Furthermore, DG significantly decreased the escape latency and search distance and increased the target crossing times of Aβ1–42-induced AD mice in the Morris water maze test. Therefore, these results demonstrated that DG could attenuate Aβ1–42-induced neuronal injury by preventing mitochondrial dysfunction and oxidative stress and improved cognitive impairment in Aβ1–42-induced AD mice, indicating that DG exerted potential beneficial effects on AD.

Chinese herbal medicine in the treatment of nonalcoholic fatty liver disease

Chinese herbal medicine has developed new therapies for nonalcoholic fatty liver disease (NAFLD) based on its unique theory system and substantial herb remedies. In this review, 21 traditional Chinese herbs were introduced for their potential benefit in the treatment of NAFLD. Majority of them are evaluated by experimental studies and few by multicenter clinical trials. Herbal monomers as berberine and resveratrol, extracts from Polygonum hypoleucum Ohwi, and Artemisia sacrorum Ledeb., and formulae including Yinchenhao Decoction (, YCHD), Qushi Huayu Decoction (, QSHYD), and Danning Tablet () were discussed in detail on their therapeutic potentials. Most of these herbal medicines were proved to improve biochemical and histological changes of NAFLD both in vitro and in vivo. Also, their therapeutic activities were associated with inhibiting lipid accumulation through adenosine monophosphate-activated protein kinase activation or upregulating low-density lipoprotein receptor (LDLR) expression, alleviating lipid peroxidation, and reducing the production of inflammatory cytokines. Although the efficacy and safety of these herbal medicines needed to be evaluated in multicenter large-scale clinical trials, Chinese medicine is promising and effective for preventing and treating NAFLD disease.

Effects of short-term anoxia treatment on browning of fresh-cut Chinese water chestnut in relation to antioxidant activity

The effects of short-term anoxia pre-treatment on browning of fresh-cut Chinese water chestnut (CWC), stored at 4°C, in relation to antioxidant activity were investigated. CWC slices were exposed to pure N2 for 4h and then stored at 4°C for 18d. Anoxia significantly inhibited browning of CWC slices during storage, accompanied by lower contents of malondialdehyde, H2O2, and lipoxygenase activity. Furthermore, anoxia induced the activities of superoxide dismutase and ascorbate peroxidase, which could benefit scavenging reactive oxygen species and alleviating lipid peroxidation. In addition, better maintenance of reducing power and free-radical-scavenging activities against α,α-diphenyl-β-picrylhydrazy (DPPH), superoxide anions and hydroxyl was observed in N2-treated CWC slices, with higher phenolic compounds and ascorbic acid contents. Collectively, these finds suggest that N2 pre-treatment enhanced enzymatic and non-enzymatic antioxidant activity in CWC slices, and thereby contributed to alleviating lipid peroxidation and maintenance of storage quality.

Gibberellin A 3 pretreatment increased antioxidative capacity of cucumber radicles and hypocotyls under suboptimal temperature

The effects of GA3 on the growth and antioxidant capacity of cucumber hypocotyls and radicles under sub-optimal temperature were investigated. The elongation of hypocotyls and radicles was significantly promoted by GA3 treatment under sub-optimal temperature, and the effects greatly depended on GA3 concentrations. In the previous reported investigation, there is not much information on the role of GA3 in modulating reactive oxygen species (ROS) under stress conditions, the present study indicated that GA3 treatment could decrease excess accumulation of ROS and alleviate lipid peroxidation which was induced by sub-optimal temperature in cucumber hypocotyls and radicles, the alleviating effects were highly correlated with the increasing activities of antioxidant enzymes including superoxide dismutase (SOD), catalase (CAT), ascorbate peroxidase (APX) and guaiacol peroxidase (GPX) as well as antioxidative activity indicated as α,α-diphenyl-β-picryllhydrazyl (DPPH) scavenging activity, hydroxyl radical (∙HO) scavenging activity and ferrous ion chelating activity. Furthermore, the increasing antioxidative activity was positively related with amylase activity in cucumber cotyledons, suggesting that the distribution of carbohydrate from cotyledons to hypocotyls and radicles might be responsible for higher antioxidant activity induced by GA3. Key words: Cucumis sativus L., gibberellin, suboptimal temperature, hypocotyls, radicles, antioxidative activity.

Protective effects of salecan against carbon tetrachloride‐induced acute liver injury in mice

Carbon tetrachloride (CCl₄) is a well-established model for screening hepato-protective drugs. The aim of the present study was to evaluate the potential protective effects of a novel soluble β-glucan salecan on acute liver injury induced by CCl₄ in mice and to further explore the underlying mechanisms. Mice were given salecan (40 mg kg⁻¹) or phosphate-buffered saline for 3 days prior to treatment with a single intraperitoneal dose of CCl₄ (1 ml kg⁻¹ body weight). Animals were sacrificed at 0, 12, 24, 48, 72 and 96 h post-injection of CCl₄. Serum liver enzyme levels, histology, lipid peroxidation, glutathione (GSH) content, expression of antioxidant enzymes and hepatocyte proliferation were subsequently evaluated. The serum levels of hepatic enzyme markers were markedly reduced in the salecan pretreatment group compared with the control group. Histopathological examination of the livers revealed that hepatocellular degeneration and necrosis were significantly attenuated at an early stage during CCl₄ intoxication and liver recovery was markedly accelerated at a later stage in salecan pre-administered mice. Furthermore, salecan administration remarkably alleviated lipid peroxidation and restored GSH depletion. Meanwhile, the expression of antioxidant genes was significantly elevated in the salecan-treated group. Interestingly, the administration of salecan remarkably enhanced hepatocyte proliferation in the recovery phase after CCl₄ injection. Taken together, these results demonstrated that salecan exhibits a protective action on acute hepatic injury induced by CCl₄ through attenuating oxidative stress and accelerating hepatocyte regeneration.

Induction of heme oxygenase-1 with β-CD-hemin complex mitigates cadmium-induced oxidative damage in the roots of Medicago sativa

Using pharmacological and biochemical approaches, the functional roles of heme oxygenase-1 (HO-1) induction in cadmium (Cd)-stressed alfalfa (Medicago sativa) seedling roots caused by a metal-organic complex (β-cyclodextrin-hemin, β-CD-hemin, CDH) and the well-known HO-1 inducer hemin, were investigated and compared. Cd-stressed seedling roots exhibited severe oxidative damage, whereas up-regulation of HO-1 by CDH and hemin pretreatment prevented this toxic response, as evidenced by the decrease of lipid peroxidation as well as the alleviation of growth inhibition and Cd accumulation. Reestablishment of glutathione (GSH) and reactive oxygen species (ROS) homeostasis were observed. Upon Cd stress, 0.01 μM CDH and 10 μM hemin pretreatment alleviated lipid peroxidation to almost the same extent and the CDH was highly potent. The modulation of the transcripts and total activities of ascorbate peroxidase (APX) and superoxide dismutase (SOD) were regulated by CDH and hemin, respectively. We also noticed that the potent HO-1 inhibitor zinc protoporphyrin IX (ZnPP) significantly reversed the CDH-driven cytoprotective roles. Additionally, β-CD was found to be ineffective in the alleviation of lipid peroxidation. Taken together, the data suggested that HO-1 induction mediated by CDH provides critical protection against Cd-induced oxidative damage and toxicity partly by lowering the Cd accumulation.

Preconditioning effect of cobalt chloride supplementation on hypoxia induced oxidative stress in male albino rats

The present study was designed to understand the preconditioning effect of cobalt chloride (CoCl2), a known hypoxia mimetic, on promoting acclimation to hypobaric hypoxia in male Sprague Dawley rats. Rats were exposed to hypoxia (7619 m) for 1,2,3 and 5 days with and without prior supplementation of cobalt chloride (12.5 mg cobalt/kg bw for 7 days). After hypoxic exposure, rats were sacrificed and various oxidative stress parameters were studied in the blood/plasma. Further protein expression studies were carried out in the heart. The results showed significant increase in lipid peroxidation and protein oxidation and decrease in reduced glutathione (GSH) in the plasma of animals exposed to hypoxia without cobalt supplementation as compared to control group. Prior administration of cobalt appreciably attenuated oxidation of lipids and proteins. There was increase in antioxidant enzyme superoxide dismutase (SOD) on exposure to hypoxia, whereas SOD levels were maintained in cobalt supplemented groups. Expressions of hypoxia inducible factor (HIF-1), hemoxygenase (HO-1) and metallothionein (MT) were higher in the cobalt supplemented group as compared to control group. Therefore, cobalt preconditioning appears to decrease oxidative stress by alleviating lipid peroxidation and maintaining higher HO-1 and MT levels leading to faster acclimation to hypobaric hypoxia.

The effects of moderately oxidised dietary oil with or without vitamin E supplementation on performance, nutrient digestibility, some blood traits, lipid peroxidation and antioxidant defence of male broilers

The experiment was conducted to determine the effects of dietary supplementation of oxidised oil with or without vitamin E on performance, nutrient digestibility, some blood traits, lipid peroxidation and antioxidant defence system of male broilers. The supplementation of oxidised oil with or without vitamin E to the grower diets did not significantly affect performance, the pH and viscosity values of excreta and nutrient digestibilities in male broilers. Oxidised oil supplementation slightly increased plasma triglyceride and cholesterol concentrations but did not alter plasma glucose concentration. Although malondialdehyde (MDA) and nitric oxide concentrations tended to be higher in the oxidised oil group, these increases were not significant. Birds fed the diet containing oxidised oil had significantly lower superoxide dismutase (SOD) activity. However, no differences were observed in glutathione peroxidase (GSH-Px) activity and uric acid concentrations of broilers fed oxidised oil as compared to the control group. Dietary vitamin E supplementation decreased MDA concentration whereas increasing SOD activity, suggesting that vitamin E supplementation reduced susceptibility to lipid peroxidation. The results showed that a milder oxidative stress occurred by supplementation of moderately oxidised oil to the diet of broilers and vitamin E supplementation had been helpful in alleviating lipid peroxidation.

Reversal of Cardiac Iron Loading and Dysfunction in Thalassemic Mice by Curcuminoids

Non-transferrin bound iron (NTBI) is found in plasma of β-thalassemia patients and causes oxidative tissue damage. Cardiac siderosis and complications are the secondary cause of death in β-thalassemia major patients. Desferrioxamine (DFO), deferiprone (DFP) and deferasirox (DFX) are promising chelators used to get negative iron balance and improve life quality. DFP has been shown to remove myocardial iron effectively. Curcuminoids (CUR) can chelate plasma NTBI, inhibit lipid peroxidation and alleviate cardiac autonomic imbalance. Effects of CUR on cardiac iron deposition and function were investigated in iron-loaded mice. Wild type ((mu)β(+/+) WT) and heterozygous β-knockout ((mu)β(th-3/+) BKO) mice (C57BL/6) were fed with ferrocene-supplemented diet (Fe diet) and coincidently intervened with CUR and DFP for 2 months. Concentrations of plasma NTBI and malondialdehyde (MDA) were measured using HPLC techniques. Heart iron concentration was determined based on atomic absorption spectrophotometry and Perl's staining methods. Short-term electrocardiogram (ECG) was recorded with AD Instruments Power Lab, and heart rate variability (HRV) was evaluated using MATLAB 7.0 program. Fe diet increased levels of NTBI and MDA in plasma, nonheme iron and iron deposit in heart tissue significantly, and depressed the HRV, which the levels were higher in the BKO mice than the WT mice. CUR and DFP treatments lowered plasma NTBI as well as MDA concentrations (p <0.05), heart iron accumulation effectively, and also improved the HRV in the treated mice. The results imply that CUR would be effective in decreasing plasma NTBI and myocardial iron, alleviating lipid peroxidation and improving cardiac function in iron-loaded thalassemic mice.

Effect of pure oxygen atmosphere on antioxidant enzyme and antioxidant activity of harvested litchi fruit during storage

The effects of pure oxygen on pericarp browning, reactive oxygen species (ROS) metabolism, antioxidant enzyme and antioxidant activity of harvested litchi fruit were investigated. Application of pure oxygen significantly prevented pericarp browning and delayed the increase in membrane permeability of litchi fruit during storage. Litchi fruit exposed to pure oxygen showed a lower level of lipid peroxides, compared to control fruit, with the delay in the increases of both H2O2 content and superoxide production rate. Furthermore, it was found that the treatment with pure oxygen induced the activities of superoxide dismutase (SOD), ascorbated peroxidase (APX) and catalase (CAT), which could be beneficial in scavenging of H2O2 and superoxide and alleviating lipid peroxidation. In addition, antioxidant ability (reducing power and free-radical scavenging activity against DPPH radical, superoxide anions and hydroxyl radical) of methanol extracts from litchi fruit pericarp declined gradually, with decreasing contents of anthocyanins and phenolic compounds, as storage time of the fruit progressed. There was a linear relationship between the contents of either anthocyanins or phenolic compounds and antioxidant ability or free radical scavenging activity. Treatment with pure oxygen markedly increased antioxidant ability, which was related to higher levels of anthocyanins and phenolic compounds, compared with those of control fruit. It is suggested that enhanced antioxidant activity and antioxidant enzyme induced by pure oxygen may contribute to alleviating lipid peroxidation and maintenance of membrane integrity, which reduced decompartmentation of enzymes and substrates, resulting in enzymatic browning.

E0375 Long-term enhanced external counterpulsation repairs platelet membrane fluidity and alleviates lipid peroxidation in patients with stable angina pectoris

ObjectiveTo explore the effect of long-term enhanced external counterpulsation (EECP) on platelet membrane fluidity (PMF) and lipid peroxidation in patients with stable angina pectoris.MethodsLong-term EECP was performed on 30 patients...

Nitric oxide alleviates lipid peroxidation induced by osmotic stress during senescence of detached leaves of Malus hupehensis Rehd.

SummaryThe protective effect of nitric oxide (NO) against membrane lipid peroxidation induced by polyethylene glycol (PEG) osmotic stress was investigated in relation to the metabolism of reactive oxygen species (ROS) and proline accumulation during the senescence of detached leaves of Malus hupehensis Rehd. in the dark. Membrane lipid peroxidation was determined by measuring the increase in malondialdehyde (MDA) content. PEG-induced osmotic stress resulted in a marked increase in the contents of MDA and proline, as well as the activities of superoxide dismutase (SOD), peroxidase (POD), catalase (CAT), and ascorbate peroxidase (APX). Sodium nitroprusside (SNP), a donor of NO, prevented the PEG-induced increase in MDA content, but, with an increase in proline content as well as increases in the activities of CAT and APX, and in the levels of superoxide anions and hydrogen peroxide (H2O2).Treatment with SNP alone also alleviated lipid peroxidation, compared to water-treated leaves, with an increased proline content and SOD activity, but decreased the levels of superoxide anions and H2O2. We concluded that NO was effective at alleviating membrane lipid peroxidation induced by osmotic stress (PEG) during the senescence of detached leaves of M. hupehensis Rehd., suggesting a similar role for NO as in the regulation of ROS-dependent lipid peroxidation in animals. The relationships between NO-mediated regulation of lipid peroxidation and ROS metabolism, as well as proline accumulation, are discussed.

D-β-Hydroxybutyrate Prevents MPP+-Induced Neurotoxicity in PC12 Cells

Numerous studies show that D-beta-Hydroxybutyrate (DbetaHB) is neuroprotective. The present study was to explore the neuroprotective effects of DbetaHB against the cell death and apoptosis induced by 1-methyl-4-phenylpyridinium ion (MPP+) in PC12 cells. PC12 cells were pretreated with DbetaHB and followed by MPP+ exposure. The cell viability was determined by MTT assay. The morphological characteristics of apoptosis was observed by Acridine Orange (AO) staining and apoptotic rates were measured by flow cytometer. The product of lipid peroxidation, malondialdehyde (MDA), was measured using thiobarbituric acid method. The mitochondrial membrane potential (MMP), intracellular ROS and total glutathione were detected by microplate reader. In PC12 cells, pretreatment with DbetaHB significantly reduced MPP+-induced the decrease of cell viability. AO staining and flow cytometric analysis found DbetaHB inhibited MPP+-induced apoptosis. The measurement of MDA formation showed that DbetaHB alleviated lipid peroxidation induced by MPP+. The loss of MMP induced by MPP+ was preventive by DbetaHB. The changes of intracellular ROS and total glutathione induced by MPP+ were reversed by DbetaHB. DbetaHB protected PC12 cells against MPP+-induced death and apoptosis.

Calcium protects Trifolium repens L. seedlings against cadmium stress

The effect of calcium (Ca(2+)) on Trifolium repens L. seedlings subjected to cadmium (Cd(2+)) stress was studied by investigating plant growth and changes in activity of antioxidative enzymes. Physiological analysis was carried out on seedlings cultured for 2 weeks on half-strength Hoagland medium with Cd(2+) concentrations of 0, 400 and 600 microM, and on corresponding medium supplied with CaCl(2) (5 mM). Exposure to increasing Cd(2+) reduced the fresh weight of the upper part (stems + leaves) of the seedlings more strongly than that of the root system. In both parts of T. repens seedlings H(2)O(2) level and lipid peroxidation increased. In the upper part, Cd(2+) exposure led to a significant decrease in the activity of superoxide dismutase, catalase and glutathione peroxidase and an increase in ascorbate peroxidase activity. In contrast, the roots showed an increase in the activity of antioxidative enzymes under Cd(2+) stress. Ca(2+) addition to medium reduced the Cd(2+) accumulation, and considerably reversed the Cd(2+)-induced decrease in fresh mass as well as the changes in lipid peroxidation in the both parts of T. repens seedlings. Ca(2+) application diminished the Cd(2+) effect on the activity of antioxidative enzymes in the upper part, even though it did not significantly affect these enzymes in the roots. So the possible mechanisms for the action of Ca(2+) in Cd(2+) stress were considered to reduce Cd(2+) accumulation, alleviate lipid peroxidation and promote activity of antioxidative enzymes.

Effect of Dietary Grape Pomace on Lipid Oxidation and Related Enzyme Activities in Rats Fed High Fat Diet

The present study was conducted to investigate the effect of dietary supplementation of grape pomace on lipid peroxidation and related enzyme activities of rats fed high fat diet. Male Sprague-Dawley rats weighing about 90 g were assigned to 4 experimental groups of 8 rats on the basis of their body weight. The high fat diet contained additional 15% lard to AIN 93-based diet. Rats were fed experimental diets containing 5% grape pomace for 4 weeks. Dietary supplementation of grape pomace reduced serum concentration of lipid peroxide in rats fed high fat diet. Hepatic concentration of lipid peroxide tended to be lower by feeding grape pomace. Hepatic total glutathione content and GSH/GSSG ratio were increased by grape pomace feeding in normal or high fat diet groups. Hepatic superoxide dismutase activity of grape pomace group with high fat diet was induced significantly compared with high fat diet group without grape pomace. Hepatic catalase activity of high fat fed rats was induced by feeding grape pomace. Grape pomace diet increased glutathione-S-transferase and glutathione peroxidase activities in rat liver fed high fat. Hepatic glucose-6-phosphatase activity was not affected by dietary supplementation of grape pomace in rats fed high fat. These results suggest that dietary supplementation of grape pomace may alleviate lipid peroxidation through antioxidant effect in rats fed high fat.

Transgene expression of human PON1 Q in mice protected the liver against CCl4‐induced injury

Oxidative stress, often in association with decreased antioxidant defenses, plays a pathogenetic role in both initiation and progression of liver injuries, leading to almost all clinical and experimental conditions of chronic liver diseases. Human paraoxonase 1 (hPON1) is a liver-synthesized enzyme possessing antioxidant properties. Here, we investigate the effects of transgene-expressed hPON1 Q on alleviating lipid peroxidation and preventing liver injury in a mouse model. The hPON1 Q gene was cloned into pcDNA3.0 plasmid and electro-transferred into mouse skeletal muscle. After CCl4 had been administrated to induce liver injury, mice were monitored for serum levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST) and malonyldialdehyde (MDA). The extent of CCl4-induced liver injury was also analyzed through histopathological observations. After gene delivery, hPON1 mRNA expression was detected in mouse muscle and serum PON1 activity was 1.5 times higher than that of the control counterpart. In the PON1 Q gene transferred mice, protection against CCl4-induced liver injury was reflected by significantly decreased serum ALT, AST and MDA levels compared to those in control mice (P < 0.01). Histological observations also revealed that hepatocyte necrosis, hemorrhage, vacuolar change and hydropic degeneration were apparent in control mice after CCl4 administration. In contrast, the damage was significantly prevented (P < 0.01) in the hPON1 Q transferred mice. Intramuscular electro-transfer of the hPON1 Q gene led to efficient expression of hPON1 in mice. Elevated levels of PON1, by virtue of its potency to alleviate oxidative stress, could protect mice from suffering CCl4-induced liver damage.

Photosynthesis of Rehmannia glutinosa subjected to drought stress is enhanced by choline chloride through alleviating lipid peroxidation and increasing proline accumulation

Rehmannia glutinosa seedlings were pretreated with choline chloride (CC) in concentrations of 0, 0.7, 2.1 and 3.5 mM, and then subjected to drought and rewatering treatment to study the effects of CC on the generation of reactive oxygen species (O 2 − , H2O2), lipid peroxidation, proline accumulation, water status and photosynthesis. The results showed that pretreatment with CC alleviated the inhibition of SOD and APX activity caused by drought stress, and therefore, the rate of O 2 − production and H2O2 concentration were reduced and lipid peroxidation decreased in pretreated plants. CC pretreatment also accelerated accumulation of proline, maintained higher Ψw and RWC, deferred leaf water loss during drought stress and retarded the drop in proline concentration after rewatering. Consequently, drought-induced decreases in Fm/F0, Fv/Fm, ΦPS2, qP, and A and increase in qNP were inhibited and the recovery of photosynthesis after rewatering was quicker in pretreated plants. Although differences in Fv/Fm, ΦPS2 and qP between treatments were not significant, there was a general trend that the effects of CC increased with the rise of its concentrations. The data suggested that 2.1 mM of CC be suitable for alleviating lipid peroxidation, promoting proline accumulation, retarding leaf water loss and improving photosynthesis of R. glutinosa seedlings under drought stress.

Neuroprotective Effects of 17β-Estradiol and Nonfeminizing Estrogens against H2O2Toxicity in Human Neuroblastoma SK-N-SH Cells

Neuroprotective effects of estrogens have been shown in various in vitro and in vivo models, but the mechanisms underlying protection by estrogen are not clear. Mounting evidence suggests antioxidant effects contribute to the neuroprotective effects of estrogens. In the present study, we assessed the protective effects of estrogens against H2O2-induced toxicity in human neuroblastoma cells and the potential mechanisms involved in this protection. We demonstrate that 17beta-estradiol (17beta-E2) increases cell survival against H2O2 toxicity in human neuroblastoma cells. 17beta-E2 effectively reduced lipid peroxidation induced by 5-min H2O2 exposure. Furthermore, 17beta-E2 exerts the protective effects by maintaining intracellular Ca2+ homeostasis, attenuating ATP depletion, ablating mitochondrial calcium overloading, and preserving mitochondrial membrane potential. Two nonfeminizing estrogens, 17alpha- and ent-estradiol, were as effective as 17beta-E2 in increasing cell survival, alleviating lipid peroxidation, preserving mitochondrial function, and maintaining intracellular glutathione levels and Ca2+ homeostasis against H2O2 insult. Moreover, the estrogen receptor antagonist fulvestrant (ICI 182,780) did not block effects of 17beta-E2, but increased cell survival and blunted intracellular Ca2+ increases. However, these estrogens failed to reduce cytosolic reactive oxygen species, even at concentrations as high as 10 microM. In conclusion, estrogens exert protective effects against oxidative stress by inhibiting lipid peroxidation and subsequently preserving Ca2+ homeostasis, mitochondrial membrane potential, and ATP levels.