Identification, functional characterization and developmental regulation of sesquiterpene synthases from sunflower capitate glandular trichomes

Background

Besides being essential for plant structure and metabolism, soluble carbohydrates play important roles in stress responses. Sucrose has been shown to confer to Arabidopsis seedlings a high level of tolerance to the herbicide atrazine, which causes reactive oxygen species (ROS) production and oxidative stress. The effects of atrazine and of exogenous sucrose on ROS patterns and ROS-scavenging systems were studied. Simultaneous analysis of ROS contents, expression of ROS-related genes and activities of ROS-scavenging enzymes gave an integrative view of physiological state and detoxifying potential under conditions of sensitivity or tolerance.

Results

Toxicity of atrazine could be related to inefficient activation of singlet oxygen (¹O₂) quenching pathways leading to ¹O₂ accumulation. Atrazine treatment also increased hydrogen peroxide (H₂O₂) content, while reducing gene expressions and enzymatic activities related to two major H₂O₂-detoxification pathways. Conversely, sucrose-protected plantlets in the presence of atrazine exhibited efficient ¹O₂ quenching, low ¹O₂ accumulation and active H₂O₂-detoxifying systems.

Conclusion

In conclusion, sucrose protection was in part due to activation of specific ROS scavenging systems with consequent reduction of oxidative damages. Importance of ROS combination and potential interferences of sucrose, xenobiotic and ROS signalling pathways are discussed.     

Increased prevalence of tumor-infiltrating regulatory T cells is closely related to their lower sensitivity to H2O2-induced apoptosis in gastric and esophageal cancer

Purpose and experimental design

Although an increase in regulatory T cells (Tregs) is observed in tumor microenvironments, the underlying mechanism is not fully clarified. Since it was suggested that Tregs showed a lower sensitivity toward oxidative stress in comparison with conventional T cells, in the present study, we investigated the H₂O₂ production and apoptosis of Tregs in gastric and esophageal cancer tissues, employing flow cytometric analysis using fresh samples (n = 93) and immunohistochemical analysis (n = 203).

Results

The increased tumor-infiltrating Tregs coexisted with elevated H₂O₂ production according to disease progression. The grade of apoptosis in Tregs was less pronounced than that in conventional T cells, and there was a positive correlation between H₂O₂ production and the grade of apoptosis in conventional T cells, while there was no correlation between H₂O₂ production and the grade of apoptosis in Tregs. Moreover, Tregs were less sensitive to H₂O₂-induced apoptosis compared with conventional T cells in vitro.

Conclusions

We have demonstrated that the increased prevalence of tumor-infiltrating Tregs closely related to their lower sensitivity to H₂O₂-induced apoptosis.     

Heme oxygenase is involved in H2O2-induced lateral root formation in apocynin-treated rice

Key message

Apocynin is a natural organic compound structurally related to vanillin. We demonstrated that hydrogen peroxide and heme oxygenase participated in apocynin-induced lateral root formation in rice.

Abstract

Apocynin, also known as acetovanillone, is a natural organic compound structurally related to vanillin. Information concerning the effect of apocynin on plants is limited. In this study, we examined the effect of apocynin on lateral root (LR) formation in rice. Treatment with apocynin induced LR formation and increased H₂O₂ production, but had no effect on nitric oxide production. Diphenyleneiodonium chloride, an inhibitor of H₂O₂ generating NADPH oxidase, was effective in reducing apocynin-induced H₂O₂ production and LR formation. Apocynin treatment also increased superoxide dismutase activity and decreased catalase activity. H₂O₂ application was able to increase the number of LRs. Moreover, H₂O₂ production caused by H₂O₂ and apocynin was localized in the root area corresponding to the LR emergence. Treatment with H₂O₂ and apocynin also increased heme oxygenase (HO) activity and induced OsHO1 mRNA expression. Lateral root formation and HO activity induced by H₂O₂ and apocynin were reduced by Zn protoporphyrin IX (the specific inhibitor of HO). Our data suggest that both H₂O₂ and HO are required for apocynin-induced LR formation in rice.     

Generation and characterization of transgenic mice expressing mitochondrial targeted red fluorescent protein selectively in neurons: modeling mitochondriopathy in excitotoxicity and amyotrophic lateral sclerosis

Background

Accumulation of aberrant proteins to form Lewy bodies (LBs) is a hallmark of Parkinson's disease (PD). Ubiquitination-mediated degradation of aberrant, misfolded proteins is critical for maintaining normal cell function. Emerging evidence suggests that oxidative/nitrosative stress compromises the precisely-regulated network of ubiquitination in PD, particularly affecting parkin E3 ligase activity, and contributes to the accumulation of toxic proteins and neuronal cell death.

Results

To gain insight into the mechanism whereby cell stress alters parkin-mediated ubiquitination and LB formation, we investigated the effect of oxidative stress. We found significant increases in oxidation (sulfonation) and subsequent aggregation of parkin in SH-SY5Y cells exposed to the mitochondrial complex I inhibitor 1-methyl-4-phenlypyridinium (MPP ⁺ ), representing an in vitro cell-based PD model. Exposure of these cells to direct oxidation via pathological doses of H₂O₂ induced a vicious cycle of increased followed by decreased parkin E3 ligase activity, similar to that previously reported following S-nitrosylation of parkin. Pre-incubation with catalase attenuated H₂O₂ accumulation, parkin sulfonation, and parkin aggregation. Mass spectrometry (MS) analysis revealed that H₂O₂ reacted with specific cysteine residues of parkin, resulting in sulfination/sulfonation in regions of the protein similar to those affected by parkin mutations in hereditary forms of PD. Immunohistochemistry or gel electrophoresis revealed an increase in aggregated parkin in rats and primates exposed to mitochondrial complex I inhibitors, as well as in postmortem human brain from patients with PD with LBs.

Conclusion

These findings show that oxidative stress alters parkin E3 ligase activity, leading to dysfunction of the ubiquitin-proteasome system and potentially contributing to LB formation.     

Glucose-6-phosphate dehydrogenase plays a pivotal role in tolerance to drought stress in soybean roots

Key message

Two soybean cultivars showed markedly different drought tolerance. G6PDH plays a central role in the process of H ₂ O ₂ regulated GR, DHAR, and MDHAR activities to maintain GSH and Asc levels.

Abstract

Glucose-6-phosphate dehydrogenase (G6PDH) plays a pivotal role in plant resistance to environmental stresses. In this study, we investigated the role of G6PDH in modulating redox homeostasis under drought stress induced by polyethylene glycol 6000 (PEG6000) in two soybean cultivars JINDOU21 (JD-21) and WDD00172 (WDD-172). The G6PDH activity markedly increased and reached a maximum at 96 h in JD-21 and 72 h in WDD-172 during PEG6000 treatments, respectively. Glucosamine (Glucm, a G6PDH inhibitor) obviously inhibited G6PDH activity in both soybeans under PEG6000 treatments. After PEG6000 treatment, JD-21 showed higher tolerance than WDD-172 not only in higher activities of superoxide dismutase (SOD), catalase (CAT), peroxidase (POD), glutathione reductase (GR), dehydroascorbate reductase (DHAR), and monodehydroascorbate reductase (MDHAR), but also in higher content of glutathione (GSH) and ascorbate (Asc). And we found that hydrogen peroxide (H₂O₂) regulated the cell length in root elongation zone. Diphenylene iodonium (DPI, a plasma membrane NADPH oxidase inhibitor) counteracted the PEG6000-induced H₂O₂ accumulation and decreased the activities of GR, DHAR, and MDHAR as well as GSH and Asc content. Furthermore, exogenous application of H₂O₂ increased the GR, DHAR, and MDHAR activities that were decreased by Glucm under drought stress. Western blot analysis showed that the G6PDH expression was stimulated by PEG6000 and buthionine sulfoximine (BSO, glutathione biosynthesis inhibitor), and blocked by Glucm, DPI and N-acetyl-l-cysteine (NAC, GSH precursor) in both cultivars. Taken together, our evidence indicates that G6PDH plays a central role in the process of H₂O₂ regulated GR, DHAR, and MDHAR activities to maintain GSH and Asc levels.     

Vasoactive intestinal peptide reduces oxidative stress in pancreatic acinar cells through the inhibition of NADPH oxidase

Vasoactive intestinal peptide (VIP) attenuates experimental acute pancreatitis (AP) by inhibition of cytokine production from inflammatory cells. It has been suggested that reactive oxygen species (ROS) as well as cytokines play pivotal roles in the early pathophysiology of AP. This study aimed to clarify the effect of VIP on the oxidative condition in pancreas, especially pancreatic acinar cells (acini). Hydrogen peroxide (H₂O₂)-induced intracellular ROS, assessed with CM-H₂DCFDA, increased time- and dose-dependently in acini isolated from rats. Cell viability due to ROS-induced cellular damage, evaluated by MTS assay, was decreased with ≥100 μmol/L H₂O₂. VIP significantly inhibited ROS production from acini and increased cell viability in a dose-dependent manner. Expression of antioxidants including catalase, glutathione reductase, superoxide dismutase (SOD) 1 and glutathione peroxidase was not altered by VIP except for SOD2. Furthermore, Nox1 and Nox2, major components of NADPH oxidase, were expressed in pancreatic acini, and significantly increased after H₂O₂ treatment. Also, NADPH oxidase activity was provoked by H₂O₂. VIP decreased NADPH oxidase activity, which was abolished by PKA inhibitor H89. These results suggested that VIP affected the mechanism of ROS production including NADPH oxidase through induction of a cAMP/PKA pathway. In conclusion, VIP reduces oxidative stress in acini through the inhibition of NADPH oxidase. These results combined with findings of our previous study suggest that VIP exerts its protective effect in pancreatic damage, not only through an inhibition of cytokine production, but also through a reduction of the injury caused by oxidative stress.     

Response characteristics of seed germination and seedling growth of Acorus tatarinowii under diesel stress

Aims

Responses of typical wetland plant Acorus tatarinowii to diesel stress were investigated to provide basis of ecological monitoring system and phytoremediation for diesel-contaminated wetland.

Methods

Greenhouse experiments were established to determine the germinability of seedlings, hydrogen peroxide in leaves, and DNA damage in roots exposed to a range of potentially phytotoxic diesel.

Results

The presence of diesel did not benefit the growth of A. tatarinowii. The germination ratio and germination rate decreased with the increase of diesel concentration, both the lowest value appeared when the concentration of diesel was 10,000 mg?kg^?1. The lowest diesel concentration (2,000 mg?kg^?1) in the soil significantly reduced the length, average diameter, and projected area of root, especially on the stress of the higher diesel concentration (4,000, 8,000, and 10,000 mg?kg^?1). Furthermore, H₂O₂ concentration in leaves rose with the increasing concentration of diesel. However, no DNA oxidative damage to root was observed in our experiment.

Conclusions

Diesel exposure significantly inhabited the seed germination, root elongation, and seedlings growth of A. tatarinowii. Diesel stress caused the accumulation of H₂O₂ in the leaves of A. tatarinowii.     

The response of the Rhizobium leguminosarum bv. trifolii wild-type and exopolysaccharide-deficient mutants to oxidative stress

Aims

The aim of this study was investigation of the response of R. leguminosarum bv. trifolii wild-type and its two rosR and pssA mutant strains impaired in exopolysaccharide (EPS) synthesis to oxidative stress conditions caused by two prooxidants: a superoxide anion generator- menadione (MQ) and hydrogen peroxide (H₂O₂).

Methods

The levels of enzymatic (catalase, superoxide dismutase, pectinase and β-glucosidase) and non-enzymatic (superoxide anion generator, formaldehyde, phenolic compounds) biomarkers were monitored using biochemical methods in both the supernatants and rhizobial cells after treatment with 0.3?mM MQ and 1.5?mM H₂O₂. The viability of bacterial cells was estimated using fluorescent dyes and confocal laser scanning microscopy. In addition, the effect of prooxidants on symbiosis of the R. leguminosarum bv. trifolii strains with clover was established.

Results

The tested stress factors significantly changed enzymatic patterns of the rhizobial strains, and the wild-type strain proved to be more resistant to these prooxidants than both pssA and rosR mutants. Significantly higher activities of both catalase and superoxide dismutase have been detected in these mutants in comparison to the wild-type strain. H₂O₂ and MQ also increased the levels of pectinase and β-glucosidase activities in the tested strains. Moreover, pre-incubation of R. leguminosarum bv. trifolii strains with the prooxidants negatively affected the viability of bacterial cells and the number of nodules elicited on clover plants.

Conclusions

EPS produced in large amounts by R. leguminosarum bv. trifolii plays a significant protective role as a barrier against oxidative stress factors and during symbiotic interactions with clover plants.     

Lipoteichoic acid induces surfactant protein-A biosynthesis in human alveolar type II epithelial cells through activating the MEK1/2-ERK1/2-NF-κB pathway

Background

Asthma is a chronic inflammatory disease of the airways but recent studies have shown that alveoli are also subject to pathophysiological changes. This study was undertaken to compare hydrogen peroxide (H₂O₂) concentrations in different parts of the lung using a new technique of fractioned breath condensate sampling.

Methods

In 52 children (9-17 years, 32 asthmatic patients, 20 controls) measurements of exhaled nitric oxide (FE_NO), lung function, H₂O₂ in exhaled breath condensate (EBC) and the asthma control test (ACT) were performed. Exhaled breath condensate was collected in two different fractions, representing mainly either the airways or the alveoli. H₂O₂ was analysed in the airway and alveolar fractions and compared to clinical parameters.

Results

The exhaled H₂O₂ concentration was significantly higher in the airway fraction than in the alveolar fraction comparing each single pair (p = 0.003, 0.032 and 0.040 for the whole study group, the asthmatic group and the control group, respectively). Asthma control, measured by the asthma control test (ACT), correlated significantly with the H₂O₂ concentrations in the alveolar fraction (r = 0.606, p = 0.004) but not with those in the airway fraction in the group of children above 12 years. FE_NO values and lung function parameters did not correlate to the H₂O₂ concentrations of each fraction.

Conclusion

The new technique of fractionated H₂O₂ measurement may differentiate H₂O₂ concentrations in different parts of the lung in asthmatic and control children. H₂O₂ concentrations of the alveolar fraction may be related to the asthma control test in children.     

Crosstalk between JNK and SUMO signaling pathways: deSUMOylation is protective against H2O2-induced cell injury

Background

Oxidative stress is a key feature in the pathogenesis of several neurological disorders. Following oxidative stress stimuli a wide range of pathways are activated and contribute to cellular death. The mechanism that couples c-Jun N-terminal kinase (JNK) signaling, a key pathway in stress conditions, to the small ubiquitin-related modifier (SUMO), an emerging protein in the field, is largely unknown.

Methodology/Principal Findings

With this study we investigated if SUMOylation participates in the regulation of JNK activation as well as cellular death in a model of H₂O₂ induced-oxidative stress. Our data show that H₂O₂ modulates JNK activation and induces cellular death in neuroblastoma SH-SY5Y cells. Inhibition of JNK''s action with the D-JNKI1 peptide rescued cells from death. Following H₂O₂, SUMO-1 over-expression increased phosphorylation of JNK and exacerbated cell death, although only in conditions of mild oxidative stress. Furthermore inhibition of SUMOylation, following transfection with SENP1, interfered with JNK activation and rescued cells from H₂O₂ induced death. Importantly, in our model, direct interaction between these proteins can occur.

Conclusions/Significance

Taken together our results show that SUMOylation may significantly contribute to modulation of JNK activation and contribute to cell death in oxidative stress conditions.     

Stress influenced the aerotolerance of <Emphasis Type="Italic">Lactobacillus rhamnosus</Emphasis> hsryfm 1301

Objective

To investigate the aerotolerance of Lactobacillus rhamnosus hsryfm 1301 and its influencing factors.

Results

The growth rate of L. rhamnosus hsryfm 1301 weakened noticeably when the concentration of supplemented H₂O₂ reached 1 mM, and only 2% of all L. rhamnosus hsryfm 1301 cells survived in MRS broth supplemented with 2 mM H₂O₂ for 1 h. After pretreatment with 0.5 mM H₂O₂, the surviving cells of L. rhamnosus hsryfm 1301 in the presence of 5 mM H₂O₂ for 1 h increased from 3.7 to 7.8 log CFU. Acid stress, osmotic stress, and heat stress at 46 °C also enhanced its aerotolerance, while heat stress at 50 °C reduced the tolerance of L. rhamnosus hsryfm 1301 to oxidative stress. Moreover, treatment with 0.5 mM H₂O₂ increased the heat stress tolerance of L. rhamnosus hsryfm 1301 by approximately 150-fold.

Conclusions

Lactobacillus rhamnosus hsryfm 1301 possesses a stress-inducible defense system against oxidative stress, and the cross-adaptation to different stresses is a promising target to increase the stress tolerance of L. rhamnosus hsryfm 1301 during probiotic food and starter culture production.

     

Comparison of two methods for the isolation of phytolith occluded carbon from plant material

Background and aims

Phytolith occluded carbon (PhytOC) is of interest for isotope studies, dating of sediments and the capture and storage of carbon. Many methodologies have been used for the isolation of phytoliths from plant material; however, there are wide disparities in the PhytOC contents when determined by different methodologies. In this study we examine the utility of the two main methods used for quantifying PhytOC.

Methods

These methods are: (1) a microwave digestion followed by a Walkley-Black digestion, and (2) H₂SO₄/H₂O₂.

Results

Method (1) produced PhytOC values over 50 times higher than those acquired by method (2). SEM examination indicated that the differences were likely due to shattering of the phytoliths by method (2) allowing consumption by the acid and peroxide of PhytOC .

Conclusion

These results indicate that for the samples analysed here: 1] the modified microwave method allowed the total PhytOC to be measured, 2] the H₂SO₄/H₂O₂ method allowed the PhytOC within the tightly packed silica matrix to be measured, and 3] the PhytOC retained within the phytolith cavities could possibly be calculated by subtracting 2] from 1]. For the samples analysed here most of the PhytOC resided in the phytolith cavities.     

Oxidative Stress Impairs the Heat Stress Response and Delays Unfolded Protein Recovery

Background

Environmental changes, air pollution and ozone depletion are increasing oxidative stress, and global warming threatens health by heat stress. We now face a high risk of simultaneous exposure to heat and oxidative stress. However, there have been few studies investigating their combined adverse effects on cell viability.

Principal Findings

Pretreatment of hydrogen peroxide (H₂O₂) specifically and highly sensitized cells to heat stress, and enhanced loss of mitochondrial membrane potential. H₂O₂ exposure impaired the HSP40/HSP70 induction as heat shock response (HSR) and the unfolded protein recovery, and enhanced eIF2α phosphorylation and/or XBP1 splicing, land marks of ER stress. These H₂O₂-mediated effects mimicked enhanced heat sensitivity in HSF1 knockdown or knockout cells. Importantly, thermal preconditioning blocked H₂O₂–mediated inhibitory effects on refolding activity and rescued HSF1 +/+ MEFs, but neither blocked the effects nor rescued HSF1 -/- MEFs. These data strongly suggest that inhibition of HSR and refolding activity is crucial for H₂O₂–mediated enhanced heat sensitivity.

Conclusions

H₂O₂ blocks HSR and refolding activity under heat stress, thereby leading to insufficient quality control and enhancing ER stress. These uncontrolled stress responses may enhance cell death. Our data thus highlight oxidative stress as a crucial factor affecting heat tolerance.     

Silicon ameliorates manganese toxicity by regulating manganese transport and antioxidant reactions in rice (Oryza sativa L.)

Background and aims

This study aimed to investigate the roles of silicon (Si) in ameliorating manganese (Mn) toxicity in two rice (Oryza sativa L.) cultivars: i.e. cv. Xinxiangyou 640 (XXY), a Mn-sensitive cultivar and cv. Zhuliangyou 99 (ZLY), a Mn-tolerant cultivar.

Methods

Plants were cultured in nutrient solution containing normal Mn (6.7 μM) or high Mn (2.0 mM), both with or without Si supply at 1.5 mM Si.

Results

Plant growth was severely inhibited by high Mn in cv. XXY, but was enhanced by Si supply. In cv. XXY, Si-enhanced tolerance resulted from a restriction of Mn transport, whereas in cv. ZLY Mn uptake was depressed. In cv. XXY, high Mn significantly increased superoxide dismutase (SOD), catalase and ascorbate peroxidase activities but decreased non-protein thiols and glutathione concentrations, leading to accumulation of H₂O₂ and malondialdehyde. The addition of Si significantly counteracted high Mn-elevated malondialdehyde and H₂O₂ concentrations and enhanced plant growth. In cv. ZLY, high Mn considerably raised SOD activities and glutathione concentrations, thus leading to relatively low oxidative damage.

Conclusions

Si-enhanced Mn tolerance was attributed mainly to restricted Mn transport in cv. XXY but to depressed Mn uptake in cv. ZLY. Silicon mainly influenced non-enzymatic antioxidants in these two rice cultivars under high Mn stress.     

Enhanced biomass and oxidative stress tolerance of <Emphasis Type="Italic">Synechococcus elongatus</Emphasis> PCC 7942 overexpressing the <Emphasis Type="Italic">DHAR</Emphasis> gene from <Emphasis Type="Italic">Brassica juncea</Emphasis>

Objectives

To improve the oxidative stress tolerance, biomass yield, and ascorbate/dehydroascorbate (AsA/DHA) ratio of Synechococcus elongatus PCC 7942 in the presence of H₂O₂, by heterologous expression of the dehydroascorbate reductase (DHAR) gene from Brassica juncea (BrDHAR).

Results

Under H₂O₂ stress, overexpression of BrDHAR in the transgenic strain (BrD) of S. elongatus greatly increased the AsA/DHA ratio. As part of the AsA recycling system, the oxidative stress response induced by reactive oxygen species was enhanced, and intracellular H₂O₂ level decreased. In addition, under H₂O₂ stress conditions, the BrD strain displayed increased growth rate and biomass, as well as higher chlorophyll content and deeper pigmentation than did wild-type and control strains.

Conclusion

By maintaining the AsA pool and redox homeostasis, the heterologous expression of BrDHAR increased S. elongatus tolerance to H₂O₂ stress, improving the biomass yield under these conditions. The results suggest that the BrD strain of S. elongatus, with its ability to attenuate the deleterious effects of ROS caused by environmental stressors, could be a promising platform for the generation of biofuels and other valuable bioproducts.

     

Arabidopsis desaturase 2 gene is involved in the regulation of cadmium and lead resistance

Aims

It was shown previously that Arabidopsis (Arabidopsis thaliana) desaturase 2 (ADS2) cDNA was isolated and it was shown that the expression of ADS2 was organ-dependent and up-regulated by low temperature. However, little is known about the role of ADS2 gene in heavy metal resistance in plants. In this study, we showed that ADS2 gene is involved in the regulation of cadmium (Cd) and lead (Pb) resistance.

Methods

For heavy metal resistance tests, seeds were germinated and grown on 1/2 MS media supplemented with the indicated concentrations of metal ions. To quantify root length, plants were grown vertically in plates. For heavy metal treatments, two-week old wild-type seedlings grown on MS media were treated with cadmium (Cd) or lead (Pb) for 24 h, and then sampled for metal content measurement and qPCR analysis.

Results

ADS2 was strongly repressed by Cd(II), and ads2-1 mutant plants showed increased Cd(II) resistance. A lower Cd content was detected in ads2-1 plants than in wild-type plants subjected to Cd(II) treatment, which was associated with activation in expression of AtPDR8 gene, a pump excluding Cd(II) and/or Cd(II)-containing toxic compounds from the cytoplasm, suggesting that ADS2-mediated Cd(II) resistance is AtPDR8 dependent. We also found that ads2-1 plants showed increased Pb(II) sensitivity, and ADS2 was strongly repressed by hydrogen peroxide (H₂O₂) but not by Pb(II). The ads2-1 mutant showed increased sensitivity to oxidative stresses mediated by H₂O₂ and paraquat, and higher levels of H₂O₂ accumulation were observed in leaves of ads2-1 plants than those of wild-type plants when subjected to Pb(II) and H₂O₂, indicating that ADS2 mediates Pb(II) resistance indirectly by impaired ROS scavenging.

Conclusions

ADS2 gene mediates Cd(II) and Pb(II) resistance, at least in part, through two distinct mechanisms, an AtPDR8-dependent mechanism and a ROS detoxification system-mediated mechanism, respectively.     

Taurine protection of PC12 cells against endoplasmic reticulum stress induced by oxidative stress

Background

Taurine is a free amino acid present in high concentrations in a variety of organs of mammalians. As an antioxidant, taurine has been found to protect cells against oxidative stress, but the underlying mechanism is still unclear.

Methods

In this report, we present evidence to support the conclusion that taurine exerts a protective function against endoplasmic reticulum (ER) stress induced by H₂O₂ in PC 12 cells. Oxidative stress was introduced by exposure of PC 12 cells to 250 uM H₂O₂ for 4 hours.

Results

It was found that the cell viability of PC 12 cells decreased with an increase of H₂O₂ concentration ranging from approximately 76% cell viability at 100 uM H₂O₂ down to 18% at 500 uM H₂O₂. At 250 uM H₂O₂, cell viability was restored to 80% by taurine at 25 mM. Furthermore, H₂O₂ treatment also caused a marked reduction in the expression of Bcl-2 while no significant change of Bax was observed. Treatment with taurine restored the reduced expression of Bcl-2 close to the control level without any obvious effect on Bax. Furthermore, taurine was also found to suppress up-regulation of GRP78, GADD153/CHOP and Bim induced by H₂O₂, suggesting that taurine may also exert a protective function against oxidative stress by reducing the ER stress.

Conclusion

In summary, taurine was shown to protect PC12 cells against oxidative stress induced by H₂O₂. ER stress was induced by oxidative stress and can be suppressed by taurine.