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BackgroundAdult asthma is phenotypically heterogeneous with unclear aetiology. We aimed to evaluate the potential contribution of environmental exposure and its ensuing response to asthma and its heterogeneity.MethodsEnvironmental risk was evaluated by assessing the records of National Health Insurance Research Database (NHIRD) and residence-based air pollution (particulate matter with diameter less than 2.5 micrometers (PM2.5) and PM2.5-bound polycyclic aromatic hydrocarbons (PAHs)), integrating biomonitoring analysis of environmental pollutants, inflammatory markers and sphingolipid metabolites in case–control populations with mass spectrometry and ELISA. Phenotypic clustering was evaluated by t-distributed stochastic neighbor embedding (t-SNE) integrating 18 clinical and demographic variables.FindingsIn the NHIRD dataset, modest increase in the relative risk with time-lag effect for emergency (N=209 837) and outpatient visits (N=638 538) was observed with increasing levels of PM2.5and PAHs. Biomonitoring analysis revealed a panel of metals and organic pollutants, particularly metal Ni and PAH, posing a significant risk for current asthma (ORs=1.28–3.48) and its severity, correlating with the level of oxidative stress markers, notably Nε-(hexanoyl)-lysine (r=0.108–0.311, p2.5exposure. Further, levels of circulating sphingosine-1-phosphate and ceramide-1-phosphate were found to discriminate asthma (pInterpretationThese results suggest the potential contribution of environmental factors from multiple sources, their ensuing oxidative stress and sphingolipid remodeling to adult asthma and its phenotypic heterogeneity.

Oxidative stress plays a crucial role in the development of diseases induced by welding fumes. To our knowledge, little information is available on the relationship between multiple heavy metal exposure and oxidative stress in welders. We assessed the relationship between multiple heavy metal exposure and oxidative damage by analyzing 174 nonsmoking male welders in a shipyard. Urinary metals were used as the internal dose of exposure to metals in welding fumes, and urinary 8-hydroxy-2'-deoxyguanosine (8-OHdG) was used as an oxidative DNA damage marker. The relationship between workers' metal levels and 8-OHdG was estimated using a multiple linear regression model. The geometric mean levels of urinary chromium (Cr), nickel (Ni), cadmium (Cd), and lead (Pb) were considerably higher in welders than in controls. Urinary Cr and Ni were determined as effective predictors of urinary 8-OHdG levels after adjusting for covariates. Oxidative DNA damage was associated with both Cr and Ni of welding fume exposure in shipyard welders (Ln Cr: β = 0.33, 95%C.I. = 0.16-0.49; Ln Ni: β = 0.27, 95%C.I. = 0.12-0.43). In this study, we investigated the significantly positive relationship between urinary metals (especially Cr and Ni) and 8-OHdG in nonsmoking shipyard welders. Moreover, the use of particulate respirators did not reduce metal exposure and oxidative damage. Therefore, we infer that hazard identification for welders should be conducted.

Certain studies have reported various insulin resistance responses to ambient heavy metal pollution, but few have reported such responses to occupational heavy metal pollution. Even fewer have demonstrated a relationship between mixture effects of heavy metals and insulin resistance in welding workers. Overall, we recruited 53 welders and 48 administrative staff from a shipyard located in northern Taiwan. Personal exposure to heavy metals was monitored for PM2.5 and urine. Blood samples from each participant were collected from the antecubital vein after fasting. Urine samples from each participant were collected in the same period as blood samples. The geometric mean levels for chromium (Cr), manganese (Mn), iron (Fe), cobalt (Co), nickel (Ni), copper (Cu), zinc (Zn), and cadmium (Cd) in the PM2.5 of the personal breathing zone and urinary Mn of welders were significantly higher than those in administrative staffs. Ambient Cr, Co, Ni, and Cu levels in the PM2.5 and urinary Cd were positively related to HOMA2-IR after adjusting for personal covariates (PM2.5-Cr: β=0.036, 95%C.I.: 0.002 to 0.070; PM2.5-Co: β=0.040, 95%C.I.: 0.002 to 0.077; PM2.5-Ni: β=0.054, 95%C.I.: 0.013 to 0.094; PM2.5-Cu: β=0.049, 95%C.I.: 0.010 to 0.088; U-Cd: β=0.209, 95%C.I.: 0.052 to 0.366, respectively). Our findings indicated the PM2.5 metal components and urinary metals were associated with increased insulin resistance in shipyard welders.

Background: Adult asthma is phenotypically heterogeneous with unclear etiology. We aimed to evaluate the potential contribution of environmental exposure and its ensuing response to asthma and its heterogeneity. Methods: Environmental risk was evaluated by assessing the records of National Health Insurance Research database (NHIRD) and residence-based air pollution [PM2.5 and PM2.5-bound polycyclic aromatic hydrocarbons (PAHs)], integrating biomonitoring analysis of environmental pollutants, inflammatory markers and sphingolipid metabolites in case-control populations with mass spectrometry and ELISA. Phenotypic clustering was evaluated by t-SNE integrating 18 clinical and demographic variables. Findings: In the NHIRD dataset, a modest increase in the relative risk with time-lag effect for emergency (N=209,837) and outpatient visits (N=638,538) was observed with increasing levels of PM2.5 and PAHs. Biomonitoring analysis revealed a panel of metals and organic pollutants, particularly metal Ni and PAH originated from multiple sources, posing a significant risk for current asthma and its severity, correlating with the level of oxidative stress markers, notably Ne-(hexanoyl)-lysine (HEL) as a marker of response in both cases and controls. Further, levels of circulating sphingosine-1-phosphate (S1P) and ceramide-1-phosphate (C1P) were found to discriminate asthma, correlating with the levels of exposure to PAH and metals, respectively, and both correlating with a panel of circulating inflammatory markers. Stratification of the combined datasets by 6 phenotypic clusters among 1,163 asthmatic subjects and those with comorbid T2DM revealed cluster-selective environmental risks and biosignatures. Interpretation: These results suggest the potential contribution of environmental factors, their ensuing oxidative stress and sphingolipid remodeling to adult asthma and its phenotypic heterogeneity. Funding Information: This work was supported, in part, by grants from National Health Research Institutes, Taiwan (EOPP10-014, EOSP07-014 and NHRI-102A1-PDCO-03010201) and Ministry of Health, Taiwan (EODOH01), National Science Council (NSC 102-2314-B-037-052), Ministry of Health (EODOH01), Ministry of Science and Technology (MOST 103-2320-B-110-001), and Academic Sinica (BM-102021170), Taiwan. Declaration of Interests: We declare no competing interests. Ethics Approval Statement: All eligible subjects were enrolled in the study after signing the informed consent approved by the respective recruitment hospitals.

Sleep disorders may pose a risk to workers in the workplace. We aimed to investigate the associations between metal fume fine particulate matter (PM2.5) and sleep quality in workers. We assessed the effects of personal exposure to metal fume PM2.5 on lung functions, urinary biomarkers, and sleep quality in shipyard welding workers. In total, 96 welding workers and 54 office workers were recruited in the present study; office workers were exposed to 82.1 ± 94.1 μg/m3 PM2.5 and welding workers were exposed to 2166.5 ± 3149.1 μg/m3. Welding workers had significantly lower levels of FEV25-75 than office workers (p

Exposure to metals poses potential health risks, including insulin resistance (IR), to those exposed to them in excess. Limited studies have examined such risks in occupational workers, including welders, and these have yielded inconsistent results. Thus, we examined the associations between exposure to welding metals and IR in welders. We recruited 78 welders and 75 administrative staff from a shipyard located in northern Taiwan. Personal exposure to heavy metals, including chromium (Cr), manganese (Mn), iron (Fe), nickel (Ni), copper (Cu), zinc (Zn), and cadmium (Cd), was monitored through particulate matter with an aerodynamic diameter of less than 2.5 μm (PM2.5) and urine analysis by inductively coupled plasma mass spectrometry (ICP–MS). After each participant fasted overnight, blood samples were collected and analyzed for IR assessment through updated homeostasis model assessment (HOMA2) modeling. Air sampling in the personal breathing zone was performed during a Monday shift prior to the blood and urine sample collection the following morning. The welders’ median personal Cr, Mn, Fe, Ni, Cu, and Zn airborne PM2.5 levels and urinary Cd levels were significantly higher than those of the administrative staff. After adjustment for covariates, logarithmic PM2.5-Mn, PM2.5-Fe, PM2.5-Cu, and PM2.5-Zn levels were positively correlated with logarithmic fasting plasma glucose (P-FGAC) levels (PM2.5-Mn: β = 0.0105, 95% C.I.: 0.0027–0.0183; PM2.5-Fe: β = 0.0127, 95% C.I.: 0.0027–0.0227; PM2.5-Cu: β = 0.0193, 95% C.I.: 0.0032–0.0355; PM2.5-Zn: β = 0.0132, 95% C.I.: 0.0005–0.0260). Logarithmic urinary Zn was positively correlated with logarithmic serum insulin and HOMA2-IR levels and negatively correlated with logarithmic HOMA2-insulin sensitivity (%S; βinsulin = 0.2171, 95% C.I.: 0.0025–0.4318; βIR = 0.2179, 95% C.I.: 0.0027–0.4330; β%S = −0.2180, 95% C.I.: −0.4334 to −0.0026). We observed that glucose homeostasis was disrupted by Mn, Fe, Cu, and Zn exposure through increasing P-FGAC and IR levels in shipyard welders.

Aim: To investigate the relationship between indium exposure and lung effects markers among indium tin oxide (ITO) manufacturing workers without job change.Methods: We enrolled 179 male workers fro...

After water imbibition, the outer layer seed coat of shaddock (Citrus grandis Osbeck) produces transparent gel-like mucilage (MSS), but its characteristics have never been studied before. This study aimed to assess the physico-chemical and functional properties of MSS. Extractions of MSS with deionized water at room temperature yielded about 3.5% based on the dry weight of seed. The major components were neutral sugars and uronic acids in the amounts of 33.5% and 49.6%, respectively. The acidic nature of MSS was confirmed by ruthenium red staining. Its water holding capacity and viscosity were 44.53 g•g-1 DW and 1660 cP at 10 g/L, respectively. MSS showed a weak quenching activity against DPPH radical, and moderate ferrous ion-chelating and superoxide anion radical scavenging activities, with IC50 value of 1.5 g/L and 1.1 g/L, respectively. A methyl thiazolyl tetrazolium (MTT) assay demonstrated that MSS significantly stimulated the viability of mouse skin fibroblasts (NIH/3T3) at 5 - 300 mg/L. These results impart the potential usefulness of the MSS to food, cosmetics and other applications.

A key step in regulating the flowering of Phalaenopsis is to control the emergence of the flower stalk or spiking. Light quality is an important factor to regulate plant reproduction. We used either red or blue light emitting diodes (LEDs) to substitute for 10% photosynthetic photon flux emitted by white fluorescent tubes as the control (WC) at approximately 70 μmole&middotm-2&middots-1 to examine the effects of enhanced red (WR) or blue (WB) light on spiking and the dawn-to-dusk fluctuations in the photosynthetic pigments and carbohydrates of Phalaenopsis aphrodite, which were grown in 7.5 cm diameter pots for six weeks. WR treatment significantly elevated the ratio of red to far-red light and the level of phytochrome photostationary state in concurrence with an increase in the spiking ratio and length, but had little effect on the concentrations of chlorophyll a and chlorophyll b in the leaf, levels of soluble sugars such as glucose, fructose, sucrose, and insoluble starch in the leaf and shortened stem, the locus of spiking, when compared to the other two treatments. Evidently, the spiking of Phalaenopsis is improved by dependent on the relative amount of active phytochrome expressed in the photostationary state.

Oxidative stress plays a crucial role in the development of diseases induced by welding fumes. To our knowledge, little information is available on the relationship between multiple heavy metal exposure and oxidative stress in welders. We assessed the relationship between multiple heavy metal exposure and oxidative damage by analyzing 174 nonsmoking male welders in a shipyard. Urinary metals were used as the internal dose of exposure to metals in welding fumes, and urinary 8-hydroxy-2&rsquo, deoxyguanosine (8-OHdG) was used as an oxidative DNA damage marker. The relationship between workers&rsquo, metal levels and 8-OHdG was estimated using a multiple linear regression model. The geometric mean levels of urinary chromium (Cr), nickel (Ni), cadmium (Cd), and lead (Pb) were considerably higher in welders than in controls. Urinary Cr and Ni were determined as effective predictors of urinary 8-OHdG levels after adjusting for covariates. Oxidative DNA damage was associated with both Cr and Ni of welding fume exposure in shipyard welders (Ln Cr: &beta, = 0.33, 95%C.I. = 0.16&ndash, 0.49, Ln Ni: &beta, = 0.27, 95%C.I. = 0.12&ndash, 0.43). In this study, we investigated the significantly positive relationship between urinary metals (especially Cr and Ni) and 8-OHdG in nonsmoking shipyard welders. Moreover, the use of particulate respirators did not reduce metal exposure and oxidative damage. Therefore, we infer that hazard identification for welders should be conducted.

AimTo investigate the relationship between indium exposure and lung effects markers among indium tin oxide (ITO) manufacturing workers without job change.MethodsWe enrolled 179 male workers from ITO target manufacturing and recycling factories in Taiwan. Plasma indium (P-In), urine indium (U-In) and creatinine adjusted U-In (U-In/Creat.) were used as internal dose of indium exposure. Plasma Krebs von den Lungen-6 (KL-6) and surfactant protein D (SP-D) were used as markers of interstitial pneumonitis. Forced vital capacity (FVC), forced expiratory volume at 1 st second (FEV1), and FEV1/FVC were also evaluated by spirometry.ResultsAfter adjusted for covariates by linear regression, plasma, urinary and creatinine adjusted indium were increased in high exposure group (P-In: β=1.13, pConclusionOur findings indicate indium exposure was related to restrictive lung dysfunction, decreased lung function for both FEV1 and FVC test but not for FEV1/FVC ratio. Meanwhile, increased plasma KL-6 in high exposure group also supports that indium exposure results in increased risk of interstitial pneumonitis among direct indium exposure workers. Our study provided an explanation to the consequence of indium exposure- interstitial pneumonitis-restrictive lung dysfunction.

We aimed to investigate indium exposure profiles and the relationship between ambient exposure and internal dose of indium among workers with different job characteristics in order to improve the work environment and protect workers from overexposure.We recruited 329 workers from indium-tin oxide (ITO) powder and target manufacturing and recycling factories. The workers were categorized into six groups, as powder, ITO target, bonding, processing, recycling process and administration department as reference group. Field and personal air sampling were performed to monitor indium concentrations of work environments and breathing zones of workers. Cumulative exposure were evaluated by respirable dust concentrations in personal sampling, exposure duration and work duration. Plasma indium (P-In), urine indium (U-In) and U-In adjusted for creatinine (U-In/creatinine) were used as internal dose.One-fourth of air indium concentrations of ITO manufacturing and recycling factories were exceeded permissible exposure limit (PEL) in Taiwan. Thirty-six percent of workers in this study exposed to unacceptable airborne concentration of indium. Over one-fifth of workers had P-In higher than Japanese biological exposure index (BEI) of 3 µg/L. After adjusting for potential confounders, significant positive were found between indium cumulative exposure and P-In (β=0.56, pWe suggest that U-In was an useful biomarker to assess indium exposure of indium manufacturing workers. The distribution and elimination of indium differed by its chemical form, which lead to characterization of the chemical form of indium is important for biomonitoring. Notably, although workers were exposed to indium below PEL, P-In still exceeded Japanese BEI. An appropriate exposure index need to be specified.

Illumination of Chlamydomonas reinhardtii cells at 1000 (high light, HL) or 3000 (very high light, VHL) µmol photons m(-2) s(-1) intensity increased superoxide anion radical (O(2)(•-)) and hydrogen peroxide (H(2)O(2)) production, and VHL illumination also increased the singlet oxygen ((1)O(2)) level. HL and VHL illumination decreased methionine sulfoxide reductase A4 (CrMSRA4) transcript levels but increased CrMSRA3, CrMSRA5 and CrMSRB2.1 transcripts levels. CrMSRB2.2 transcript levels increased only under VHL conditions. The role of reactive oxygen species (ROS) on CrMSR expression was studied using ROS scavengers and generators. Treatment with dimethylthiourea (DMTU), a H(2)O(2) scavenger, suppressed HL- and VHL-induced CrMSRA3, CrMSRA5 and CrMSRB2.1 expression, whereas H(2)O(2) treatment stimulated the expression of these genes under 50 µmol photons m(-2) s(-1) conditions (low light, LL). Treatment with diphenylamine (DPA), a (1)O(2) quencher, reduced VHL-induced CrMSRA3, CrMSRA5 and CrMSRB2.2 expression and deuterium oxide, which delays (1)O(2) decay, enhanced these gene expression, whereas treatment with (1)O(2) (rose bengal, methylene blue and neutral red) or O(2)(•-) (menadione and methyl viologen) generators under LL conditions induced their expression. DPA treatment inhibited the VHL-induced decrease in CrMSRA4 expression, but other ROS scavengers and ROS generators did not affect its expression under LL or HL conditions. These results demonstrate that the differential expression of CrMSRs under HL illumination can be attributed to different types of ROS. H(2)O(2), O(2) (•-) and (1)O(2) modulate CrMSRA3 and CrMSRA5 expression, whereas H(2)O(2) and O(2)(•-) regulate CrMSRB2.1 and CrMSRB2.2 expression, respectively. (1)O(2) mediates the decrease of CrMSRA4 expression by VHL illumination, but ROS do not modulate its decrease under HL conditions.

Nitric oxide (NO) has emerged as a fundamental signal molecule involved in the responses of plant to stress. A role for NO in the regulation of methionine sulfoxide reductase (MSR) mRNA expression and high light acclimation was studied in a green macroalga Ulva fasciata Delile. Transfer from darkness to high light (≥1,200 μmol photons m(-2) s(-1)) inhibited photosynthesis and growth but increased NO production and UfMSRA and UfMSRB transcripts. Treatment with an NO scavenger, 2-(4-carboxy- phenyl)-4,4,5,5-tetramethyl-imidazoline-1-oxyl-3-oxide (cPTIO), at 1,200 μmol photons m(-2) s(-1) caused a further growth inhibition accompanied by an inhibition of the increase of UfMSRA and UfMSRB transcripts by high light, while treatment with an NO generator, sodium nitroprusside (SNP), alleviated the growth inhibition and enhanced UfMSRA and UfMSRB expression. Exposure to moderate light (300 μmol photons m(-2) s(-1)) conditions also increased UfMSRA and UfMSRB transcripts, which were not affected by cPTIO treatment but were enhanced by SNP treatment. So, NO does not mediate the up-regulation of UfMSR genes by transfer to moderate light possibly as a precautionary mechanism in the sense of increasing light intensities in the daytime. In conclusion, NO production can be induced in U. fasciata upon exposure to high light for up-regulation of UfMSRA and UfMSRB expression but the level of NO production is not sufficient for acquisition of full tolerance to high light stress. Enhanced NO production by an exogenously applied NO generator can effectively trigger the high light acclimation process, including UfMSRA and UfMSRB expression.

The molecular acclimation of intertidal green macroalga Ulva fasciata Delile to high salinity stress were examined by the construction of a forward cDNA library via the suppressive subtractive hybridization between 30‰ and 90‰ (24 h) and by the time course dynamics of several abundantly expressed genes. Among the genes with known sequences, the expressed sequence tags are abundant in the function of protein synthesis (ribosomal protein) and destination. The cDNAs of ATP-dependent Clp protease (UfClpC), 20S proteasome β-subunit type 1 domain (UfPbf1), ubiquitin-conjugating enzyme E2 I (UfUbc9), and heat shock protein 90A (UfHsp90A) were cloned. UfClpC transcript increased 3 h after 90‰ treatment, followed by a decrease, while UfPbf1 and UfUbc9 transcripts increased after 12 h and decreased at 48 h. The transcripts of UfHsp90A increased 1 h after 90‰ treatment, followed by a drop and to the control level at 48 h. Protease activity increased 3 h after 90‰ treatment and decreased to the control level at 48 h. H₂O₂ contents increased 1 h after 90‰ treatment and then remained unchanged, but protein carbonyl group contents increased after 48 h. The treatments of reactive oxygen species scavengers partially alleviated 90‰ damage (partial growth rescue) and suppressed the increases in H₂O₂ content, protein carbonyl group content, protease activity, and UfClpC, UfPbf1, UfUbc9, and UfHsp90A transcripts by 90‰. The induction of specific chaperones and proteases at the molecular level for protein quality control can be considered as one of the molecular mechanisms of hypersalinity acclimation in U. fasciata.

Methionine (Met) residues of proteins can be oxidized by reactive oxygen species (ROS) with the formation of two epimers of methionine sulfoxide, S-MetSO and R-MetSO, which are reduced back to methionine by methionine sulfoxide reductase A (MSRA) and B (MSRB), respectively. UfMSRA and UfMSRB were cloned from the marine macroalga Ulva fasciata Delile, and the role of retrograde signal in gene expression was studied. Transcripts of UfMSRA and UfMSRB were increased after light exposure with a peak at 1 h. Treatment of photosynthetic electron transport inhibitors, 3-(3,4-dichlorophenyl)-1,1-dimethylurea (DCMU), 2,5-dibromo-3-methyl-6-isopropyl-p-benzoquinone (DBMIB), or stigmatellin, promoted the light-activated increase in UfMSRA transcripts, and a PSI electron donor, 2,6-dichlorophenolindophenol (DCPIP), reversed their effects. Increase of UfMSRB transcript by light was inhibited by DCMU and DBMIB treatments, and their effects were not reversed by DCPIP. Stigmatellin treatment did not affect UfMSRB transcripts. Thus, a relatively oxidized state of electron transport downstream from the cytochrome b6f (cytb6 f ) complex is involved in the light up-regulation of UfMSRA gene expression, and a more reduced state of Qo of the cytb6 f complex is required for the light activation of gene expression of UfMSRB.

Full-length protein disulfide isomerase (UfPDI) cDNA was cloned from the intertidal macroalga Ulva lactuca Linnaeus. Modulation of UfPDI expression by stresses and polyamines (PA) was studied. UfPDI transcription and enzyme activity were increased by hypersalinity (90) or high light illumination (1,200 μmol photons · m(-2) · s(-1) ), decreased by the addition of 100 μM CuSO4 . An exposure to a salinity of 90 decreased PA contents. Treating with PA biosynthetic inhibitors, D-arginine (D-Arg) or α-methyl ornithine (α-MO), led to a further decrease and also inhibited UfPDI expression and recovery of the growth rate. These results suggest that PAs are required to activate UfPDI expression with hypersalinity, even PA contents are decreased at a salinity of 90. The induction of UfPDI expression by hypersalinity of 90 and tolerance to hypersalinity could be enhanced if internal PA contents rise. Sung et al. (2011b) showed that PA contents could be increased by pretreating with putrescine (Put, 1 mM), spermidine (Spd, 1 mM), or spermine (Spm, 1 mM) at a salinity of 30. Therefore, PA pretreatment effect on UfPDI expression was examined. Pretreatment with Spd and Spm, but not with Put, enhanced UfPDI expression after transferred to a salinity of 90 and restored the growth rate. In conclusion, induction of UfPDI expression by Spd or Spm before exposure to hypersaline conditions and continuous up-regulation after hypersalinity exposure are required for the acquisition of hypersalinity tolerance in the intertidal green macroalga U. lactuca.

Nitric oxide (NO) was produced in Chlamydomonas reinhardtii cells 30 min after illumination at a very high light intensity of 3,000 µmol m⁻² s⁻¹ (VHL) followed by singlet oxygen (¹O₂) production, lipid peroxidation, expression of oxidative stress-related genes, irreversible PSII inactivation and cell death. Treatment with 2-(4-carboxyphenyl)-4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide (cPTIO), an NO scavenger, effectively reduced ¹O₂ levels and VHL damage, while treatment with diphenylamine (DPA), an ¹O₂ scavenger, only slightly reduced NO levels, though VHL damage was still effectively reduced. In the presence of cPTIO, the decline in minimum (Fo, Ft) and maximum (Fm, Fm') fluorescence after 60 min of VHL illumination can be slowed, and after recovery to 50 µmol m⁻² s⁻¹ conditions, PSII activity (Fv/Fm, Fv'/Fm') and PSII donor-side and acceptor-side electron transfer were partially restored. This finding indicates that ¹O₂ production is induced by NO through inhibition of PSII electron transfer under VHL conditions. VHL illumination caused a decrease in carotenoid contents but a transient increase in the transcription of two enzymes involved in carotenoid synthesis, phytoene synthase (PSY) and phytoene desaturase (PDS), at 30 min followed by a decrease at 60 min. The VHL-induced decrease in PDS transcription can be inhibited in the presence of cPTIO. The results of the present study show that NO generated in C. reinhardtii cells under VHL conditions induces ¹O₂ accumulation due to a decrease in the ¹O₂-scavenging capacity caused by NO-mediated inhibition of carotenoid synthesis and PSII electron transport, which, in turn, leads to oxidative damage and cell death.

A gene (UfCBR) encoding carotene biosynthesis-related (CBR) protein that potentially functions for the dissipation of excessive energy has been cloned from the intertidal green macroalga Ulva fasciata Delile. Hypersalinity and high light ≥300 µmol m(-2) s(-1) increased both UfCBR mRNA level and non-photochemical quenching (NPQ). The increase of UfCBR mRNA level and NPQ by high light was inhibited by treatment of photosynthetic electron transport inhibitor, 3-(3,4-dichlorophenyl)-1,1-dimethylurea or 2,5-dibromo-3-methyl-6-isopropyl-p-benzoquinone, but not by stigmatellin, an inhibitor that blocks electron transfer from quinol oxidase to iron-sulfur protein in cytochrome b(6) f complex. Treatment of dimethylthiourea, an H(2) O(2) scavenger, under 1200 µmol m(-2) s(-1) condition inhibited H(2) O(2) accumulation but did not affect UfCBR mRNA level, while treatment of H(2) O(2) in 150 µmol m(-2) s(-1) condition decreased UfCBR mRNA level. Thus, an reactive oxygen species-independent redox control via a more reduced state downstream the cytochrome b(6) f complex is involved in high light up-regulation of UfCBR expression in U. fasciata. The expression of UfCBR in U. fasciata against oxidative stress occurring in high light or high salinity in relation to NPQ is discussed.