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Protection effect of nitric oxide on photosynthesis in rice under heat stress

100%

Song L. , Yue L. , Zhao H. , Hou M.

Acta Physiologiae Plantarum

2013

tom 35

nr 12

The effect of exogenous applied nitric oxide on photosynthesis under heat stress was investigated in rice seedlings. High temperature resulted in significant reductions of the net photosynthetic rate (P N) due to non-stomatal components. Application of nitric oxide donors, sodium nitroprusside (SNP) or S-nitrosoglutathione (GSNO), dramatically alleviated the decrease of P N induced by high temperature. Chlorophyll fluorescence measurement revealed that high temperature caused significant increase of the initial fluorescence (F o) and non-photochemical quenching (NPQ) whereas remarkable decrease of the maximal fluorescence (F m), the maximal efficiency of PSII photochemistry (F v/F m), the actual PSII efficiency (ΦPSII), and photochemical quenching (q p). In the presence of SNP or GSNO pretreatment, the increase of F o and decrease of F m, F v/F m, ΦPSII and q p were markedly mitigated, but NPQ was further elevated. Moreover, with SNP or GSNO pretreatment, H2O2 accumulation and electrolyte leakage induced by heat treatment were significantly reduced, whereas zeaxanthin content and carotenoid content relative to chlorophyll were elevated. The potassium salt of 2-(4-carboxyphenyl)-4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide (cPTIO), a specific NO scavenger, arrested NO donors mediated effects. These results suggest that NO can effectively protect photosynthesis from damage induced by heat stress. The activation effect of NO on photosynthesis may be mediated by acting as ROS scavenging, or/and alleviating oxidative stress via maintaining higher carotenoid content relative to chlorophyll or/and enhancing thermal dissipation of excess energy through keeping higher level of zeaxanthin content under heat stress.

Effect of varying NaCl doses on flavonoid production in suspension cells of Ginkgo biloba : relationship to chlorophyll fluorescence, ion homeostasis, antioxidant system and ultrastructure

63%

Chen Y. , Lin F. , Yang H. , Yue L. , Hu F. , Wang J. , Luo Y. , Cao F.

Acta Physiologiae Plantarum

2014

tom 36

nr 12

Ginkgo suspension cells were used to investigate the mechanism that governs the shift between primary and secondary metabolism under NaCl elicitation. The production of three flavonol glycosides, chlorophyll fluorescence, ion content, the antioxidant system, and the cellular ultrastructure in the presence of NaCl doses from 5 to 175 mM were examined. At low salt doses (5–50 mM), cell growth and flavonol glycosides accumulation were stimulated without damaging cell structure or inducing oxidative stress by maintaining high K⁺ and chlorophyll content. At moderate salt doses (75–125 mM), the cells could withstand the salt stress without an impact on survival by changing internal cellular structure, maintaining high levels of K⁺ and Ca²⁺ and increasing anti-oxidative enzyme activities rather than flavonol glycosides to counteract the inhibition of the photosystem II, the accumulation of Na⁺ and hydrogen peroxide (H₂O₂) in the cells. This allowed cells to divert their metabolism from growth to defense-related pathways and tolerate NaCl stress. At higher salinity (150–175 mM), the cellular structure was damaged, and the high Na⁺ and low K⁺ content led to osmotic stress, and therefore, the stimulation of peroxidase (POD) and catalase (CAT) was not enough to cope with high H₂O₂ accumulation. The high production of flavonol glycosides may be a response of elicitation stimulation to serious damage at 175 mM NaCl. In conclusion, the use of 175 mM NaCl may be desirable for the induction of flavonol glycoside production in Ginkgo suspension cells.

The mitochondria mediate the induction of NOX1 gene expression by aldosterone in an ATF-1-dependent manner

63%

Fu Y. , Shi G. , Wu Y. , Kawai Y. , Qing T. , Yue L. , Xia Q. , Miyamori I. , Fan C.

Cellular and Molecular Biology Letters

2011

tom 16

nr 2

High aldosterone (Ald) levels can induce hypertrophy of vascular smooth muscle cells (VSMCs), which carries high risks of heart failure. A previous study showed that Ald induces hypertrophy of VSMCs by up-regulating NOX1, a catalytic subunit of NADPH oxidase that produces superoxides. However, the precise mechanism remains unknown. Diphenylene iodonium (DPI) is known as an inhibitor of complex I in the mitochondrial respiratory chain, and it was also found to almost completely suppress the induction of NOX1 mRNA and the phosphorylation of activating transcription factor (ATF-1) by PGF2α or PDGF in a rat VSMC cell line. In this study, we found that the Ald-induced phosphorylation of ATF-1 and NOX1 expression was significantly suppressed by DPI. Silencing of ATF-1 gene expression attenuated the induction of NOX1 mRNA expression, and over-expression of ATF-1 restored Ald-induced NOX1 expression. On the basis of this data, we show that the mitochondria mediate aldosterone-induced NOX1 gene expression in an ATF-1-dependent manner.