Correction to: The Effects of 50 nm Unmodified Nano-ZnO on Lipid Metabolism and Semen Quality in Male Mice

Biological Trace Element Research - The original version of this article unfortunately contained a mistake. The correct title should be “The Effects of 50 nm Unmodified Nano-ZnO on Lipid...     

H2O2作为根源信号介导盐胁迫诱导的蚕豆气孔关闭反应

H2O2作为信号分子可被多种胁迫诱导产生并在细胞内积累,进而参与调节植物的抗逆反应。文章通过远红外热成像观察等实验发现,根部NaCl胁迫可诱导蚕豆气孔关闭,叶片温度上升,叶片内Na+和H2O2含量增加,蒸腾流汁液中H2O2浓度升高。另外,NaCl可直接诱导离体蚕豆根产生H2O2,却不能影响表皮条内H2O2含量。NaCl胁迫条件下产生的蒸腾流汁液可直接诱导表皮条气孔关闭,该过程可被抗氧化剂抗坏血酸(AsA)所逆转。这些结果表明,H2O2作为盐胁迫的根源信号,可能通过维管系统运输参与调节蚕豆气孔的关闭反应。     

Regulation of reproduction- and biomarker-related gene expression by sex steroids in the livers and ovaries of adult female western mosquitofish (Gambusia affinis)

To assess the adverse toxicological effects of steroid hormones on western mosquitofish (Gambusia affinis), 180 adult females were exposed to individual or binary combinations of progesterone (1μg/L), testosterone (1μg/L) and 17β-estradiol (1μg/L) for eight days. The expression patterns of vitellogenin, estrogen receptor, androgen receptor, metallothionein, and cytochrome P450 1A genes in mosquitofish varied according to tissue as well as the specificity of steroids. Treatment by progesterone or testosterone alone inhibited target gene expression in the livers. The expression levels of both vitellogenin A and vitellogenin B mRNAs were up-regulated by17β-estradiol, and a parallel induction of estrogen receptor α mRNA expression was also observed in the livers. In addition, 17β-estradiol treatment alone suppressed androgen receptor α, metallothionein and cytochrome P450 1A mRNA expression in the livers. In general, multiple hormone treatments had different effects on target gene expression compared with corresponding hormone alone. The results demonstrate that steroid hormones cause multiple biological responses including the expression of vitellogenin, estrogen receptor and androgen receptor mRNA in the hormone signaling pathways and the expression of metallothionein and cytochrome P450 1A mRNA in the xenobiotic signaling pathway.     

不同培养条件对拟南芥根细胞膜片钳记录的影响

本文以沙培养法、蛭石培养法、土培养法、水培养法和MS培养基等不同的方法培养拟南芥(Arabidopsis thaliana),分析了不同培养方法对根生长发育的影响,并分别分离根的原生质体.在膜片钳记录中对不同来源的根原生质体状态进行了比较.结果表明,土培养法分离的原生质体最适于膜片钳记录.     

NO可能作为H2O2的下游信号介导ABA诱导的蚕豆气孔关闭

ABA、H2O2和硝普钠(SNP)均能诱导蚕豆气孔关闭.NO的清除剂c-PTIO可以减轻由ABA或H2O2所诱导的蚕豆气孔关闭的程度,而过氧化氢酶(CAT)则不能减轻NO诱导的气孔关闭程度.激光共聚焦显微检测结果显示,10μmo1/L的ABA处理后,胞内H2O2的产生速率明显高于NO的产生速率;CAT几乎可完全抑制ABA所诱导的DAF的荧光增加;外源H2O2能显著诱导胞内DAF的荧光增加;c-PTIO对ABA诱导的DCF荧光略有促进作用,但外源SNP不能诱导胞内DCF荧光增加.这些结果表明,在ABA诱导气孔关闭过程中,H2O2可能在NO的上游起作用并受NO的负反馈调节.     

茉莉酸甲酯抑制拟南芥根伸长生长电生理学机制

以外源茉莉酸甲酯(JA-Me)处理拟南芥,运用膜片钳技术研究JA-Me、过氧化氢(H2O2)和内向K+通道之间的关系,以探讨茉莉酸类物质(JAs)抑制根伸长生长分子机制。检测到10-4mol/L的JA-Me能抑制根细胞质膜内向K+电流,表明可能与根的伸长生长有关,并且发现H2O2可能作为第二信使参与了JAs抑制根伸长生长的过程,H2O2介导的JA-Me对根细胞内向K+通道的抑制是根生长受抑的可能电生理机制。     

过氧化氢对蚕豆气孔运动和质膜K+通道的影响

不同浓度H2O2可使蚕豆(ViciafabaL.)叶片气孔关闭,抑制气孔张开,10mmol/L的H2O2最有效,10μmol/L的H2O2仍明显使气孔关闭。且10μmol/L的H2O2抑制气孔张开作用能被EGTA所消除,表明Ca2+参与低浓度H2O2使气孔关闭的过程。2mmol/L的H2O2可使质膜内向K+通道电流明显减小,而外向K+通道电流显著增加。因此,H2O2促进蚕豆气孔关闭主要是通过抑制K+通过保卫细胞质膜内向流入,或加强K+外向流出实现的。     

Response of fine roots to precipitation change: A meta-analysis北大核心CSCD

Aims The response of fine roots to soil moisture is very sensitive. Climate change scenarios predict changes in precipitation which influence soil moisture directly. Plants optimize resource acquisition by fine root morphological plasticity and biomass redistribution when soil moisture changes. Therefore, it is important to study the effect of precipitation increase and decrease on fine roots and reveal the response of ecosystem carbon cycling to global climate change. Methods We collected 202 sets of data from 48 published domestic and foreign articles, and analized the responses of fine root biomass, production, turnover, root length density, specific root length and soil microbial biomass carbon which reflects fine root decomposition dynamic to precipitation change by the meta-analysis. RR++ (weighted response ratio) was used to quantify the effect size of the response of fine roots to precipitation change. Important findings (1) The significance and magnitude of the precipitation effects on fine roots varied among plant types. Shrub fine roots had stronger response than tree fine roots. (2) The response of fine roots differed across soil depth. Fine root had most significant responses when the precipitation increased or decreased 50%. A 50% increase in precipitation had a significant positive impact on both fine root biomass in 20–40 cm soil and specific root length in 0–10 cm soil depth. A 50% decreased in precipitation had a significant negative impact on fine root production in 20–40 cm soil but positive impact on root length density in 0–10 cm soil. (3) The duration of experiment affected the response of fine roots, fine roots responded to precipitation changes (increase and decrease) by morphological plasticity in short-term experiments, and by biomass redistribution in long-term experiments. (4) Increasing precipitation contributed to the nutrient release of fine roots, because soil microbes accelerated the decomposability of fine roots due to sufficient substrate resources stimulated their own activity. © 2018 Editorial Office of Chinese Journal of Plant Ecology. All rights reserved.     

TIPE2 Inhibits Lung Cancer Growth Attributing to Promotion of Apoptosis by Regulating Some Apoptotic Molecules Expression

Recent studies found that TIPE2 was involved in cancer development. However, little is known about TIPE2 in lung cancer. Our study aims to clarify the role of TIPE2 in lung carcinogenesis. We examined the expression of TIPE2 in lung squamous cancer (LSC), small cell lung cancer and lung adenocarcinoma (AdC) tissues and found that TIPE2 expression was lost in small cell lung cancer, compared with adjacent non-tumor tissues. Overexpression of TIPE2 significantly inhibited the growth of lung cancer cell H446 in vitro and even suppressed tumor formation in vivo. Flow cytometry analysis found TIPE2 overexpression promoted apoptosis of H446. In TIPE2 over-expression cells, caspase-3, caspase-9, and Bax were significantly up-regulated while Bcl-2 was down-regulated. Moreover, coincident results were shown by immunohistochemistry in tumors from nude mice. TIPE2 inhibited the phosphorylation of Akt, while promoting the phosphorylation of P38, but had no effect on IκBα and ERK pathway. Taken together, TIPE2 promoted lung cancer cell apoptosis through affecting apoptosis-related molecules caspase-3, caspase-9, Bcl-2 and Bax, possibly via regulating P38 and Akt pathways, indicating that TIPE2 might be a novel marker for lung cancer diagnosis and therapy.