内生细菌对盐胁迫下小麦幼苗脯氨酸和丙二醛的影响

以周麦18为试验材料,以内生菌252和254为供试菌株,试验采用盆栽法设置盐胁迫组、盐胁迫接菌组和对照组,研究不同盐浓度胁迫下接菌处理对小麦幼苗脯氨酸(Pro,proline)和丙二醛(MDA,malondialdehyde)含量的影响。结果表明:小麦幼苗在盐胁迫环境下,随着培养时间和盐浓度增加,盐胁迫组Pro含量先升后降。在前中期,盐胁迫组小麦Pro含量逐渐积累,提高了小麦抗逆性;在后期Pro含量较中期有一定程度下降,小麦逐渐对盐环境产生适应性。随着盐浓度升高,盐胁迫组小麦在不同培养阶段对盐环境的抵抗能力不同,每个时期对盐抵抗能力有一阈值,超过此盐浓度Pro含量下降,抵抗能力减弱。接菌处理后,小麦Pro含量升高,提高了抗盐胁迫能力,第14天时修复效果最明显,接菌252处理组和254处理组分别在盐浓度为200 mmol/L和250 mmol/L时高出盐胁迫组133.48%和91.48%。盐胁迫组MDA含量随时间延长先降后升,与Pro含量变化趋势相反。在前中期,盐胁迫组小麦膜质过氧化程度不高,对小麦正常代谢活动尚未造成严重影响,在后期MDA含量升高,盐胁迫组小麦逐渐枯萎。接菌后,降低了幼苗细胞膜脂化程度,提高了小麦存活率,促进幼苗生长,MDA含量在21 d时均低于盐胁迫组,修复效果显著。     

有机污染物芘胁迫下白菜生理特性变化规律

为探究多环芳烃芘对白菜生理特性的影响,通过盆栽实验对华北地区常见的11种白菜进行不同浓度芘胁迫下的培养,研究白菜生理指标的变化规律。结果表明：白菜的种类和芘的浓度对白菜生理指标（生物量、丙二醛、叶绿素）均有显著影响,且随芘浓度变化,不同种类白菜的生理指标呈现不同的变化规律。白菜的生物量随芘的添加呈现两种变化：一是随芘添加浓度增加白菜生物量逐渐下降;二是在中低浓度芘（5、15、45 mg/kg）处理白菜生物量升高,高浓度（135、405 mg/kg）胁迫下生物量下降。白菜的丙二醛（MDA）含量随芘浓度的增加,表现出3种不同规律：各浓度之间均无显著性差异,MDA含量逐渐升高,以及显著低于对照组。叶绿素含量随芘浓度的增加,主要呈现出先下降后上升和逐渐上升2种变化趋势。京春白（JCB）和中白50（ZB-50）对芘的胁迫具有良好的耐受性,生理指标变化较小;中浓度芘胁迫下京翠60（JC-60）和京春绿（JCL）较为敏感,高浓度下京秋65（JQ-65）和吉红308（JH-308）生理指标变化显著,可以作为中低浓度和高浓度芘污染土壤指示作物。     

Oxidants and antioxidants in myocardial infarction (MI): Investigation of ischemia modified albumin,malondialdehyde, superoxide dismutase and catalase in individuals diagnosed with ST elevated myocardial infarction (STEMI) and non-STEMI (NSTEMI)

BackgroundCoronary ischemia can lead to myocardial damage and necrosis. The pathogenesis of cardiovascular diseases often includes increased oxidative stress and decreased antioxidant defense. The study aimed to assess levels of ischemia modified albumin (IMA), malondialdehyde acid (MDA), superoxide dismutase (SOD), and catalase in individuals diagnosed with ST elevated myocardial infarction (STEMI) and non-STEMI.MethodsThe present study prospectively included 50 STEMI patients, 55 NSTEMI patients, and 55 healthy subjects. Only patients who were recently diagnosed with STEMI or NSTEMI were included in this study. IMA, MDA, SOD, and catalase activities were measured spectrophotometrically. Significant coronary artery lesions were determined by angiography.ResultsPatients with ACS had significantly greater IMA and MDA values than the healthy controls (p<0.001). Besides, patients with STEMI had IMA levels that were significantly greater than those of the patients with NSTEMI (p<0.001), while the reverse was true for MDA levels (p<0.001). The healthy controls had the highest levels of SOD and catalase levels, followed by patients with STEMI and patients with NSTEMI, respectively (p<0.001). There was a significant negative correlation among MDA and SOD with catalase levels (r = -0.771 p<0.001 MDA vs catalase; r = -0.821 p<0.001 SOD vs catalase).ConclusionsData obtained in this study reveals that compared to healthy controls, STEMI and NSTEMI patients had increased levels of MDA and IMA and decreased levels of SOD and catalase.     

Neuroprotection against CCl4 induced brain damage with crocin in Wistar rats

Owing to its lipophilic property, carbon tetrachloride (CCl₄) is rapidly absorbed by both the liver and brain. We investigated the protective effects of crocin against brain damage caused by CCl₄. Fifty rats were divided into five groups of ten: control, corn oil, crocin, CCl₄ and CCl₄ + crocin. CCl₄ administration decreased glutathione (GSH) and total antioxidant status (TAS) levels, and catalase (CAT) activity, while significant increases were observed in malondialdehyde (MDA) and total oxidant status (TOS) levels and superoxide dismutase (SOD) activity. The cerebral cortex nuclear lamina developed a spongy appearance, neuronal degeneration was observed in the hippocampus, and heterochromatic and pyknotic neurons with increased cytoplasmic eosinophilia were observed in the hippocampus after CCl₄ treatment. Because crocin exhibits strong antioxidant properties, crocin treatment increased GSH and TAS levels and CAT activities, and decreased MDA and TOS levels and SOD activity; significant improvements also were observed in histologic architecture. We found that crocin administration nearly eliminated CCl₄ induced brain damage by preventing oxidative stress.     

Oxidative stress in small-for-gestational age (SGA) term newborns and their mothers

This study used malondialdehyde (MDA) determination by HPLC and enzymatic assays for total serum peroxides and antioxidant capacity to evaluate oxidative stress in 47 healthy full-term small-for-gestational age (SGA) newborns vs 67 appropriate-for-gestational age (AGA) newborns. Blood samples were collected at delivery from umbilical cord artery and vein and from peripheral blood of the babies on the third day after birth. Blood samples of mothers were also collected and compared with blood of 29 normal non-pregnant women (NPW). Serum peroxide values were significantly higher in both groups of mothers than in NPW, decreasing towards the third day in AGA mothers, while persisting in SGA mothers. Antioxidant capacity of sera of both groups of mothers was lower than NPW. Both SGA mothers and babies had increased MDA at delivery, unlike AGA counterparts. MDA levels in umbilical vein were higher than in umbilical arteries, while immunohistochemistry revealed abundant presence of 4-hydroxynonenal (HNE)-protein adducts only in stroma of the SGA placenta. These results show that both mothers and babies are exposed to oxidative stress during and after delivery, which is more pronounced and persistent in the perinatal period of the SGA group, while lipid peroxidation in placenta could play a role in SGA pathophysiology.     

An inter-laboratory validation of methods of lipid peroxidation measurement in UVA-treated human plasma samples

Abstract

Lipid peroxidation products like malondialdehyde, 4-hydroxynonenal and F₂-isoprostanes are widely used as markers of oxidative stress in vitro and in vivo. This study reports the results of a multi-laboratory validation study by COST Action B35 to assess inter-laboratory and intra-laboratory variation in the measurement of lipid peroxidation. Human plasma samples were exposed to UVA irradiation at different doses (0, 15 J, 20 J), encoded and shipped to 15 laboratories, where analyses of malondialdehyde, 4-hydroxynonenal and isoprostanes were conducted. The results demonstrate a low within-day-variation and a good correlation of results observed on two different days. However, high coefficients of variation were observed between the laboratories. Malondialdehyde determined by HPLC was found to be the most sensitive and reproducible lipid peroxidation product in plasma upon UVA treatment. It is concluded that measurement of malondialdehyde by HPLC has good analytical validity for inter-laboratory studies on lipid peroxidation in human EDTA-plasma samples, although it is acknowledged that this may not translate to biological validity.     

Tiller number is altered in the ascorbic acid-deficient rice suppressed for l-galactono-1,4-lactone dehydrogenase

The tiller of rice (Oryza sativa L.), which determines the panicle number per plant, is an important agronomic trait for grain production. Ascorbic acid (Asc) is a major plant antioxidant that serves many functions in plants. l-Galactono-1,4-lactone dehydrogenase (GLDH, EC 1.3.2.3) is an enzyme that catalyzes the last step of Asc biosynthesis in plants. Here we show that the GLDH-suppressed transgenic rices, GI-1 and GI-2, which have constitutively low (between 30% and 50%) leaf Asc content compared with the wild-type plants, exhibit a significantly reduced tiller number. Moreover, lower growth rate and plant height were observed in the Asc-deficient plants relative to the trait values of the wild-type plants at different tillering stages. Further examination showed that the deficiency of Asc resulted in a higher lipid peroxidation, a loss of chlorophyll, a loss of carotenoids, and a lower rate of CO₂ assimilation. In addition, the level of abscisic acid was higher in GI-1 plants, while the level of jasmonic acid was higher in GI-1 and GI-2 plants at different tillering stages. The results we presented here indicated that Asc deficiency was likely responsible for the promotion of premature senescence, which was accompanied by a marked decrease in photosynthesis. These observations support the conclusion that the deficiency of Asc alters the tiller number in the GLDH-suppressed transgenics through promoting premature senescence and changing phytohormones related to senescence.     

Hydrogen sulfide donor sodium hydrosulfide-improved heat tolerance in maize and involvement of proline

Hydrogen sulfide (H₂S) has long been considered as a phytotoxin, but nowadays as a cell signal molecule involved in growth, development, and the acquisition of stress tolerance in higher plants. In the present study, hydrogen sulfide donor, sodium hydrosulfide (NaHS), pretreatment markedly improved germination percentage of seeds and survival percentage of seedlings of maize under heat stress, and alleviated an increase in electrolyte leakage of roots, a decrease in tissue vitality and an accumulation of malondialdehyde (MDA) in coleoptiles of maize seedlings. In addition, pretreatment of NaHS could improve the activity of Δ¹-pyrroline-5-carboxylate synthetase (P5CS) and lower proline dehydrogenase (ProDH) activity, which in turn induced accumulation of endogenous proline in maize seedlings. Also, application of proline could enhance endogenous proline content, followed by mitigated accumulation of MDA and increased survival percentage of maize seedlings under heat stress. These results suggest that sodium hydrosulfide pretreatment could improve heat tolerance of maize and the acquisition of this heat tolerance may be involved in proline.     

Hydrogen sulfide protects SH-SY5Y neuronal cells against d-galactose induced cell injury by suppression of advanced glycation end products formation and oxidative stress

d-Galactose is widely used as an agent to cause aging effects in experimental animals. The present study aims to investigate the effects of hydrogen sulfide (H₂S) in human neuroblastoma SH-SY5Y cells exposed to d-galactose. Cells were pretreated with NaHS, an H₂S donor, and then exposed to d-galactose (25–400 mM for 48 h). We found that NaHS pretreatment significantly reversed the d-galactose-induced cell death and cellular senescence. MTT assay shows that NaHS significantly increased cell viability from 62.31 ± 1.29% to 72.34 ± 0.46% compared with d-galactose (200 mM) treatment group. The underlying mechanism appeared to involve a reduction by NaHS in the formation of advanced glycation end products (AGEs), which are known to contribute to the progression of age-related diseases. In addition, NaHS decreased the elevation of reactive oxygen species from 151.17 ± 2.07% to 124.8 ± 2.89% and malondialdehyde from 1.72 ± 0.07 to 1.10 ± 0.08 (nmol/mg protein) in SH-SY5Y cells after d-galactose exposure. NaHS also stimulated activities of superoxide dismutase from 0.42 ± 0.05 to 0.73 ± 0.04 (U/mg protein) and glutathione peroxidase from 3.98 ± 0.73 to 14.73 ± 0.77 (nmol/min/mg protein) and upregulated the gene expression levels of copper transport protein ATOX1, glutathione synthetase (GSS) and thioredoxin reductase 1 (TXNRD1) while down-regulated aldehyde oxidase 1 (AOX1). In summary, our data indicate that H₂S may have potentially anti-aging effects through the inhibition of AGEs formation and reduction of oxidative stress.     

人参皂苷Rg1对MDA诱导小鼠间充质干细胞凋亡的保护作用

目的：观察人参皂苷Rg1 （Ginsenoside Rg1,GS-Rg1）对丙二醛（Malondialdehyde,MDA）诱导的小鼠骨髓间充质干细胞（Mesenchymal stem cells,MSCs）凋亡的保护作用,并探讨其作用的可能机制.方法：以不同剂量（10、50、100 mg/L）人参皂苷Rg1预处理24 h,在小鼠骨髓MSC体外培养体系中加入MDA,TUNEL法,流式细胞术检测MSC凋亡率,Q-RT-PCR和Westen印迹分析检测Bcl-2、Bax和Caspase-3表达.结果：GS-Rg1可以减少TUNEL阳性细胞百分率及亚G1峰凋亡细胞百分率,增加Bcl-2mRNA及蛋白的表达水平,降低Bax和Caspase-3mRNA及蛋白表达水平.结论：GS-Rg1对MDA诱导小鼠间充质干细胞凋亡具有保护作用,其作用机制可能与增加Bc1-2表达,降低Bax和Caspase-3表达有关.