多囊卵巢综合征患者血清VitD水平及与炎症因子之间的相关性研究

目的 了解多囊卵巢综合征（PCOS）患者血清中25-羟维生素D（25-OH-VitD3）水平情况,并探讨其与白细胞介素-6（IL-6）、肿瘤坏死因子（TNF-α）、转化生长因子（TGF-β）、单核细胞趋化蛋白-1（MCP-1）及C-反应蛋白（CRP）之间的相关性。方法 选择2017年8月—2018年12月来医院妇科门诊就诊并确诊为PCOS的患者共135例作为PCOS组,选择同期来医院体检的健康妇女共120例作为对照组,采用化学发光法检测血清中25-OH-VitD3水平,免疫比浊法检测CRP水平及采用酶联免疫吸附法（ELISA）检测IL-6、TNF-α及TGF-β水平,并对检测结果进行统计学分析。结果 PCOS组患者血清中25-OH-VitD3水平为31.87±6.29 nmol/L,明显低于对照组的65.08±13.76 nmol/L,差异有统计学意义（t=3.190,P<0.05）。PCOS组患者血清IL-6、TNF-α、TGF-β、MCP-1及CRP水平分别为23.71±11.23 ng/L、20.54±3.16 ng/L、76.54±8.03 ng/L、375.92±40.15 ng/L及13.48±3.10 mg/L,均明显高于对照组,差异均有统计学意义（t=9.065,8.091,10.178,13.052,7.059,Ps<0.05）。通过Pearson相关性分析,25-OH-VitD3水平与IL-6、TNF-α、TGF-β、MCP-1及CRP水平均呈明显的负相关（r= -0.562,-0.628,-0.780,-0.850,-0.505,Ps<0.05）。结论 25-OH-VitD3低表达水平可能通过其免疫调节及抑制炎症因子生成能力下降,引起各种炎症因子水平升高,导致PCOS的发病。因此,维生素D可能与PCOS病的发生和发展有密切关系。     

Circulating levels of apoptotic markers and oxidative stress parameters in women with polycystic ovary syndrome: a case-controlled descriptive study

Context: Apoptotic dysregulation plays a role in the pathogenesis of polycystic ovary syndrome (PCOS).

Objective: To evaluate circulatory apoptotic markers and oxidative stress in patients with PCOS.

Materials and methods: Forty-four women with PCOS, and 44 healthy women as controls were enrolled in the study. Oxidative stress parameters and caspases levels were measured in serum.

Results: The caspase 9 level was significantly lower and related with oxidant status in patients with PCOS, while the circulating levels of caspases 3 and 7 were statistically similar in both groups.

Discussion: This study is the first report demonstrating the circulating levels of apoptotic markers and their relationship with oxidant status in PCOS.

Conclusion: The circulating caspase 9 and oxidant status might contribute to apoptotic dysregulation in PCOS.     

Characterization of LY231617 protection against hydrogen peroxide toxicity

The compound LY231617 [2,6-bis(1,1-dimethylethyl)-4-[[(1-ethyl)amino]methyl]phenol hydrochloride] has been reported to afford significant neuroprotection against hydrogen peroxide (H2O2)-induced toxicity in vitro and global ischemia in vivo. We now report on further mechanistic studies of H2O2 toxicity and protection by LY231617. Brief exposure to H2O2 (15 min) elicited an oxidative insult comparable with that generated by overnight treatment. H2O2-mediated cellular degeneration was characterized using lactate dehydrogenase (LDH) release, changes in total glutathione, and a new marker of oxidative stress, 8-epiprostaglandin F2alpha (8-isoprostane). LY231617 attenuated H2O2-mediated degeneration under a variety of exposure conditions, including a more clinically relevant posttreatment paradigm. Levels of 8-isoprostane paralleled LDH release under various treatment paradigms of 100 microM H2O2 +/- 5 microM drug. In contrast, despite affording significant protection, LY231617 had modest to no effects on cellular levels of glutathione. Taken together, these results are consistent with a membrane site of action for LY231617 and suggest that the compound affords cytoprotection via its antioxidant properties.     

Antiarthritic and antiinflammatory propensity of 4-methylesculetin,a coumarin derivative

Coumarins are a group of natural compounds widely distributed in plants. Of late, coumarins and their derivatives have grabbed much attention from the pharmacological and pharmaceutical arena due to their broad range of therapeutical qualities. A coumarin derivative 4-methylesculetin (4-ME) has known to possess effective antioxidant and radical-scavenging properties. Recently they have also shown to down regulate nuclear factor-kappa B (NF-κB) and protein kinase B (Akt) that play a vital role in inflammation and apoptosis. In view of this, the present study investigated the anti-arthritic potentiality of 4-ME by assessing its ability to inhibit cartilage and bone degeneration, inflammation and associated oxidative stress. Arthritis being a debilitating joint disease, results in the deterioration of extracellular matrix (ECM) of cartilage and synovium. Participation of both enzymatic and non-enzymatic factors in disease perpetuation is well documented. The present study demonstrated the mitigation of augmented serum levels of hyaluronidase and matrix metalloproteinases (MMP-13, MMP-3 and MMP-9) responsible for cartilage degeneration by 4-ME. It also protected bone resorption by reducing the elevated levels of bone-joint exoglycosidases, cathepsin-D and tartrate resistant acid phosphatases. Further, 4-ME significantly ameliorated the upregulated non-enzymatic inflammatory markers like TNF-α, IL-1β, IL-6, COX-2 and PGE₂. Besides, 4-ME effectively stabilized the arthritis-induced oxidative stress by restoring the levels of reactive oxygen species, lipid and hydro peroxides and antioxidant enzymes such as superoxide dismutase, catalase and glutathione-S-transferase. Thus, the study suggests that 4-ME could be an effective agent to treat arthritis and associated secondary complications like oxidative stress.     

Evaluation of the Rho A/Rho-kinase pathway in the uterus of the rat model of polycystic ovary syndrome

The aim of this study was to investigate the expression of RhoA/Rho-kinase in the uterus and the effect of Rho-kinase inhibitors on uterine contractions of dehydroepiandrosterone (DHEA) induced polycystic ovary syndrome (PCOS) rats. Forty-four female Sprague-Dawley (21 days old) rats divided into three groups: The control group (n?=?14, any procedure was not performed), vehicle group (n?=?14, 0.2?ml of sesame oil, subcutaneous injection, 20 days) and PCOS group (n?=?16, DHEA 6?mg/100?g in 0.2?ml of sesame oil, subcutaneous injection, 20 days). The myometrium thickness and uterine wet weight were assessed. The mRNA and protein expressions of Rho A, the effect of Rho-kinase inhibitors (fasudil and Y-27632) on KCl, carbachol, and PGF2α induced contractions were evaluated in the uterus. In the PCOS group, the myometrium thickness and uterine wet weight significantly increased compared to the control group and vehicle group. The mRNA expression level and the immunoreactive score of Rho A, ROCK 1, ROCK 2 were similar in all groups. In the PCOS group, KCl, carbachol, and PGF2α induced uterine contractions significantly increased compared to the control group and vehicle group. Fasudil and Y-27632 significantly inhibited KCl, carbachol, and PGF2α induced uterine contractions in all groups. In conclusion, the expression of Rho A, ROCK 1, ROCK 2 not changed although myometrium thickness, uterine wet weight and the contractile responses of uterus increased in the PCOS group. The results suggest that the Rho-kinase inhibitors effectively suppressed increased contractions in the PCOS group they might be potential therapeutic agents.     

Contrasting association of Leptin receptor polymorphisms and haplotypes with polycystic ovary syndrome in Bahraini and Tunisian women: a case–control study

Background: The present study examined the contribution of ethnicity to the association of leptin receptor gene (LEPR) gene variants with polycystic ovary syndrome (PCOS) in Tunisian and Bahraini Arabic-speaking women.Methods: Subjects consisted of 320 women with PCOS, and 446 eumenorrhic women from Tunisia, and 242 women with PCOS and 238 controls from Bahrain. Genotyping of (exonic) rs1137100 and rs1137101 and (intronic) rs2025804 LEPR variants was done by allelic exclusion.Results: The minor allele frequencies (MAFs) of rs1137100 and rs1137101 were significantly different between PCOS cases and control women from Bahrain but not Tunisia, and LEPR rs1137101 was associated with increased PCOS susceptibility only in Bahraini subjects. Furthermore, rs1137100 was associated with decreased PCOS risk among Bahrainis under codominant and recessive models; rs1137100 was negatively associated with PCOS in Tunisians after controlling for testosterone. In addition, rs2025804 was associated with increased PCOS risk among Tunisian but not Bahraini women, after adjusting for key covariates. Negative correlation was seen between rs1137101 and triglycerides in Tunisians, while homeostasis model assessment of insulin resistance (HOMA-IR) and insulin correlated with rs2025804 and rs1137101 among Bahraini subjects, and rs1137101 correlated with estradiol and prolactin. Taking TAG haplotype as common, positive association of TAA and negative association of TGG haplotype with PCOS was seen among Bahraini women; no three-locus PCOS-associated haplotypes were found in Tunisians.Conclusions: The present study is the first to demonstrate the contribution of ethnicity to the association of LEPR gene variants with PCOS, thereby highlighting the significance of controlling for ethnicity in gene association investigations.     

Effects of the pharmacologic manipulation of testosterone on cognitive functioning in women with polycystic ovary syndrome: a randomized, placebo-controlled treatment study

In a previous study, we found that women with polycystic ovary syndrome (PCOS), an endocrine disorder characterized by chronic hyperandrogenism, performed more poorly than healthy, matched controls on a number of neuropsychological tests, in particular tests of verbal fluency, verbal memory, manual dexterity, and visuospatial working memory. This randomized, placebo-controlled trial was undertaken to investigate whether pharmacologic manipulation of free testosterone (free T) levels in women with PCOS might affect their performance on cognitive tests. Nineteen women with PCOS completed a battery of neuropsychological tests before and after 3 months of treatment with either an anti-androgen (cyproterone acetate) plus estrogen or with a placebo. Hormone treatment of women with PCOS caused a significant reduction in their free T levels but did not affect performance on tests visuospatial ability, verbal memory, manual dexterity, or perceptual speed. Women treated with hormone therapy did, however, demonstrate an improvement in their performance on a test of verbal fluency compared to their pre-treatment scores. These findings suggest that changes in free T levels do not have a significant impact on cognitive performance in women with PCOS, although reductions in free T may be beneficial for verbal fluency.     

The protective effect of sulforaphane against oxidative stress in granulosa cells of patients with polycystic ovary syndrome (PCOS) through activation of AMPK/AKT/NRF2 signaling pathway

Increased production of reactive oxygen species (ROS) in granulosa cells (GCs) causes oxidative stress (OS) and plays a role in pathogenesis of polycystic ovary syndrome (PCOS). Sulforaphane (SFN) has received a great deal of attention as potent antioxidant because of its ability to induce expression of antioxidant enzymes through nuclear factor (erythroid-derived 2)-like 2 (NRF2) signaling pathway. Therefore, the present study was done to investigate the protective effect of SFN against OS in granulosa-lutein cells (GLCs) of patients with PCOS through activation of AMP-activated protein kinase (AMPK)/AKT/NRF2 signaling pathway. GLCs were isolated from patients with PCOS and healthy fertile women, as control group, during egg retrieval procedure. Level of intracellular ROS and apoptosis was determined in the isolated cells. For investigating the protective effect of SFN against ROS production and apoptosis in GLCs, the cells were cultured for 24 h in the presence or absence of SFN. Finally, expression of AMPK, AKT, and NRF2 proteins and genes was evaluated by western blotting and quantitative real-time polymerase chain reaction (qRT-PCR), respectively. The results indicated the increased ROS and apoptosis levels in GLCs isolated from patients with PCOS compared to the control group. Addition of SFN to culture medium of GLCs of patients with PCOS reduced intracellular ROS and apoptosis levels, and increased expression of AMPK, AKT, and NRF2 proteins and genes. Our findings demonstrated the protective effect of SFN against OS by lowering level of ROS and apoptosis possibly through activation of AMPK, AKT, and NRF2 proteins and genes expression.     

Nrf2抗氧化的分子调控机制

Nrf2是调控细胞氧化应激反应的重要转录因子,同时也是维持细胞内氧化还原稳态的中枢调节者。Nrf2通过诱导调控一系列抗氧化蛋白的组成型和诱导型表达,可以减轻活性氧和亲电体引起的细胞损伤,使细胞处于稳定状态,维持机体氧化还原动态平衡。本研究为了从分子层面深入探讨剖析Nrf2发挥抗氧化功能的作用机制,通过查找阅读大量相关文献并进行整理归纳,最终从Nrf2的结构与激活、Nrf2抗氧化功能以及Nrf2抗氧化的分子调控机制三个方面进行了概述分析。其中在对Nrf2抗氧化的分子调控机制的探讨部分,既探析了对Nrf2起激活作用的相关调节因子的作用机制,又分析了Nrf2被激活后对其下游多种抗氧化因子及谷胱甘肽氧化还原系统的诱导调控机制,以期较深入了解Nrf2抵抗机体氧化应激损伤作用及其抗氧化分子调控机制。     

A novel procedure for the assessment of the antioxidant capacity of food components

Carbonylation, an oxidative modification of the amino group of arginine and lysine residues caused by reactive oxygen species, has emerged as a new type of oxidative damage. Protein carbonylation has been shown to exert adverse effects on various protein functions. Recently, the role of food components in the attenuation of oxidative stress has been the focus of many studies. Most of these studies focused on the chemical properties of food components. However, it is also important to determine their effects on protein functions via post-translational modifications. In this study, we developed a novel procedure for evaluating the antioxidant capacity of food components. Hydrogen peroxide (H₂O₂)-induced protein carbonylation in HL-60 cells was quantitatively analyzed by using fluorescent dyes (Cy5–hydrazide dye and IC3–OSu dye), followed by sodium dodecyl sulfate–polyacrylamide gel electrophoresis (SDS–PAGE) and fluorescence determination. Among a panel of food components tested, quinic acid, kaempferol, saponin, squalene, trigonelline, and mangiferin were shown to be capable of suppressing protein carbonylation in HL-60 cells. Our results demonstrated that this fluorescence labeling/SDS–PAGE procedure allows for the detection of oxidative stress-induced protein carbonylation with high sensitivity and quantitative accuracy. This method should be useful for the screening of new antioxidant food components as well as the analysis of their suppression mechanism.     

Arjunolic acid: A new multifunctional therapeutic promise of alternative medicine

Importance of the field

In recent years, a number of studies describing the effective therapeutic strategies of medicinal plants and their active constituents in traditional medicine have been reported. Indeed, tremendous demand for the development and implementation of these plant derived biomolecules in complementary and alternative medicine is increasing and appear to be promising candidates for pharmaceutical industrial research. These new molecules, especially those from natural resources, are considered as potential therapeutic targets, because they are derived from commonly consumed foodstuff and are considered to be safe for humans.

Areas covered in this review

This review highlights the beneficial role of arjunolic acid, a naturally occurring chiral triterpenoid saponin, in various organ pathophysiology and the underlying mechanism of its protective action. Studies on the biochemistry and pharmacology suggest the potential use of arjunolic acid as a novel promising therapeutic strategy.

What the readers will gain

The multifunctional therapeutic application of arjunolic acid has already been documented by its various biological functions including antioxidant, anti-fungal, anti-bacterial, anticholinesterase, antitumor, antiasthmatic, wound healing and insect growth inhibitor activities. The scientific basis behind its therapeutic application as a cardioprotective agent in traditional medicine is justified by its ability to prevent myocardial necrosis and apoptosis, platelet aggregation, coagulation and lowering of blood pressure, heart rate, as well as cholesterol levels. Its antioxidant property coupled with metal chelating property (by its two hydroxyl groups) protects different organs from metal and drug-induced organ pathophysiology. Arjunolic acid also plays a beneficial role in the pathogenesis of diabetes and its associated complications. The mechanism of cytoprotection of arjunolic acid, at least in part, results from the detoxification of reactive oxygen species (ROS) produced in the respective pathophysiology. In addition to its other biological functions, it also possesses vibrant insecticidal properties and it has the potential to be used as a structural molecular framework for the design of molecular receptors in the general area of supramolecular chemistry and nanochemistry. Esters of arjunolic acid function as organogelators which has wide application in designing thermochromic switches and sensor devices. Arjunolic acid derived crown ether is an attractive candidate for the design of molecular receptors, biomimetics and supramolecular systems capable of performing some biological functions.

Home message

This review would provide useful information about the recent progress of natural product research in the domain of clinical science. This review also aims to untie the multifunctional therapeutic application of arjunolic acid, a nanometer-long naturally occurring chiral triterpenoid biomolecule.     

Heterologous expression of a novel psychrophilic Cu/Zn superoxide dismutase from Deschampsia antarctica

Superoxide dismutase (SOD) catalyzes the conversion of the superoxide radical (O₂⁻) into oxygen and hydrogen peroxide. Deschampsia antarctica is a plant that grows in Antarctica and survives to extreme low temperature and high UV radiation, thus it is an ideal model to study novel antioxidants. A cDNA Cu/Zn-SOD gene from D. antarctica was cloned into a pET vector and expressed in Escherichia coli BL21-SI. 112 mg/L of recombinant Cu/Zn-SOD was attained in batch cultures in bioreactor. Using Ni-affinity gel chromatography, the recombinant Cu/Zn-SOD was recovered with a purity of 90% and a specific enzyme activity of 749 at 25 °C. However, zymogram test showed that the enzyme has more activity at 4 °C. This D. antarctica SOD could be used to reduce the oxidation of refrigerated and frozen foods.     

A combination of five mechanisms confers a high tolerance for aluminum to a wild species of Poaceae,Andropogon virginicus L.

How can high tolerance against aluminum (Al) toxicity be obtained in plants? To address this question, tolerant mechanisms were characterized in a highly Al tolerant wild species of Poaceae, Andropogon virginicus L. A. virginicus showed an Al-stress-induced synthesis and secretion of citrate and malate in roots. This mechanism may help to suppress an increase of toxic Al ions in the root region. Microscopic observation of the morin-stained leaves indicated that the Al transferred to shoots was specifically accumulated in the trichomes and spikes of the leaves and that some portion of the accumulated Al was furthermore secreted as sap from the tips of trichomes. Al-induced synthesis of poly-phenolic compounds including anthocyanin also occurred in roots as a long term response to Al toxicity and anthocyanin production did not co-localize with either Al accumulation, nitric oxide (NO) production or lipid peroxides production in the roots. It was suggested that oxidative damage caused by Al stress was suppressed in these areas where anthocyanin was localized. Moreover, induction of NO production occurred in roots within 24 h of Al treatment. Our results suggested that NO could not efficiently ameliorate the Al-dependent nuclei deformation and DNA fragmentation, but could function as a trigger to stimulate anti-peroxidation enzymes under Al stress. Collectively the results suggested that A. virginicus manifests its high Al tolerance by a unique combination of effective mechanisms.     

HSPB5 (αB-crystallin) confers protection against paraquat-induced oxidative stress at the organismal level in a tissue-dependent manner

Oxidative stress is one of the major and continuous stresses, an organism encounters during its lifetime. Tissues such as the brain, liver and muscles are more prone to damage by oxidative stress due to their metabolic activity, differences in physiological and adaptive processes. One of the defence mechanisms against continuous oxidative stress is a set of small heat shock proteins. αB-Crystallin/HSPB5, a small heat shock protein, gets upregulated under stress and acts as a molecular chaperone. In addition to acting as a molecular chaperone, HSPB5 is shown to have a role in other cytoprotective functions such as inhibition of apoptosis, prevention of oxidative stress and stabilisation of cytoskeletal system. Such protection in vivo, at the organism level, particularly in a tissue-dependent manner, has not been investigated. We have expressed HSPB5 in fat body (liver), neurons and specifically in dopaminergic and motor neurons in Drosophila and investigated its protective effect against paraquat-induced oxidative stress. We observed that expression of HSPB5 in neurons and fat body confers protection against paraquat-induced oxidative stress. Expression in dopaminergic neurons showed a higher protective effect. Our results clearly establish the protective ability of HSPB5 in vivo; the extent of protection, however, varies depending on the tissue in which it is expressed. Interestingly, neuronal expression of HSPB5 resulted in an improvement in negative geotropic behaviour, whereas specific expression in muscle tissue did not show such a beneficial effect.     

Association of TNF-alpha,IL-6 and IL-1beta gene polymorphisms with polycystic ovary syndrome: a meta-analysis

Background

Several studies on the association of TNF-alpha (−308 G/A), IL-6 (−174 G/C) and IL-1beta (−511 C/T) polymorphisms with polycystic ovary syndrome (PCOS) risk have reported conflicting results. The aim of the present study was to assess these associations by meta-analysis.

Results

A total of 14 eligible articles (1665 cases/1687 controls) were included in this meta-analysis. The results suggested that there was no obvious association between the TNF-alpha (−308 G/A) polymorphism and PCOS in the overall population or subgroup analysis by ethnicity, Hardy–Weinberg equilibrium (HWE) in controls, genotyping method, PCOS diagnosis criteria, and study sample size. Also, no obvious association was found between the TNF-alpha (−308 G/A) polymorphism and obesity in patients with PCOS (body mass index [BMI] ≥ 25 kg/m² vs. BMI < 25 kg/m²). Regarding the IL-6 (−174 G/C) polymorphism, also no association was found in the overall population in heterozygote comparison, dominant model, and recessive model. Even though an allelic model (odds ratio [OR] = 0.63, 95% confidence interval [CI] = 0.41–0.96) and a homozygote comparison (OR = 0.52, 95% CI = 0.30–0.93) showed that the IL-6 (−174 G/C) polymorphism was marginally associated with PCOS. Further subgroup analysis suggested that the effect size was not significant among HWE in controls (sample size ≤ 200) and genotyping method of pyrosequencing under all genetic models. Similarly, there was no association between the IL-1beta (−511 C/T) polymorphism and PCOS in the overall population or subgroup analysis under all genetic models. Furthermore, no significant association was found between the IL-1beta (−511 C/T) polymorphism and several clinical and biochemical parameters in patients with PCOS.

Conclusions

The results of this meta-analysis suggest that the TNF-alpha (−308 G/A), IL-6 (−174 G/C), and IL-1beta (−511 C/T) polymorphisms may not be associated with PCOS risk. However, further case–control studies with larger sample sizes are needed to confirm our results.

Electronic supplementary material

The online version of this article (doi:10.1186/s12863-015-0165-4) contains supplementary material, which is available to authorized users.     

Molecular mechanisms of oxidative stress resistance induced by resveratrol: Specific and progressive induction of MnSOD

trans-Resveratrol (3,4′,5-trihydroxystilbene; RES), a polyphenol found in particularly high concentrations in red wine, has recently attracted intense interest for its potentially beneficial effects on human health. Here, we report the effects of long-term exposure to micromolar concentrations of RES on antioxidant and DNA repair enzyme activities in a human cell line (MRC-5). RES had either no effect on, or reduced the activities of glutathione peroxidase, catalase and CuZn superoxide dismutase (SOD), in treatments lasting up to 2 weeks. RES failed to induce activities of the DNA base excision repair enzymes apurinic/apyrimidinic endonuclease and DNA polymerase β. However, it dramatically and progressively induced mitochondrial MnSOD expression and activity. Two weeks exposure to RES increased MnSOD protein level 6-fold and activity 14-fold. Thus, long-term exposure of human cells to RES results in a highly specific upregulation of MnSOD, and this may be an important mechanism by which it elicits its effects in human cells.     

Nontargeted metabolomic analysis of skeletal muscle in a dehydroepiandrosterone‐induced mouse model of polycystic ovary syndrome

Polycystic ovary syndrome (PCOS) is the most common endocrinopathy and an important metabolic disorder in women of reproductive age. Insulin resistance (IR) is one of its most important clinical features in patients with PCOS. Androgen excess‐induced mitochondrial dysfunction contributes to skeletal muscle IR in dehydroepiandrosterone (DHEA)‐induced PCOS mice. The effect of androgen excess on the skeletal muscle, however, is incompletely characterized. A nontargeted metabolomics approach was thus applied to analyze the metabolites in skeletal muscle of DHEA‐induced PCOS mice. Data from metabolomic analysis revealed the significant changes in 32 metabolites and the marked impact of five metabolic pathways. ATP production was also found to be significantly reduced in skeletal muscle of DHEA mice. Combined with the quantification of type I and II myofibers and lipid measurement in the skeletal muscle of the mice, the results from the present study supported the role of mitochondrial impairment rather than lipid accumulation in the pathogenesis of skeletal muscle IR in DHEA‐induced PCOS mice. In summary, we show here for the first time the profile of the metabolites in the skeletal muscle of DHEA‐induced PCOS mice which exhibit IR. The work would help better understand the pathology of skeletal muscle IR in PCOS.     

Chronic exposure to 50Hz magnetic fields causes a significant weakening of antioxidant defence systems in aged rat brain

Several studies suggest that extremely low-frequency magnetic fields (ELF-MFs) may enhance the free radical endogenous production. It is also well known that one of the unavoidable consequences of ageing is an overall oxidative stress-based decline in several physiological functions and in the general resistance to stressors. On the basis of these assumptions, the aim of this study was to establish whether the ageing process can increase susceptibility towards widely present ELF-MF-mediated pro-oxidative challenges. To this end, female Sprague-Dawley rats were continuously exposed to a sinusoidal 50Hz, 0.1mT magnetic field for 10 days. Treatment-induced changes in the major antioxidant protection systems and in the neurotrophic support were investigated, as a function of the age of the subjects. All analyses were performed in brain cortices, due to the high susceptibility of neuronal cells to oxidative injury. Our results indicated that ELF-MF exposure significantly affects anti-oxidative capability, both in young and aged animals, although in opposite ways. Indeed, exposed young individuals enhanced their neurotrophic signalling and anti-oxidative enzymatic defence against a possible ELF-MF-mediated increase in oxygen radical species. In contrast, aged subjects were not capable of increasing their defences in response to ELF-MF treatment but, on the contrary, they underwent a significant decrease in the major antioxidant enzymatic activities. In conclusion, our data seem to suggest that the exposure to ELF-MFs may act as a risk factor for the occurrence of oxidative stress-based nervous system pathologies associated with ageing.     

Molecular mapping of gene Gm-6(t) which confers resistance against four biotypes of Asian rice gall midge in China

The Chinese rice cultivar Duokang #1 carries a single dominant gene Gm-6(t) that confers resistance to the four biotypes of Asian rice gall midge (Orseolia oryzae Wood-Mason) known in China. Bulked segregant analysis was performed on progeny of a cross between Duokang #1 and the gall midge-susceptible cultivar Feng Yin Zhan using the RAPD method. The RAPD marker OPM06₍₁₄₀₀₎ amplified a locus linked to Gm-6(t). The locus was subsequently mapped to rice chromosome 4 in a region flanked by cloned RFLP markers RG214 and RG163. Fine mapping of Gm-6(t) revealed that markers RG214 and RG476 flanked the gene at distances of 1.0 and 2.3 cM, respectively. Another gall midge resistance gene, Gm-2, mapped previously to chromosome 4, is located about 16 cM from Gm-6(t), to judge by data from a segregating population derived from a cross between Duokang #1 and the Indian cultivar Phalguna that carries Gm-2. We developed a PCR-based marker-assisted selection kit for transfer of the Gm-6(t) gene into Ming Hui 63 and IR50404, two parental lines commonly used in hybrid rice production in China. The kit contains PCR primer pairs based on the terminal sequences of the RG214 and RG476 clones. Polymorphism between Duokang #1 and the hybrid parental lines was found at these markers after digestion of the PCR products with specific restriction endonucleases. The kit will accelerate introduction of gall midge resistance into hybrid rice in China. Received: 18 May 2000 / Accepted: 9 March 2001