Single intravenous injection of plasmid DNA encoding human paraoxonase-1 inhibits hyperlipidemia in rats

Paraoxonase-1 (PON1, EC 3.1.8.1) is a high-density lipoprotein (HDL)-associated antioxidant enzyme, and its activity correlates negatively with the level of plasma low-density lipoprotein cholesterol (LDL-C) and triglyceridemia (TG). In this study, we examined the therapeutic effect of plasmid DNA containing the human PON1 gene (pcDNA/PON1) in hyperlipidemic model rats. The rats were fed a high-fat and high-cholesterol diet for 25 days to produce a hyperlipidemic animal model. Single intravenous injection of pcDNA/PON1 into model rats prevented dyslipidemia and hepatic lipid accumulation. The mechanisms of pcDNA/PON1 in treating hyperlipidemia were associated with increases of serum antioxidant PON1 and SOD activities, and with reduction of the levels of total cholesterol (TC), LDL-C and TG. The results suggest the potential therapeutic effect of pcDNA/PON1 on hyperlipidemia.     

Inhibition of dark‐induced stomatal closure by fusicoccin involves a removal of hydrogen peroxide in guard cells of Vicia faba

Fusicoccin (FC) treatment prevents dark‐induced stomatal closure, the mechanism of which is still obscure. By using pharmacological approaches and laser‐scanning confocal microscopy, the relationship between FC inhibition of dark‐induced stomatal closure and the hydrogen peroxide (H₂O₂) levels in guard cells in broad bean was studied. Like ascorbic acid (ASA), a scavenger of H₂O₂ and diphenylene iodonium (DPI), an inhibitor of H₂O₂‐generating enzyme NADPH oxidase, FC was found to inhibit stomatal closure and reduce H₂O₂ levels in guard cells in darkness, indicating that FC‐caused inhibition of dark‐induced stomatal closure is related to the reduction of H₂O₂ levels in guard cells. Furthermore, like ASA, FC not only suppressed H₂O₂‐induced stomatal closure and H₂O₂ levels in guard cells treated with H₂O₂ in light, but also reopened the stomata which had been closed by darkness and reduced the level of H₂O₂ that had been generated by darkness, showing that FC causes H₂O₂ removal in guard cells. The butyric acid treatment simulated the effects of FC on the stomata treated with H₂O₂ and had been closed by dark, and on H₂O₂ levels in guard cells of stomata treated with H₂O₂ and had been closed by dark, and both FC and butyric acid reduced cytosol pH in guard cells of stomata treated with H₂O₂ and had been closed by dark, which demonstrates that cytosolic acidification mediates FC‐induced H₂O₂ removal. Taken together, our results provide evidence that FC causes cytosolic acidification, consequently induces H₂O₂ removal, and finally prevents dark‐induced stomatal closure.     

Different enhancement of senescence induced by metabolic products of Alternaria alternata in tobacco leaves of different ages

The purpose of this study was to explore the mechanisms by which Alternaria alternata damages tobacco (Nicotiana tabacum) leaves. Treatment with A. alternata metabolic products enhanced senescence in leaves of different ages, as indicated by the significant decrease in chlorophyll, soluble protein, photosynthetic O₂ evolution and catalase (CAT, EC 1.11.1.6) activity as well as an increase in H₂O₂ content. The induction of senescence by A. alternata metabolic products increased as the age of the leaves increased. A. alternata metabolic products greatly influenced the behavior of photosystem II (PSII) in the leaves: oxygen evolving complex (OEC) activity and electron transport from primary quinone electron acceptor of PS II (Q_A) to secondary quinone electron acceptor of PS II (Q_B) were both significantly inhibited. This inhibition also became more pronounced in older leaves. In vitro experiments revealed that, without the influence of natural senescence, the A. alternata metabolic products directly inhibited the activity of a commercial CAT solution and inhibited photosynthetic O₂ evolution, which resulted in excess PSII excitation pressure and an overaccumulation of H₂O₂ in leaf segments. These results suggest that the significant declines in photosynthesis and CAT activity induced by the metabolic products of A. alternata were important contributors to the overaccumulation of reactive oxygen species (ROS), which accelerated senescence in tobacco leaves. The fact that the enhancement of senescence was getting more pronounced with the age of tobacco leaves might be related to the fact that older leaves already had higher H₂O₂ levels and less antioxidant activity as reflected in lower CAT activity.     

彩色马铃薯色素相关基因座的种类、功能与染色体定位(英文)

综述了与彩色马铃薯色素产生与分布相关基因座的观念起源、种类、功能和染色体定位。与彩色马铃薯色素相关基因座的观念起源于试图解释四倍体和二倍体马铃薯块茎和其他部位颜色呈现遗传行为的两个遗传模式。与彩色马铃薯色素相关的13个基因座可划分为4类,第1、第2和第3类分别与马铃薯花色苷的合成、酰化和分布有关,第4类与马铃薯类胡萝卜素的产生相关。基因座I,P,R和Y分别编码一个MYB结构域转录因子、类黄酮3′,5′-羟化酶、二氢黄酮醇4-还原酶和β-胡萝卜素羟化酶。基因座之间复杂多样的互作综合决定了彩色马铃薯色素特别是花色苷的产生与分布。基因座D和R定位在马铃薯的2号染色体上,E,F,I和PSC在10号染色体上,P在11号染色体上,Y在3号染色体上。可为彩色马铃薯颜色呈现的遗传机理探索提供参考。     

Hepatoprotective effect of a protein-enriched fraction from the maggots (Musca domestica) against CCl4-induced hepatic damage in rats

The hepatoprotective potential of a protein-enriched fraction (PEF) isolated from the maggots of housefly (Musca domestica) was evaluated in rats against carbon tetrachloride (CCl₄)-induced acute hepatic damage. Activities of serum aspartate aminotransferase and alanine aminotransferase increased by 4- and 13-fold induced by CCl₄, were significantly inhibited by pretreatment with 50, 100 and 200 mg PEF/kg. The formation of malondialdehyde was also significantly decreased in PEF-treated group compared with CCl₄-treated group. The treatments with PEF also elevated total protein levels significantly. These results were further supplemented by histopathological examination of liver sections. Hyperplasia of kupffer cells was observed after treatment with PEF (100 and 200 mg/kg). We conclude that PEF is effective in this model of liver damage.     

Chinese white Rongchang pig does not have the dominant white allele of KIT but has the dominant black allele of MC1R

The mast/stem cell growth factor receptor (KIT) and melanocortin receptor 1 (MC1R) mutations are responsible for coat color phenotypes in domestic pigs. Rongchang is a Chinese indigenous pig breed with a white coat color phenotype. To investigate the genetic variability of the KIT and MC1R genes and their possible association with the coat color phenotype in this breed, a gene duplication and splice mutation of KIT were diagnosed in a sample of 93 unrelated Rongchang animals. The results show that Rongchang pigs have a single copy of KIT without the splice mutation at the first nucleotide of intron 17, indicating that the dominant white I allele of KIT is not responsible for their white phenotype. The KIT mRNA and MC1R coding sequences were also determined in this breed. Three putative amino acid substitutions were found in the KIT gene between Rongchang and Western white pigs, their association with the Rongchang white phenotype remains unknown. For the MC1R gene, Rongchang pigs were demonstrated to have the same dominant black allele (E(D1)) as other Chinese breeds, supporting the previous conclusion that Chinese and Western pigs have independent domestication origin. We also clarified that the Rongchang white phenotype was recessive to nonwhite color phenotypes. Our results provide a good starting point for the identification of the mutations underlying the white coat color in Rongchang pigs.     

神经途径在肢体缺血预处理抗脑缺血/再灌注损伤中的作用

目的：探讨神经途径在肢体缺血预处理（limbi schemic preconditioning,LIP）抗脑缺血／再灌注损伤中的作用。方法：脑缺血采用四血管闭塞模型,重复短暂夹闭放松大鼠双侧股动脉3次作为LIP。将凝闭椎动脉的大鼠随机分为sham组、脑缺血组、股神经切断＋脑缺血组、LIP＋脑缺血组、股神经切断＋LIP＋脑缺血组。于Sham手术和脑缺血后7d处死大鼠,硫堇染色观察海马CA1区锥体神经元迟发性死亡的变化。于Sham手术和脑缺血后6h心脏灌注固定大鼠,免疫组化法测定海马CAI区c-Fos表达的变化。结果：硫堇染色结果显示,与sham组比较。脑缺血组和股神经切断＋脑缺血组大鼠海马CAI区均有明显组织损伤。LIP＋脑缺血组CAI区无明显细胞缺失,神经元密度明显高于脑缺血组（P〈0．01）。而股神经切断＋LIP＋脑缺血组大鼠海马CA1区明显损伤,锥体细胞缺失较多,与LIP＋脑缺血组组比较,神经元密度显著降低（P〈O．01）,提示LIP前切断双侧股神经取消了LIP抗脑缺血／再灌注损伤作用。c—Fos免疫组化染色结果显示,Sham组海马CAI区未见明显的c-Fos蛋白表达。脑缺血组海马CAI区偶见c—Fm的阳性表达。LIP＋脑缺血组c—Fos表达增强,数量增加,与Sham组和脑缺血组比较。c-Fos阳性细胞数和光密度均明显升高（P〈0．01）。而股神经切断＋LIP＋脑缺血组c-Fos表达明显减少,仅见少量弱阳性e-Fos表达。结论：LIP可通过神经途径发挥抗脑缺血／再灌注损伤作用,而LIP诱导c—Fos表达增加可能是LIP诱导脑缺血耐受神经途径的一个环节。