1-甲基环丙烯对砀山酥梨黑皮病的控制效果及机理研究

以砀山酥梨果实为材料,研究了0.5和1.0μL·L-11-甲基环丙烯(1-MCP)处理对(2±0.5)℃冷藏梨果实黑皮病发生的抑制效应及相关生理指标变化,同时分别考察了采收期(9月5日、15日、25日)和贮藏包装方式(纸箱和塑料箱)对1-MCP控制砀山酥梨黑皮病效应的影响.结果显示:(1)0.5和1.0μL·L-11-MCP处理均可显著抑制梨果实在贮藏期黑皮病的发生,且1.0μL·L-11-MCP处理效果更佳;延迟采收能显著降低黑皮病发病率,并以9月下旬采收、1.0μL·L-11-MCP处理的果实黑皮病发病率最低(0.0%);1-MCP处理时塑料箱包装和纸箱包装在黑皮病发病率方面没有显著差异,但纸箱较塑料箱包装的果实腐烂率高.(2)随着1-MCP处理浓度增加,冷藏过程中梨果皮过氧化物酶(POD)活性增强,对果实丙二醛(MDA)和总酚含量、多酚氧化酶(PPO)活性和细胞膜透性的升高抑制作用加剧,使之维持较高抗氧化活性;同时也抑制了果皮α-法尼烯、共轭三烯含量的上升,且抑制程度越明显,果实黑皮指数越低.研究表明,1-MCP通过保持果皮抗氧化活性和抑制α-法尼烯代谢两条途径共同控制砀山酥梨黑皮病发生;9月下旬采收的果实采用1.0μL·L-11-MCP处理控制黑皮病效果最佳.     

1-MCP对梨采后某些生理生化指标的影响

1.0μL·L-1 1-MCP抑制梨品种"京白"、"五九香"、"锦香"果实采后呼吸速率.随着冷藏期的延长,货架期间经1-MCP处理的果实呼吸速率逐渐上升;冷藏后货架期间1-MCP延缓果实硬度下降,梨果实的酸度、淀粉、果皮叶绿素含量得以保持,但作用大小因品种而异;1-MCP还可以抑制"锦香"梨冷藏和货架期间黑皮病的发生,防止果实腐烂.     

甜柿采后生理特性及对1-MCP处理的反应

以甜柿品种‘阳丰’为材料,在20℃和0℃贮藏条件下研究了1-MCP(1-甲基环丙烯)处理对不同成熟度甜柿果实采后乙烯释放速率、呼吸速率和品质特性的影响。结果表明:1-MCP处理可延缓贮藏和货架期间甜柿果实的软化、抑制呼吸速率和可溶性固形物含量(SSC)的变化,但对乙烯释放速率的作用不一致。1-MCP处理对成熟度I果实的效果优于成熟度Ⅱ。低温贮藏虽然能显著延缓果实硬度的下降,但在0℃贮藏30、60和90 d后7 d货架期结束时,对照果完全软化,而经1-MCP处理后果实果肉硬度仍保持“脆”性。因此,贮前0.50μL.L-11-MCP处理结合低温贮藏是延长‘阳丰’甜柿贮藏期的有效途径,具有广泛的应用前景。     

不同后熟期‘菊水’梨果实对外源乙烯和1-MCP处理的生理响应

用80uL·L-1外源乙烯和1.0 uL·L-11-甲基环丙烯(1-MCP)处理不同后熟期'菊水'梨果实,分析处理后果实品质和生理指标在(25±1)℃贮藏温度下的变化特征.结果显示:在采收当天(采后0 d)和呼吸跃变初期(采后4 d),外源乙烯处理能明显促进果实硬度和可溶性同形物含量(SSC)的下降,降低活性氧清除酶(SOD、CAT和APX)的活性,提高呼吸速率和乙烯释放速率,促进果实后熟,1-MCP处理却表现出与乙烯相反的效应,且采收当天比呼吸跃变初期的作用效果更明显;在呼吸跃变中期(采后12 d),外源乙烯和1-MCP处理效果均不明显.研究发现,外源乙烯能促进果实后熟而1-MCP却抑制果实后熟,其效果因处理果实后熟期的不同而存在显著差异,果实后熟程度越高,其处理的效果越不明显.     

1-MCP对冷藏食荚豌豆衰老及品质的影响

研究了0.5、l和2μL/L的l-MCP处理对l℃贮藏食荚豌豆衰老及品质变化的影响.结果表明,采用l和2uL/L的1-MCP处理可有效抑制食荚豌豆呼吸、乙烯释放和超氧阴离子(O-2)生成,同时保持豆荚中较高的超氧化物歧化酶(SOD)、抗坏血酸过氧化物酶(AsA-POD)活性和叶绿素、抗坏血酸(AsA)含量,减少豆荚中MDA、纤维素含量的积累和豆荚腐烂指数的增加,延缓了其衰老进程和品质的下降.0.5 uL/L浓度的1-MCP处理对食荚豌豆采后衰老及品质无明显影响.     

1-MCP对‘珍珠’番石榴采后生理和品质的影响

为探讨改善番石榴贮藏性能的方法,番石榴(Psidium guajava L. ‘Pearl’)果实用1-甲基环丙烯(1-MCP)结合冷藏(15℃)处理,研究其贮藏生理和品质的变化。结果表明：1 μL L-1 1-MCP处理能有效抑制番石榴果实软化和果皮退绿;1-MCP处理抑制了可溶性固形物(TSS)含量上升和维生素C含量的下降;同时,超氧化物歧化酶(SOD)、过氧化氢酶(CAT)和过氧化物酶(POD)活性升高,多酚氧化酶(PPO)活性下降,延缓了果实中丙二醛(MDA)的积累。因此,1-MCP处理结合低温可有效改善珍珠番石榴的贮藏性能。 关键词：番石榴;1-MCP;贮藏生理;品质     

'嘎拉'苹果对不同浓度1-MCP处理的反应

以'嘎拉'('Kid's Orange'×'Delicious')苹果为试材,研究了0℃贮藏期间及贮藏30、60、90和120 d后转入室温7d货架期间1-MCP(1-甲基环丙烯)对果实呼吸速率、乙烯释放速率、品质和蛋白质变化的影响.结果表明,1-MCP处理显著抑制嘎拉苹果贮藏期间和贮后货架期间呼吸和乙烯释放速率,延缓果实硬度、可滴定酸含量的下降,对可溶性固形物含量无影响.对照果实在贮藏过程中,出现5条明显的特异性蛋白条带,1-MCP处理能抑制特异蛋白表达.300 nL·L-1浓度1-MCP处理与600 nL·L-11-MCP处理作用效果无显著差异.     

一氧化氮(NO)对采后青椒某些生理生化特性与品质的影响

不同浓度(0.1、0.5、1.0μmol·L-1)NO气体处理青椒果实的结果表明:0.5和1.0μmol·L.NO显著地抑制青椒果实的呼吸速率,延缓维生素C(VC)降解,0.5 μmol·L-1NO显著抑制多酚氧化酶(PPO)活性.各处理对果实中叶绿素和丙二醛(MDA)含量与未理的之间无显著差异.     

1-MCP和CO2对‘南果梨’冷藏后货架期能量代谢特性的影响

分别对‘南果梨’果实采用0.75μL/L 1-甲基环丙烯(1-MCP)在20℃熏蒸20h后装入保鲜袋(0.02mm)、用2%CO2充气果实包装袋(0.04mm)、以保鲜袋果实为对照,各处理组果实均置于(0±1)℃贮藏5个月后移至室温下(18℃±3℃),测定各处理果实在货架期间的褐变度以及果实线粒体蛋白含量、MDA含量、ATP含量,以明确1-MCP和CO2对南果梨冷藏后果实货架期的能量代谢特性。结果显示:(1)1-MCP和CO2处理可不同程度延缓南果梨冷藏后货架期果实果心褐变指数和褐变度,且1-MCP处理效果更好,但CO2处理在货架后期反而使果实褐变度较对照提高。(2)1-MCP和CO2处理可有效抑制果实MDA含量增加,延缓细胞膜透性的升高,保持细胞完整性。(3)1-MCP处理有利于提高货架前期果实中线粒体蛋白质含量,能够在货架后期保持较高的ATP含量和能荷水平,而CO2处理在货架前期果实内含有较高水平的ATP,促进了果实内的能荷水平。研究发现,1-MCP和CO2处理均可以通过影响南果梨果实的能量代谢特性从而影响果实的成熟衰老进程,且1-MCP处理可以抑制货架前期的ATP含量和能量供应,有利于保持细胞膜完整性,抑制果心褐变的发生,延缓果实成熟衰老进程;而2%CO2处理与对照相比对果实能量代谢特性的影响不大。     

1-MCP对室温贮藏下不同成熟度猕猴桃的生理效应

以适期采收(成熟度Ⅰ)和晚采收(成熟度Ⅱ)的'海沃德'猕猴桃果实为材料,研究0.5 μL·L~(-1) 1-甲基环丙烯(1-MCP)处理对室温贮藏(20℃)条件下两种果实的生理生化指标的影响.结果显示:1-甲基环丙烯(1-MCP)处理能有效延缓贮藏期间两种成熟度果实的硬度、可滴定酸含量、维生素C含量的下降,显著降低二者的乙烯释放速率和呼吸强度及其峰值,提高果实的POD、CAT和SOD活性.与成熟度Ⅰ相比,成熟度Ⅱ果实的硬度下降较快,且丙二醛含量和呼吸速率却明显较高,呼吸速率和乙烯释放量高峰时间相对提前.研究表明,在相同的贮藏条件下,晚采收的'海沃德'猕猴桃果实成熟衰老进程明显快于适期采收果实,贮藏效果较差;1-MCP能够明显延长猕猴桃果实的贮藏时间,表现出显著的保鲜效果.     

Investigation of the mechanism of temperature sensitivity of the electroreceptors of ampullae of lorenzini

In experiments on Black Sea skates (Raja clavata), the potential of the receptor epithelium of the ampullae of Lorenzini and spike activity of single nerve fibers connected to them were investigated during electrical and temperature stimulation. Usually the potential within the canal was between 0 and –2 mV, and the input resistance of the ampulla 250–400 k. Heating of the region of the receptor epithelium was accompanied by a negative wave of potential, an increase in input resistance, and inhibition of spike activity. With worsening of the animal's condition the transepithelial potential became positive (up to +10 mV) but the input resistance of the ampulla during stimulation with a positive current was nonlinear in some cases: a regenerative spike of positive polarity appeared in the channel. During heating, the spike response was sometimes reversed in sign. It is suggested that fluctuations of the transepithelial potential and spike responses to temperature stimulation reflect changes in the potential difference on the basal membrane of the receptor cells, which is described by a relationship of the Nernst's or Goldman's equation type.I. P. Pavlov Institute of Physiology, Academy of Sciences of the USSR, Leningrad. I. M. Sechenov, Institute of Evolutionary Physiology and Biochemistry, Academy of Sciences of the USSR, Leningrad. Pacific Institute of Oceanology, Far Eastern Scientific Center, Academy of Sciences of the USSR, Vladivostok. Translated from Neirofiziologiya, Vol. 12, No. 1, pp. 67–74, January–February, 1980.     

Shapes of curves of pH-dependence of reactions

A simple case is considered in which the rate of a two-step reaction depends on pH because the intermediate formed in the first step has to gain (or lose) a proton before it can react in the second step, and in which the rate-determining step therefore changes with pH. The curves of reaction rate against pH are shown to be symmetrical, and the sharpest peak possible has a width at half its height of 1.53pH units, i.e. of 2log(3+2 radical2). Any particular curve for this situation proves to be identical with a curve that could be generated for the pH-dependence of a single-step reaction in which the rate is proportional to the concentration of a particular ionic form of a reactant. Curves for the latter situation, however, can have forms impossible for the former case in which the rate-determining step changes, but only if the protonations that activate and deactivate the reactant are co-operative. The peak can then become even sharper, and its width at half its height can fall to 1.14pH units, i.e. to 2log(2+ radical3).     

Overview of mechanisms of action of lycopene

Dietary intakes of tomatoes and tomato products containing lycopene have been shown to be associated with decreased risk of chronic diseases such as cancer and cardiovascular diseases in numerous studies. Serum and tissue lycopene levels have also been inversely related to the risk of lung and prostate cancers. Lycopene functions as a very potent antioxidant, and this is clearly a major important mechanism of lycopene action. In this regard, lycopene can trap singlet oxygen and reduce mutagenesis in the Ames test. However, evidence is accumulating for other mechanisms as well. Lycopene at physiological concentrations can inhibit human cancer cell growth by interfering with growth factor receptor signaling and cell cycle progression specifically in prostate cancer cells without evidence of toxic effects or apoptosis of cells. Studies using human and animal cells have identified a gene, connexin 43, whose expression is upregulated by lycopene and which allows direct intercellular gap junctional communication (GJC). GJC is deficient in many human tumors and its restoration or upregulation is associated with decreased proliferation. The combination of low concentrations of lycopene with 1,25-dihydroxyvitamin D3 exhibits a synergistic effect on cell proliferation and differentiation and an additive effect on cell cycle progression in the HL-60 promyelocytic leukemia cell line, suggesting some interaction at a nuclear or subcellular level. The combination of lycopene and lutein synergistically interact as antioxidants, and this may relate to specific positioning of different carotenoids in membranes. This review will focus on the growing body of evidence that carotenoids have unexpected biologic effects in experimental systems, some of which may contribute to their cancer preventive properties in models of carcinogenesis. Consideration of solubility in vitro, comparison with doses achieved in humans by dietary means, interactions with other phytochemicals, and other potential mechanisms such as stimulation of xenobiotic metabolism, inhibition of cholesterogenesis, modulation of cyclooxygenase pathways, and inhibition of inflammation will be considered. This review will point out areas for future research where more evidence is needed on the effects of lycopene on the etiology of chronic disease.